Base de dados : MEDLINE
Pesquisa : D06.472.699.649 [Categoria DeCS]
Referências encontradas : 790 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 79 ir para página                         

  1 / 790 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28278220
[Au] Autor:Lim H; Powell S; Mcnamara HC; Howie AF; Doust A; Bowman ME; Smith R; Norman JE; Stock SJ
[Ad] Endereço:Tommy's Centre for Maternal and Fetal Health, MRC Centre for Reproductive Health, University of Edinburgh Queen's Medical Research Institute, Edinburgh, United Kingdom.
[Ti] Título:Placental hormone profiles as predictors of preterm birth in twin pregnancy: A prospective cohort study.
[So] Source:PLoS One;12(3):e0173732, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The objective of the study was to analyse placental hormone profiles in twin pregnancies to determine if they could be used to predict preterm birth. STUDY DESIGN: Progesterone, estradiol, estriol and corticotropin-releasing hormone were measured using competitive immunoassay and radioimmunoassay in serum and saliva samples of 98 women with twin pregnancies,at 3 or more gestational timepoints. Hormone profiles throughout gestation were compared between very preterm (<34 weeks; n = 8), preterm (<37 weeks; n = 40) and term (37+ weeks; n = 50) deliveries. RESULTS: No significant differences were found between preterm and term deliveries in either absolute hormone concentrations or ratios. Estimated hormone concentrations and ratios at 26 weeks did not appear to predict preterm delivery. Salivary and serum hormone concentrations were generally poorly correlated. CONCLUSION: Our results suggest that serial progesterone, estradiol, estriol and corticotropin-releasing hormone measurements in saliva and serum are not robust biomarkers for preterm birth in twin pregnancies.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Trabalho de Parto Prematuro/diagnóstico
Hormônios Placentários/sangue
[Mh] Termos MeSH secundário: Adolescente
Adulto
Hormônio Liberador da Corticotropina/sangue
Estradiol/sangue
Estriol/sangue
Feminino
Idade Gestacional
Seres Humanos
Recém-Nascido
Trabalho de Parto Prematuro/sangue
Trabalho de Parto Prematuro/prevenção & controle
Valor Preditivo dos Testes
Gravidez
Segundo Trimestre da Gravidez
Gravidez de Gêmeos
Progesterona/sangue
Estudos Prospectivos
Radioimunoensaio
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; TWIN STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Placental Hormones); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 9015-71-8 (Corticotropin-Releasing Hormone); FB33469R8E (Estriol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173732


  2 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28043376
[Au] Autor:Wojciechowska A; Mlynarczuk J; Kotwica J
[Ad] Endereço:Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
[Ti] Título:Disorders in barrier protein mRNA expression and placenta secretory activity under the influence of polychlorinated biphenyls in vitro.
[So] Source:Theriogenology;89:9-19, 2017 Feb.
[Is] ISSN:1879-3231
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pregnancy disorders are often correlated with the presence of organic pollutants in the tissues of living bodies. The aim of this study was to investigate the effects (over 24 and 48 hours) of polychlorinated biphenyls (PCBs) 153, 126, and 77 at doses of 1, 10, and 100 ng/mL on barrier function and secretory activity in cow placentome sections collected during the second trimester of pregnancy. None of the PCBs affected the viability of the sections (P > 0.05). Polychlorinated biphenyl 153 decreased (P < 0.05) connexin 26 (Cx 26) mRNA expression, and all three PCBs reduced (P < 0.05) Cx 43 mRNA expression. Cx 32 mRNA expression showed a downward trend (P > 0.05) under the influence of PCBs 126 and 77. Moreover, PCBs 153 and 126 increased keratin 8 (KRT8) mRNA expression, whereas all PCBs decreased (P < 0.05) placenta specific protein 1 (PLAC-1) mRNA expression without changing (P > 0.05) hypoxia inducible factor 1α (HIF1α) mRNA expression. Concomitantly, PCBs 153 and 126 stimulated (P < 0.05) cyclooxygenase 2 (COX-2) mRNA expression, all PCBs increased (P < 0.05) prostaglandin E2 synthase (PGES) mRNA expression, and PCBs 126 and 77 increased prostaglandin E2 (PGE2) secretion. All three PCBs decreased (P < 0.05) prostaglandin F2α synthase (PGFS) mRNA expression and prostaglandin F2α (PGF2α) secretion. In addition, all three PCBs increased (P < 0.05) neurophysin I/oxytocin (NP-I/OT) mRNA expression and OT secretion but did not affect peptidyl-glycine-α-amidating monooxygenase (PGA) mRNA expression (P > 0.05). Moreover, the PCBs increased (P < 0.05) estradiol (E2) secretion, whereas progesterone (P4) secretion remained unchanged (P > 0.05). These changes could affect trophoblast invasion and uterine contractility and thus impact the course of gestation and/or fetal development in the cow.
