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  1 / 3055 MEDLINE  
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[PMID]:28202518
[Au] Autor:Sundaram KM; Zhang Y; Mitra AK; Kouadio JK; Gwin K; Kossiakoff AA; Roman BB; Lengyel E; Piccirilli JA
[Ad] Endereço:Department of Biochemistry & Molecular Biology, and Chemistry, The University of Chicago, Chicago, Illinois.
[Ti] Título:Prolactin Receptor-Mediated Internalization of Imaging Agents Detects Epithelial Ovarian Cancer with Enhanced Sensitivity and Specificity.
[So] Source:Cancer Res;77(7):1684-1696, 2017 Apr 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Poor prognosis of ovarian cancer, the deadliest of the gynecologic malignancies, reflects major limitations associated with detection and diagnosis. Current methods lack high sensitivity to detect small tumors and high specificity to distinguish malignant from benign tissue, both impeding diagnosis of early and metastatic cancer stages and leading to costly and invasive surgeries. Tissue microarray analysis revealed that >98% of ovarian cancers express the prolactin receptor (PRLR), forming the basis of a new molecular imaging strategy. We fused human placental lactogen (hPL), a specific and tight binding PRLR ligand, to magnetic resonance imaging (gadolinium) and near-infrared fluorescence imaging agents. Both in tissue culture and in mouse models, these imaging bioconjugates underwent selective internalization into ovarian cancer cells via PRLR-mediated endocytosis. Compared with current clinical MRI techniques, this targeted approach yielded both enhanced signal-to-noise ratio from accumulation of signal via selective internalization and improved specificity conferred by PRLR upregulation in malignant ovarian cancer. These features endow PRLR-targeted imaging with the potential to transform ovarian cancer detection. .
[Mh] Termos MeSH primário: Imagem por Ressonância Magnética/métodos
Neoplasias Epiteliais e Glandulares/diagnóstico por imagem
Neoplasias Ovarianas/diagnóstico por imagem
Receptores da Prolactina/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Endocitose
Feminino
Gadolínio DTPA
Seres Humanos
Camundongos
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Ovarianas/metabolismo
Lactogênio Placentário/metabolismo
Prolactina/metabolismo
Receptores da Prolactina/análise
Sensibilidade e Especificidade
Análise Serial de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Prolactin); 9002-62-4 (Prolactin); 9035-54-5 (Placental Lactogen); K2I13DR72L (Gadolinium DTPA)
[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:170217
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-1454


  2 / 3055 MEDLINE  
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[PMID]:27743526
[Au] Autor:Hughes CK; Xie MM; McCoski SR; Ealy AD
[Ad] Endereço:Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.
[Ti] Título:Activities for leptin in bovine trophoblast cells.
[So] Source:Domest Anim Endocrinol;58:84-89, 2017 Jan.
[Is] ISSN:1879-0054
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Leptin is involved in various reproductive processes in humans and rodents, including placental development and function. The specific ways that leptin influences placental development and function in cattle are poorly understood. This work was completed to explore how leptin regulates hormone, cytokine and metalloprotease transcript abundance, and cell proliferation in cultured bovine trophoblast cells. In the first set of studies, cells were cultured in the presence of graded recombinant bovine leptin concentrations (0, 10, 50, 250 ng/mL) for 6 or 24 h. Transcript profiles were examined from extracted RNA. Leptin supplementation did not affect abundance of the maternal recognition of pregnancy factor, interferon-tau (IFNT), but leptin increased (P < 0.05) abundance of chorionic somatomammotropin hormone 2 (CSH2; ie, placental lactogen) at both 6 and 24 h at each concentration tested. At 24 h, the greatest CSH2 abundance (P < 0.05) was detected in cells supplemented with 50 ng/mL leptin. Transcript abundance of the remodeling factor, metalloprotease 2 (MMP2), was greater (P < 0.05) in leptin-treated cells at 24 h but not at 6 h. The 24 h MMP2 response was greatest (P < 0.05) at 250 ng/mL. Transcript abundance for MMP9 was not altered by leptin treatment. In a separate set of studies, cell proliferation assays were completed. Leptin supplementation did not affect bovine trophoblast cell line proliferation at any dose tested. In conclusion, leptin supplementation did not affect bovine trophoblast cell proliferation or IFNT expression, but leptin increases CSH2 and MMP2 transcript abundance. Both of these factors are involved with peri-implantation and postimplantation placental development and function, and this implicates leptin as a potential mediator of early placental development and function in cattle.