[Mh] Termos MeSH primário: Poluentes Ambientais/toxicidade
Placenta/efeitos dos fármacos
Bifenilos Policlorados/toxicidade
Proteoma/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Conexinas/genética
Conexinas/metabolismo
Relação Dose-Resposta a Droga
Feminino
Regulação da Expressão Gênica
Placenta/metabolismo
Placenta/secreção
Hormônios Placentários/genética
Hormônios Placentários/secreção
Gravidez
Prostaglandinas/secreção
Proteoma/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (Environmental Pollutants); 0 (Placental Hormones); 0 (Prostaglandins); 0 (Proteome); 0 (RNA, Messenger); DFC2HB4I0K (Polychlorinated Biphenyls)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE


  3 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27894940
[Au] Autor:Wojciechowska A; Mlynarczuk J; Kotwica J
[Ad] Endereço:Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Tuwima 10, 10-747 Olsztyn, Poland.
[Ti] Título:Changes in the mRNA expression of structural proteins, hormone synthesis and secretion from bovine placentome sections after DDT and DDE treatment.
[So] Source:Toxicology;375:1-9, 2017 Jan 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Disorders in the barrier function and secretory activity of the placenta can be caused by xenobiotics (XB) present in the environment and their accumulation in tissues of living organisms. Thus, the aim of this study was to investigate the effect of 1,1,1-trichloro-2,2,-bis-4-chlorophenyl-ethane (DDT) and its metabolite 1,1-dichloro-2,2-bis-4-chlorophenyl-ethene (DDE) (for 24 or 48h) at doses of 1, 10 or 100ng/ml on the function of cow placentome sections in the second trimester of pregnancy. DDT and DDE affected neither (P>0.05) the viability nor hypoxia inducible factor 1 (HIF1α) mRNA expression of the sections. XB decreased (P<0.05) connexin (Cx) 26, 32, 43 and placenta-specific 1 (PLAC-1) mRNA expression but did not affect (P>0.05) keratin 8 (KRT8) mRNA expression. DDT and DDE also reduced (P<0.05) prostaglandin F2α (PGF2α) synthase (PGFS) mRNA expression, while DDT increased (P<0.05) prostaglandin E2 (PGE2) synthase (PGES) mRNA expression. Neither cyclooxygenase 2 (COX-2) mRNA expression nor PGF2α and PGE2 secretion were affected. Both DDT and DDE increased (P<0.05) neurophysin I/oxytocin (NP1/OT) mRNA expression and oxytocin (OT), oestradiol (E2) and progesterone (P4) secretion while DDT stimulated only 3ß-hydroxysteroid dehydrogenase (3ßHSD) and cholesterol side-chain cleavage enzyme (CYP11A1) mRNA expression (P<0.05). In summary, DDT and DDE impaired the barrier function and secretory activity of the placenta. Thus, these compounds can disrupt trophoblast invasion, myometrium contractility and gas/nutrient exchange throughout pregnancy in cows.
[Mh] Termos MeSH primário: DDT/toxicidade
Diclorodifenil Dicloroetileno/toxicidade
Placenta/efeitos dos fármacos
Placenta/metabolismo
Hormônios Placentários/biossíntese
RNA Mensageiro/biossíntese
[Mh] Termos MeSH secundário: Animais
Bovinos
Conexinas/biossíntese
Conexinas/genética
Relação Dose-Resposta a Droga
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Inseticidas/toxicidade
Placenta/secreção
Hormônios Placentários/genética
Hormônios Placentários/secreção
Gravidez
Proteínas da Gravidez/biossíntese
Proteínas da Gravidez/genética
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (Insecticides); 0 (PLAC1 protein, human); 0 (Placental Hormones); 0 (Pregnancy Proteins); 0 (RNA, Messenger); 4M7FS82U08 (Dichlorodiphenyl Dichloroethylene); CIW5S16655 (DDT)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE


  4 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27899144
[Au] Autor:Hookham MB; Ali IH; O'Neill CL; Hackett E; Lambe MH; Schmidt T; Medina RJ; Chamney S; Rao B; McLoone E; Sweet D; Stitt AW; Brazil DP
[Ad] Endereço:Centre for Experimental Medicine, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7BL, UK.
[Ti] Título:Hypoxia-induced responses by endothelial colony-forming cells are modulated by placental growth factor.
[So] Source:Stem Cell Res Ther;7(1):173, 2016 Nov 29.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Endothelial colony-forming cells (ECFCs), also termed late outgrowth endothelial cells, are a well-defined circulating endothelial progenitor cell type with an established role in vascular repair. ECFCs have clear potential for cell therapy to treat ischaemic disease, although the precise mechanism(s) underlying their response to hypoxia remains ill-defined. METHODS: In this study, we isolated ECFCs from umbilical cord blood and cultured them on collagen. We defined the response of ECFCs to 1% O exposure at acute and chronic time points. RESULTS: In response to low oxygen, changes in ECFC cell shape, proliferation, size and cytoskeleton phenotype were detected. An increase in the number of senescent ECFCs also occurred as a result of long-term culture in 1% O . Low oxygen exposure altered ECFC migration and tube formation in Matrigel®. Increases in angiogenic factors secreted from ECFCs exposed to hypoxia were also detected, in particular, after treatment with placental growth factor (PlGF). Exposure of cells to agents that stabilise hypoxia-inducible factors such as dimethyloxalylglycine (DMOG) also increased PlGF levels. Conditioned medium from both hypoxia-treated and DMOG-treated cells inhibited ECFC tube formation. This effect was reversed by the addition of PlGF neutralising antibody to the conditioned medium, confirming the direct role of PlGF in this effect. CONCLUSIONS: This study deepens our understanding of the response of ECFCs to hypoxia and also identifies a novel and important role for PlGF in regulating the vasculogenic potential of ECFCs.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Células Endoteliais/fisiologia
Hipóxia/metabolismo
Hipóxia/patologia
Fator de Crescimento Placentário/metabolismo
Hormônios Placentários/metabolismo
[Mh] Termos MeSH secundário: Aminoácidos Dicarboxílicos/metabolismo
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Células Cultivadas
Colágeno/metabolismo
Meios de Cultivo Condicionados/metabolismo
Combinação de Medicamentos
Células Progenitoras Endoteliais/metabolismo
Sangue Fetal/metabolismo
Sangue Fetal/fisiologia
Seres Humanos
Laminina/metabolismo
Neovascularização Fisiológica/fisiologia
Proteoglicanas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids, Dicarboxylic); 0 (Culture Media, Conditioned); 0 (Drug Combinations); 0 (Laminin); 0 (PGF protein, human); 0 (Placental Hormones); 0 (Proteoglycans); 119978-18-6 (matrigel); 144589-93-5 (Placenta Growth Factor); 9007-34-5 (Collagen); VVW38EB8YS (oxalylglycine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE


  5 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27018791
[Au] Autor:Gonzalez PN; Gasperowicz M; Barbeito-Andrés J; Klenin N; Cross JC; Hallgrímsson B
[Ad] Endereço:Instituto de Genética Veterinaria, CCT-CONICET, La Plata, Argentina.