[Mh] Termos MeSH primário: Bovinos
Leptina/fisiologia
Trofoblastos/fisiologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/fisiologia
Células Cultivadas
Feminino
Expressão Gênica/efeitos dos fármacos
Interferon Tipo I
Leptina/administração & dosagem
Metaloproteinase 2 da Matriz/genética
Placenta/fisiologia
Lactogênio Placentário/genética
Gravidez
Proteínas da Gravidez
RNA Mensageiro/análise
Proteínas Recombinantes/administração & dosagem
Trofoblastos/citologia
Trofoblastos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Type I); 0 (Leptin); 0 (Pregnancy Proteins); 0 (RNA, Messenger); 0 (Recombinant Proteins); 0 (trophoblastin); 9035-54-5 (Placental Lactogen); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161016
[St] Status:MEDLINE


  3 / 3055 MEDLINE  
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[PMID]:27669115
[Au] Autor:Mukai Y; Hoshi F; Sato S
[Ad] Endereço:School of Nutrition and Dietetics, Faculty of Health and Social Work, Kanagawa University of Human Services, Kanagawa, Japan. mukai-skr@kuhs.ac.jp.
[Ti] Título:Effect of fructose on the phosphorylation of AMP-activated protein kinase and acetyl-CoA carboxylase in HepG2 cells stimulated with placental lactogen.
[So] Source:Birth Defects Res B Dev Reprod Toxicol;107(4-5):206-210, 2016 Aug.
[Is] ISSN:1542-9741
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: High fructose intake induces disruption of lipid metabolism via AMP-activated protein kinase (AMPK) signaling in the liver and peripheral tissues. Maternal lipid metabolism is physiologically altered by the activity of pregnancy hormones such as human placental lactogen (PL). To elucidate the influence of high fructose intake on hepatic lipid metabolism during pregnancy, we examined the effects of fructose on lipid metabolism via the AMPK pathway in hepatocytes stimulated with PL. METHODS: Human hepatoma cells (HepG2) were treated with D(-)-fructose in the presence or absence of PL. Intracellular lipid contents were measured. The total and phosphorylated protein content of AMPK and acetyl-CoA carboxylase (ACC) was quantified by Western blotting. RESULTS: The intracellular triacylglycerol level in fructose-treated HepG2 cells decreased significantly compared with that in untreated cells in the presence, but not absence, of PL. AMPK and ACC phosphorylation increased significantly and concentration-dependently in fructose-treated HepG2 cells in the presence of PL. CONCLUSION: Our results suggest that fructose treatment reduces triacylglycerol levels via AMPK/ACC signaling in PL-stimulated hepatocytes. These findings suggest that high fructose intake during pregnancy might impair lipid metabolism in the maternal liver.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Acetil-CoA Carboxilase/metabolismo
Frutose/toxicidade
Hepatócitos/efeitos dos fármacos
Lactogênio Placentário/farmacologia
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Acetil-CoA Carboxilase/genética
Células Hep G2
Hepatócitos/metabolismo
Seres Humanos
Metabolismo dos Lipídeos/efeitos dos fármacos
Fosforilação
Transdução de Sinais
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Triglycerides); 30237-26-4 (Fructose); 9035-54-5 (Placental Lactogen); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160927
[St] Status:MEDLINE
[do] DOI:10.1002/bdrb.21186


  4 / 3055 MEDLINE  
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[PMID]:27615133
[Au] Autor:Baeyens L; Hindi S; Sorenson RL; German MS
[Ad] Endereço:Diabetes Center, University of California San Francisco, San Francisco.