[Ti] Título:Chronic Protein Restriction in Mice Impacts Placental Function and Maternal Body Weight before Fetal Growth.
[So] Source:PLoS One;11(3):e0152227, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mechanisms of resource allocation are essential for maternal and fetal survival, particularly when the availability of nutrients is limited. We investigated the responses of feto-placental development to maternal chronic protein malnutrition to test the hypothesis that maternal low protein diet produces differential growth restriction of placental and fetal tissues, and adaptive changes in the placenta that may mitigate impacts on fetal growth. C57BL/6J female mice were fed either a low-protein diet (6% protein) or control isocaloric diet (20% protein). On embryonic days E10.5, 17.5 and 18.5 tissue samples were prepared for morphometric, histological and quantitative RT-PCR analyses, which included markers of trophoblast cell subtypes. Potential endocrine adaptations were assessed by the expression of Prolactin-related hormone genes. In the low protein group, placenta weight was significantly lower at E10.5, followed by reduction of maternal weight at E17.5, while the fetuses became significantly lighter no earlier than at E18.5. Fetal head at E18.5 in the low protein group, though smaller than controls, was larger than expected for body size. The relative size and shape of the cranial vault and the flexion of the cranial base was affected by E17.5 and more severely by E18.5. The junctional zone, a placenta layer rich in endocrine and energy storing glycogen cells, was smaller in low protein placentas as well as the expression of Pcdh12, a marker of glycogen trophoblast cells. Placental hormone gene Prl3a1 was altered in response to low protein diet: expression was elevated at E17.5 when fetuses were still growing normally, but dropped sharply by E18.5 in parallel with the slowing of fetal growth. This model suggests that nutrients are preferentially allocated to sustain fetal and brain growth and suggests the placenta as a nutrient sensor in early gestation with a role in mitigating impacts of poor maternal nutrition on fetal growth.
[Mh] Termos MeSH primário: Dieta com Restrição de Proteínas
Desenvolvimento Fetal/fisiologia
Placenta/fisiologia
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Encéfalo/fisiologia
Caderinas/genética
Caderinas/metabolismo
Desenvolvimento Embrionário
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Hormônios Placentários/genética
Hormônios Placentários/metabolismo
Gravidez
Prolactina/genética
Prolactina/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cadherins); 0 (Pcdh12 protein, mouse); 0 (Placental Hormones); 9002-62-4 (Prolactin)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160329
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0152227


  6 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26918450
[Au] Autor:Vert A; Castro J; Ribó M; Benito A; Vilanova M
[Ad] Endereço:Laboratori d'Enginyeria de Proteïnes, Departament de Biologia, Facultat de Ciències, Universitat de Girona, Girona, Spain.
[Ti] Título:A nuclear-directed human pancreatic ribonuclease (PE5) targets the metabolic phenotype of cancer cells.
[So] Source:Oncotarget;7(14):18309-24, 2016 Apr 05.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ribonucleases represent a new class of antitumor RNA-damaging drugs. However, many wild-type members of the vertebrate secreted ribonuclease family are not cytotoxic because they are not able to evade the cytosolic ribonuclease inhibitor. We previously engineered the human pancreatic ribonuclease to direct it to the cell nucleus where the inhibitor is not present. The best characterized variant is PE5 that kills cancer cells through apoptosis mediated by the p21(WAF1/CIP1) induction and the inactivation of JNK. Here, we have used microarray-derived transcriptional profiling to identify PE5 regulated genes on the NCI/ADR-RES ovarian cancer cell line. RT-qPCR analyses have confirmed the expression microarray findings. The results show that PE5 cause pleiotropic effects. Among them, it is remarkable the down-regulation of multiple genes that code for enzymes involved in deregulated metabolic pathways in cancer cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Redes e Vias Metabólicas/genética
Neoplasias Ovarianas/patologia
Ribonuclease Pancreático/farmacologia
Proteínas Supressoras de Tumor/biossíntese
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Regulação para Baixo/efeitos dos fármacos
Feminino
Glucose/metabolismo
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Redes e Vias Metabólicas/efeitos dos fármacos
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/metabolismo
Hormônios Placentários/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Ribonuclease Pancreático/metabolismo
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Placental Hormones); 0 (Reactive Oxygen Species); 0 (Tumor Suppressor Proteins); 120178-77-0 (placental ribonuclease inhibitor); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.1.27.5 (Ribonuclease, Pancreatic); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160227
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.7579


  7 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26893355
[Au] Autor:Tsai YC; Cooke NE; Liebhaber SA
[Ad] Endereço:Department of Genetics and Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, PA 19104, USA.