[Ti] Título:ß-Cell adaptation in pregnancy.
[So] Source:Diabetes Obes Metab;18 Suppl 1:63-70, 2016 Sep.
[Is] ISSN:1463-1326
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pregnancy in placental mammals places unique demands on the insulin-producing ß-cells in the pancreatic islets of Langerhans. The pancreas anticipates the increase in insulin resistance that occurs late in pregnancy by increasing ß-cell numbers and function earlier in pregnancy. In rodents, this ß-cell expansion depends on secreted placental lactogens that signal through the prolactin receptor. Then at the end of pregnancy, the ß-cell population contracts back to its pre-pregnancy size. In the current review, we focus on how glucose metabolism changes during pregnancy, how ß-cells anticipate these changes through their response to lactogens and what molecular mechanisms guide the adaptive compensation. In addition, we summarize current knowledge of ß-cell adaptation during human pregnancy and what happens when adaptation fails and gestational diabetes ensues. A better understanding of human ß-cell adaptation to pregnancy would benefit efforts to predict, prevent and treat gestational diabetes.
[Mh] Termos MeSH primário: Adaptação Fisiológica
Proliferação Celular
Glucose/metabolismo
Células Secretoras de Insulina/metabolismo
Insulina/secreção
Gravidez/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Gestacional/metabolismo
Feminino
Seres Humanos
Resistência à Insulina
Células Secretoras de Insulina/citologia
Camundongos
Lactogênio Placentário/metabolismo
Período Pós-Parto
Ratos
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Insulin); 333DO1RDJY (Serotonin); 9035-54-5 (Placental Lactogen); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160913
[St] Status:MEDLINE
[do] DOI:10.1111/dom.12716


  5 / 3055 MEDLINE  
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[PMID]:27208323
[Au] Autor:Retnakaran R; Ye C; Kramer CK; Connelly PW; Hanley AJ; Sermer M; Zinman B
[Ad] Endereço:Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, Canada Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada rretnakaran@mtsinai.on.ca.
[Ti] Título:Maternal Serum Prolactin and Prediction of Postpartum ß-Cell Function and Risk of Prediabetes/Diabetes.
[So] Source:Diabetes Care;39(7):1250-8, 2016 07.
[Is] ISSN:1935-5548
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The insulin resistance of mid- to late pregnancy poses a physiologic stress test for the pancreatic ß-cells, which must respond by markedly increasing their secretion of insulin. This response is achieved through an expansion of ß-cell mass induced by the hormones prolactin and human placental lactogen (HPL). Conversely, the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) has recently emerged as a negative regulator of ß-cell function in pregnancy. Given their respective roles in the ß-cell response to the stress test of gestation, we hypothesized that antepartum prolactin, HPL, and CMPF may relate to a woman's underlying glucoregulatory physiology and hence to her metabolic status after pregnancy. RESEARCH DESIGN AND METHODS: Three hundred and sixty-seven women underwent measurement of fasting serum prolactin, HPL, and CMPF in the late-2nd/early-3rd trimester, followed by an oral glucose tolerance test (OGTT) at 3 months postpartum that enabled assessment of glucose tolerance, insulin sensitivity/resistance, and ß-cell function (Insulin Secretion-Sensitivity Index-2 [ISSI-2]). RESULTS: The postpartum OGTT identified 301 women with normal glucose tolerance (NGT) and 66 with prediabetes or diabetes. Serum prolactin in pregnancy was higher in women with postpartum NGT compared with those with postpartum prediabetes/diabetes (mean 98.2 vs. 80.2 ng/mL, P = 0.0003), whereas HPL and CMPF did not differ between the groups. On multiple linear regression analyses, antepartum prolactin was an independent determinant of postpartum ISSI-2 (ß = 0.0016, t = 2.96, P = 0.003). Furthermore, higher serum prolactin in pregnancy independently predicted a lower risk of postpartum prediabetes/diabetes (odds ratio 0.50, 95% CI 0.35-0.72, P = 0.0002). CONCLUSIONS: Serum prolactin in pregnancy predicts postpartum ß-cell function and risk of prediabetes/diabetes.
[Mh] Termos MeSH primário: Diabetes Gestacional/sangue
Intolerância à Glucose/sangue
Células Secretoras de Insulina/fisiologia
Estado Pré-Diabético/sangue
Prolactina/sangue
[Mh] Termos MeSH secundário: Adulto
Glicemia/metabolismo
Feminino
Furanos/sangue
Teste de Tolerância a Glucose/métodos
Seres Humanos
Insulina/sangue
Resistência à Insulina/fisiologia
Lactogênio Placentário/sangue
Período Pós-Parto/fisiologia
Valor Preditivo dos Testes
Gravidez
Complicações na Gravidez/sangue
Terceiro Trimestre da Gravidez
Propionatos/sangue
Estudos Prospectivos
Análise de Regressão
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid); 0 (Blood Glucose); 0 (Furans); 0 (Insulin); 0 (Propionates); 9002-62-4 (Prolactin); 9035-54-5 (Placental Lactogen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171112
[Lr] Data última revisão:
171112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160522
[St] Status:MEDLINE
[do] DOI:10.2337/dc16-0043


  6 / 3055 MEDLINE  
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[PMID]:27124574
[Au] Autor:Al-Soudy AS; Nakanishi T; Mizuno S; Hasegawa Y; Shawki HH; Katoh MC; Basha WA; Ibrahim AE; El-Shemy HA; Iseki H; Yoshiki A; Hiromori Y; Nagase H; Takahashi S; Oishi H; Sugiyama F
[Ad] Endereço:Laboratory Animal Resource Center, University of Tsukuba, Tsukuba, Ibaraki, Japan.
[Ti] Título:Germline recombination in a novel Cre transgenic line, Prl3b1-Cre mouse.
[So] Source:Genesis;54(7):389-97, 2016 07.
[Is] ISSN:1526-968X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spermatogenesis is a complex and highly regulated process by which spermatogonial stem cells differentiate into spermatozoa. To better understand the molecular mechanisms of the process, the Cre/loxP system has been widely utilized for conditional gene knockout in mice. In this study, we generated a transgenic mouse line that expresses Cre recombinase under the control of the 2.5 kbp of the Prolactin family 3, subfamily b, member 1 (Prl3b1) gene promoter (Prl3b1-cre). Prl3b1 was initially reported to code for placental lactogen 2 (PL-2) protein in placenta along with increased expression toward the end of pregnancy. PL-2 was found to be expressed in germ cells in the testis, especially in spermatocytes. To analyze the specificity and efficiency of Cre recombinase activity in Prl3b1-cre mice, the mice were mated with reporter R26GRR mice, which express GFP ubiquitously before and tdsRed exclusively after Cre recombination. The systemic examination of Prl3b1-cre;R26GRR mice revealed that tdsRed-positive cells were detected only in the testis and epididymis. Fluorescence imaging of Prl3b1-cre;R26GRR testes suggested that Cre-mediated recombination took place in the germ cells with approximately 74% efficiency determined by in vitro fertilization. In conclusion, our results suggest that the Prl3b1-cre mice line provides a unique resource to understand testicular germ-cell development. genesis 54:389-397, 2016. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Proteínas Imediatamente Precoces/biossíntese
Proteínas Tirosina Fosfatases/biossíntese
Espermatogênese/genética
Espermatozoides/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica no Desenvolvimento
Técnicas de Inativação de Genes
Células Germinativas/crescimento & desenvolvimento
Células Germinativas/metabolismo
Proteínas Imediatamente Precoces/genética
Masculino
Camundongos
Lactogênio Placentário/genética
Proteínas Tirosina Fosfatases/genética
Espermatozoides/crescimento & desenvolvimento
Células-Tronco/metabolismo
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immediate-Early Proteins); 0 (Ptp4a3 protein, mouse); 0 (placental lactogen II); 9035-54-5 (Placental Lactogen); EC 3.1.3.48 (Protein Tyrosine Phosphatases)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160429
[St] Status:MEDLINE
[do] DOI:10.1002/dvg.22944


  7 / 3055 MEDLINE  
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[PMID]:26944942
[Au] Autor:Janssen AB; Tunster SJ; Heazell AE; John RM
[Ad] Endereço:Cardiff School of Biosciences, Cardiff University, Cardiff, Wales, CF10 3AX, UK. JensenAB1@cardiff.ac.uk.