[Ti] Título:Long-range looping of a locus control region drives tissue-specific chromatin packing within a multigene cluster.
[So] Source:Nucleic Acids Res;44(10):4651-64, 2016 Jun 02.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The relationships of higher order chromatin organization to mammalian gene expression remain incompletely defined. The human Growth Hormone (hGH) multigene cluster contains five gene paralogs. These genes are selectively activated in either the pituitary or the placenta by distinct components of a remote locus control region (LCR). Prior studies have revealed that appropriate activation of the placental genes is dependent not only on the actions of the LCR, but also on the multigene composition of the cluster itself. Here, we demonstrate that the hGH LCR 'loops' over a distance of 28 kb in primary placental nuclei to make specific contacts with the promoters of the two GH genes in the cluster. This long-range interaction sequesters the GH genes from the three hCS genes which co-assemble into a tightly packed 'hCS chromatin hub'. Elimination of the long-range looping, via specific deletion of the placental LCR components, triggers a dramatic disruption of the hCS chromatin hub. These data reveal a higher-order structural pathway by which long-range looping from an LCR impacts on local chromatin architecture that is linked to tissue-specific gene regulation within a multigene cluster.
[Mh] Termos MeSH primário: Cromatina/química
Hormônio do Crescimento Humano/genética
Região de Controle de Locus Gênico
Família Multigênica
[Mh] Termos MeSH secundário: Animais
Fator de Ligação a CCCTC
Cromatina/metabolismo
Hormônio do Crescimento/genética
Seres Humanos
Camundongos Transgênicos
Especificidade de Órgãos
Hormônios Placentários/genética
Regiões Promotoras Genéticas
Proteínas Repressoras/metabolismo
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCCTC-Binding Factor); 0 (CTCF protein, human); 0 (Chromatin); 0 (Ctcf protein, mouse); 0 (GH2 protein, human); 0 (Placental Hormones); 0 (Repressor Proteins); 12629-01-5 (Human Growth Hormone); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160220
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw090


  8 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26671184
[Au] Autor:Liao S; Vickers MH; Stanley JL; Ponnampalam AP; Baker PN; Perry JK
[Ad] Endereço:Liggins Institute (S.L., M.H.V., J.L.S., A.P.P., P.N.B., J.K.P.), University of Auckland, Auckland 1023, New Zealand; Gravida: National Centre for Growth and Development (S.L., M.H.V., J.L.S., A.P.P., P.N.B., J.K.P.), Auckland 1142, New Zealand; and The First Affiliated Hospital (S.L.), Sun Yat-sen
[Ti] Título:The Placental Variant of Human Growth Hormone Reduces Maternal Insulin Sensitivity in a Dose-Dependent Manner in C57BL/6J Mice.