[Ti] Título:Placental PHLDA2 expression is increased in cases of fetal growth restriction following reduced fetal movements.
[So] Source:BMC Med Genet;17:17, 2016 Mar 05.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Maternal perception of reduced fetal movements (RFM) is associated with increased risk of fetal growth restriction (FGR) and stillbirth, mediated by placental insufficiency. The maternally expressed imprinted gene PHLDA2 controls fetal growth, placental development and placental lactogen production in a mouse model. A number of studies have also demonstrated abnormally elevated placental PHLDA2 expression in human growth restricted pregnancies. This study examined whether PHLDA2 was aberrantly expressed in placentas of RFM pregnancies resulting in delivery of an FGR infant and explored a possible relationship between PHLDA2 expression and placental lactogen release from the human placenta. METHODS: Villous trophoblast samples were obtained from a cohort of women reporting RFM (N = 109) and PHLDA2 gene expression analysed. hPL levels were assayed in the maternal serum (N = 74). RESULTS: Placental PHLDA2 expression was significantly 2.3 fold higher in RFM pregnancies resulting in delivery of an infant with FGR (p < 0.01), with highest levels of PHLDA2 expression in the most severe cases. Placental PHLDA2 expression was associated with maternal serum hPL levels (r = -0.30, p = 0.008, n = 74) although this failed to reach statistical significance in multiple linear regression analysis controlling for birth weight (p = 0.07). CONCLUSIONS: These results further highlight a role for placental PHLDA2 in poor perinatal outcomes, specifically FGR associated with RFM. Furthermore, this study suggests a potential relationship between placental PHLDA2 expression and hPL production by the placenta, an association that requires further investigation in a larger cohort.
[Mh] Termos MeSH primário: Retardo do Crescimento Fetal/genética
Movimento Fetal
Proteínas Nucleares/genética
Placenta/metabolismo
[Mh] Termos MeSH secundário: Estudos de Coortes
Feminino
Desenvolvimento Fetal
Regulação da Expressão Gênica
Seres Humanos
Recém-Nascido
Modelos Lineares
Masculino
Lactogênio Placentário/sangue
Gravidez
Resultado da Gravidez
Natimorto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (TSSC3 protein); 9035-54-5 (Placental Lactogen)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160306
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-016-0279-1


  8 / 3055 MEDLINE  
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[PMID]:26887431
[Au] Autor:Baker CM; Goetzmann LN; Cantlon JD; Jeckel KM; Winger QA; Anthony RV
[Ad] Endereço:Animal Reproduction and Biotechnology Laboratory, Department of Biomedical Sciences, Colorado State University, Fort Collins, Colorado.
[Ti] Título:Development of ovine chorionic somatomammotropin hormone-deficient pregnancies.
[So] Source:Am J Physiol Regul Integr Comp Physiol;310(9):R837-46, 2016 May 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intrauterine growth restriction (IUGR) is a leading cause of neonatal mortality and morbidity. Chorionic somatomammotropin hormone (CSH), a placenta-specific secretory product found at high concentrations in maternal and fetal circulation throughout gestation, is significantly reduced in human and sheep IUGR pregnancies. The objective of this study was to knock down ovine CSH (oCSH) expression in vivo using lentiviral-mediated short-hairpin RNA to test the hypothesis that oCSH deficiency would result in IUGR of near-term fetal lambs. Three different lentiviral oCSH-targeting constructs were used and compared with pregnancies (n = 8) generated with a scrambled control (SC) lentiviral construct. Pregnancies were harvested at 135 days of gestation. The most effective targeting sequence, "target 6" (tg6; n = 8), yielded pregnancies with significant reductions (P ≤ 0.05) in oCSH mRNA (50%) and protein (38%) concentrations, as well as significant reductions (P ≤ 0.05) in placental (52%) and fetal (32%) weights compared with the SC pregnancies. Fetal liver weights were reduced 41% (P ≤ 0.05), yet fetal liver insulin-like growth factor-I (oIGF1) and -II mRNA concentrations were reduced (P ≤ 0.05) 82 and 71%, respectively, and umbilical artery oIGF1 concentrations were reduced 62% (P ≤ 0.05) in tg6 pregnancies. Additionally, fetal liver oIGF-binding protein (oIGFBP) 2 and oIGFBP3 mRNA concentrations were reduced (P ≤ 0.05), whereas fetal liver oIGFBP1 mRNA concentration was not impacted nor was maternal liver oIGF and oIGFBP mRNA concentrations or uterine artery oIGF1 concentrations (P ≥ 0.10). Based on our results, it appears that oCSH deficiency does result in IUGR, by impacting placental development as well as fetal liver development and function.
[Mh] Termos MeSH primário: Retardo do Crescimento Fetal/veterinária
Lactogênio Placentário/deficiência
Prenhez
Ovinos/fisiologia
[Mh] Termos MeSH secundário: Animais
Blastocisto/fisiologia
Feminino
Desenvolvimento Fetal
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Técnicas de Silenciamento de Genes
Inativação Gênica
Lentivirus
Placenta/fisiologia
Gravidez
Prenhez/fisiologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno
Somatomedinas/genética
Somatomedinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Somatomedins); 9035-54-5 (Placental Lactogen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160219
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00311.2015


  9 / 3055 MEDLINE  
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[PMID]:26352728
[Au] Autor:Ishii T; Matsuo N; Sato S; Ogata T; Tamai S; Anzo M; Kamimaki T; Sasaki G; Inokuchi M; Hori N; Amano N; Narumi S; Shibata H; Hasegawa T
[Ad] Endereço:Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan.
[Ti] Título:Human Chorionic Gonadotropin Stimulation Test in Prepubertal Children with Micropenis Can Accurately Predict Leydig Cell Function in Pubertal or Postpubertal Adolescents.
[So] Source:Horm Res Paediatr;84(5):305-10, 2015.
[Is] ISSN:1663-2826
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: To evaluate the accuracy of the human chorionic gonadotropin (hCG) stimulation test in children with micropenis in predicting later Leydig cell function. METHODS: We conducted a retrospective investigation of testosterone response to a 3-day hCG test (3,000 IU/m2/day) in prepuberty to indicate the need for hormone replacement therapy (HRT) in adolescence. RESULTS: Fifty Japanese boys (range, 0.8-15.4 years of age; median, 8.9) with micropenis were enrolled. Thirty-four spontaneously developed puberty and preserved the ability of testosterone production (group 1), while 16 did not develop any pubertal signs without HRT (group 2). Serum testosterone levels after the hCG test (post-hCG T) in group 2 (range, <0.05-1.1 ng/ml; median, 0.24) were significantly lower than in group 1 (range, 0.5-8.7 ng/ml; median, 2.4; p < 0.0001). Based on true positives who required continuous HRT, the area under the receiver-operating characteristics curve for post-hCG T was 0.983 [95% confidence interval (CI), 0.90-1.00]. The post-hCG T cut-off level corresponding to the Youden index was 1.1 ng/ml (95% CI, 1.0-1.1), with a sensitivity of 100.0% (95% CI, 79.4-100.0) and a specificity of 94.1% (95% CI, 80.3-99.3). CONCLUSIONS: The hCG test in prepubertal children with micropenis can be useful for predicting Leydig cell function in pubertal or postpubertal adolescents. The post-hCG T cut-off level of 1.1 ng/ml is recommended to screen for those who will likely require HRT for pubertal development.