[So] Source:Endocrinology;157(3):1175-86, 2016 Mar.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human placental GH variant (GH-V) is secreted continuously from the syncytiotrophoblast layer of the placenta during pregnancy and is thought to play a key role in the maternal adaptation to pregnancy. Maternal GH-V concentrations are closely related to fetal growth in humans. GH-V has also been proposed as a potential candidate to mediate insulin resistance observed later in pregnancy. To determine the effect of maternal GH-V administration on maternal and fetal growth and metabolic outcomes during pregnancy, we examined the dose-response relationship for GH-V administration in a mouse model of normal pregnancy. Pregnant C57BL/6J mice were randomized to receive vehicle or GH-V (0.25, 1, 2, or 5 mg/kg · d) by osmotic pump from gestational days 12.5 to 18.5. Fetal linear growth was slightly reduced in the 5 mg/kg dose compared with vehicle and the 0.25 mg/kg groups, respectively, whereas placental weight was not affected. GH-V treatment did not affect maternal body weights or food intake. However, treatment with 5 mg/kg · d significantly increased maternal fasting plasma insulin concentrations with impaired insulin sensitivity observed at day 18.5 as assessed by homeostasis model assessment. At 5 mg/kg · d, there was also an increase in maternal hepatic GH receptor/binding protein (Ghr/Ghbp) and IGF binding protein 3 (Igfbp3) mRNA levels, but GH-V did not alter maternal plasma IGF-1 concentrations or hepatic Igf-1 mRNA expression. Our findings suggest that at higher doses, GH-V treatment can cause hyperinsulinemia and is a likely mediator of the insulin resistance associated with late pregnancy.
[Mh] Termos MeSH primário: Hormônio do Crescimento Humano/farmacologia
Resistência à Insulina
Insulina/metabolismo
Hormônios Placentários/farmacologia
Prenhez/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Proteínas de Transporte/efeitos dos fármacos
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Ingestão de Alimentos/efeitos dos fármacos
Feminino
Desenvolvimento Fetal/efeitos dos fármacos
Seres Humanos
Fator de Crescimento Insulin-Like I/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/genética
Fator de Crescimento Insulin-Like I/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Gravidez
Prenhez/metabolismo
RNA Mensageiro/efeitos dos fármacos
Proteínas Recombinantes/farmacologia
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (IGFBP5-interacting protein, mouse); 0 (Insulin); 0 (Placental Hormones); 0 (RNA, Messenger); 0 (Recombinant Proteins); 0 (insulin-like growth factor-1, mouse); 0 (somatotropin-binding protein); 12629-01-5 (Human Growth Hormone); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160227
[Lr] Data última revisão:
160227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151217
[St] Status:MEDLINE
[do] DOI:10.1210/en.2015-1718


  9 / 790 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26589570
[Au] Autor:Ringholm L; Juul A; Pedersen-Bjergaard U; Thorsteinsson B; Damm P; Mathiesen ER
[Ad] Endereço:Center for Pregnant Women with Diabetes, Rigshospitalet, Copenhagen, Denmark; Department of Endocrinology, Rigshospitalet, Copenhagen, Denmark; Steno Diabetes Center, Gentofte, Denmark. Electronic address: enel@dadlnet.dk.
[Ti] Título:Lower levels of placental growth hormone in early pregnancy in women with type 1 diabetes and large for gestational age infants.
[So] Source:Growth Horm IGF Res;25(6):312-5, 2015 Dec.