[Mh] Termos MeSH primário: Doenças dos Genitais Masculinos/diagnóstico
Células Intersticiais do Testículo/efeitos dos fármacos
Pênis/anormalidades
Lactogênio Placentário/farmacologia
[Mh] Termos MeSH secundário: Adolescente
Grupo com Ancestrais do Continente Asiático
Criança
Pré-Escolar
Hormônio Foliculoestimulante/sangue
Hormônio Liberador de Gonadotropina/sangue
Hormônio Liberador de Gonadotropina/farmacologia
Terapia de Reposição Hormonal
Seres Humanos
Lactente
Masculino
Pênis/anatomia & histologia
Pênis/crescimento & desenvolvimento
Puberdade
Estudos Retrospectivos
Estimulação Química
Testosterona/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33515-09-2 (Gonadotropin-Releasing Hormone); 3XMK78S47O (Testosterone); 9002-68-0 (Follicle Stimulating Hormone); 9035-54-5 (Placental Lactogen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151120
[Lr] Data última revisão:
151120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150910
[St] Status:MEDLINE
[do] DOI:10.1159/000439234


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[PMID]:26269505
[Au] Autor:Rawn SM; Huang C; Hughes M; Shaykhutdinov R; Vogel HJ; Cross JC
[Ad] Endereço:Department of Comparative Biology & Experimental Medicine, University of Calgary, Calgary, Alberta, Canada Department of Biochemistry & Molecular Biology, University of Calgary, Calgary, Alberta, Canada.
[Ti] Título:Pregnancy Hyperglycemia in Prolactin Receptor Mutant, but Not Prolactin Mutant, Mice and Feeding-Responsive Regulation of Placental Lactogen Genes Implies Placental Control of Maternal Glucose Homeostasis.
[So] Source:Biol Reprod;93(3):75, 2015 Sep.
[Is] ISSN:1529-7268
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pregnancy is often viewed as a conflict between the fetus and mother over metabolic resources. Insulin resistance occurs in mothers during pregnancy but does not normally lead to diabetes because of an increase in the number of the mother's pancreatic beta cells. In mice, this increase is dependent on prolactin (Prl) receptor signaling but the source of the ligand has been unclear. Pituitary-derived Prl is produced during the first half of pregnancy in mice but the placenta produces Prl-like hormones from implantation to term. Twenty-two separate mouse genes encode the placenta Prl-related hormones, making it challenging to assess their roles in knockout models. However, because at least four of them are thought to signal through the Prl receptor, we analyzed Prlr mutant mice and compared their phenotypes with those of Prl mutants. We found that whereas Prlr mutants develop hyperglycemia during gestation, Prl mutants do not. Serum metabolome analysis showed that Prlr mutants showed other changes consistent with diabetes. Despite the metabolic changes, fetal growth was normal in Prlr mutants. Of the four placenta-specific, Prl-related hormones that have been shown to interact with the Prlr, their gene expression localizes to different endocrine cell types. The Prl3d1 gene is expressed by trophoblast giant cells both in the labyrinth layer, sitting on the arterial side where maternal blood is highest in oxygen and nutrients, and in the junctional zone as maternal blood leaves the placenta. Expression increases during the night, though the increase in the labyrinth is circadian whereas it occurs only after feeding in the junctional zone. These data suggest that the placenta has a sophisticated endocrine system that regulates maternal glucose metabolism during pregnancy.
[Mh] Termos MeSH primário: Comportamento Alimentar
Glucose/metabolismo
Hiperglicemia/genética
Placenta/metabolismo
Prolactina/genética
Receptores da Prolactina/genética
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Pressão Sanguínea
Ritmo Circadiano
Feminino
Homeostase
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Mutação/genética
Lactogênio Placentário
Gravidez
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Receptors, Prolactin); 9002-62-4 (Prolactin); 9035-54-5 (Placental Lactogen); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150814
[St] Status:MEDLINE
[do] DOI:10.1095/biolreprod.115.132431



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