[Is] ISSN:1532-2238
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate whether levels of placental growth hormone (GH) and Insulin-like Growth Factor-I (IGF-I) are associated with development of LGA infants in pregnant women with type 1 diabetes. DESIGN: Observational study of 103 consecutive pregnant women with long-term type 1 diabetes and median HbA1c 6.6% (range 4.9-10.5) (49 mmol/mol (30-91)) in early pregnancy. At 8, 14, 21, 27 and 33 weeks weight was recorded and blood was sampled for measurements of placental GH, IGF-I and HbA1c. LGA was defined as birth weight >90th percentile after adjustment for gender and gestational age. RESULTS: Throughout pregnancy placental GH levels were similar in 51 (50%) women delivering LGA infants compared with the remaining women except at 8 weeks where placental GH levels were lower in women with LGA infants (1.1 ng/ml (0.1-4.3) vs. 1.7 (0.3-11.7), p = 0.04). IGF-I levels were similar in women with and without LGA infants (p=0.97). Gestational age at first blood sampling was similar in women with and without LGA infants (60 days (37-89) vs. 61.5 (42-94), p = 0.42). Placental GH levels at 14 weeks correlated negatively with weight gain in early pregnancy (r=-0.32, p=0.002). As predictors of LGA infants,multivariate logistic regression analysis identified placental GH levels at 8 weeks (OR 0.4 (95% CI: 0.2-0.9), p = 0.02), HbA1c at 33 weeks (3.6 (1.3-9.9), p = 0.01) and parity ≥1 (3.1 (1.3-7.5), p = 0.01) after adjustment for pre-pregnancy BMI. CONCLUSIONS: Women delivering LGA infants had lower placental GH levels in early pregnancy. Growth factors and maternal weight gain in early pregnancy may be important for healthy fetal growth.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/metabolismo
Macrossomia Fetal/metabolismo
Hormônio do Crescimento/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Placenta/metabolismo
Hormônios Placentários/metabolismo
Gravidez em Diabéticas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Feminino
Hemoglobina A Glicada/metabolismo
Seres Humanos
Recém-Nascido
Modelos Logísticos
Análise Multivariada
Gravidez
Ganho de Peso
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GH2 protein, human); 0 (Glycated Hemoglobin A); 0 (IGF1 protein, human); 0 (Placental Hormones); 0 (hemoglobin A1c protein, human); 67763-96-6 (Insulin-Like Growth Factor I); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151122
[St] Status:MEDLINE


  10 / 790 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26186596
[Au] Autor:Pidoux G; Gerbaud P; Guibourdenche J; Thérond P; Ferreira F; Simasotchi C; Evain-Brion D; Gil S
[Ad] Endereço:INSERM, U1139, Paris, France; Université Paris Descartes, Paris, France; Université Paris-Sud, Faculté de Pharmacie, Châtenay-Malabry Cedex, France.
[Ti] Título:Formaldehyde Crosses the Human Placenta and Affects Human Trophoblast Differentiation and Hormonal Functions.
[So] Source:PLoS One;10(7):e0133506, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chorionic villus of the human placenta is the source of specific endocrine functions and nutrient exchanges. These activities are ensured by the syncytiotrophobast (ST), which bathes in maternal blood. The ST arises and regenerates throughout pregnancy by fusion of underlying cytotrophoblasts (CT). Any anomaly of ST formation or regeneration can affect pregnancy outcome and fetal growth. Because of its direct interaction with maternal blood, the ST is sensitive to drugs, pollutants and xenohormones. Ex vivo assays of perfused cotyledon show that formaldehyde, a common pollutant present in furniture, paint and plastics, can accumulate in the human placenta and cross to the fetal compartment. By means of RT-qPCR, immunoblot and immunocytochemistry experiments, we demonstrate in vitro that formaldehyde exerts endocrine toxicity on human trophoblasts, including a decrease in the production of protein hormones of pregnancy. In addition, formaldehyde exposure triggered human trophoblast fusion by upregulating syncitin-1 receptor expression (ASC-type amino-acid transporter 2: ASCT2). Moreover, we show that formaldehyde-exposed trophoblasts present an altered redox status associated with oxidative stress, and an increase in ASCT2 expression intended to compensate for this stress. Finally, we demonstrate that the adverse effects of formaldehyde on trophoblast differentiation and fusion are reversed by N-acetyl-L-cysteine (Nac), an antioxidant.
[Mh] Termos MeSH primário: Diferenciação Celular
Formaldeído/toxicidade
Hormônios Placentários/metabolismo
Trofoblastos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Sistema ASC de Transporte de Aminoácidos/genética
Sistema ASC de Transporte de Aminoácidos/metabolismo
Células Cultivadas
Feminino
Seres Humanos
Troca Materno-Fetal
Antígenos de Histocompatibilidade Menor
Estresse Oxidativo
Circulação Placentária
Gravidez
Trofoblastos/citologia
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Transport System ASC); 0 (Minor Histocompatibility Antigens); 0 (Placental Hormones); 0 (SLC1A5 protein, human); 1HG84L3525 (Formaldehyde)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150718
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0133506



página 1 de 79 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde