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Pesquisa : G07.345.500.325.235 [Categoria DeCS]
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[PMID]:28460045
[Au] Autor:Lekva T; Roland MCP; Michelsen AE; Friis CM; Aukrust P; Bollerslev J; Henriksen T; Ueland T
[Ad] Endereço:Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, 0027 Oslo, Norway.
[Ti] Título:Large Reduction in Adiponectin During Pregnancy Is Associated With Large-for-Gestational-Age Newborns.
[So] Source:J Clin Endocrinol Metab;102(7):2552-2559, 2017 Jul 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Fetuses exposed to an obese intrauterine environment are more likely to be born large-for-gestational age (LGA) and are at increased risk of obesity in childhood and cardiovascular disease and/or type 2 diabetes mellitus as adults, but which factors that influence the intrauterine environment is less clear. Objective: To investigate the association between circulating levels of leptin and adiponectin, measured multiple times during pregnancy, and birth weight and prevalence of LGA or small-for-gestational-age infants. The association between birth weight and messenger RNA (mRNA) expression of adiponectin receptors and genes involved in nutrient transport in the placenta was also investigated. Design: Population-based prospective cohort [substudy of the STORK study (STORe barn og Komplikasjoner, translated as Large Babies and Complications)] from 2001 to 2008. Setting: University hospital. Patients or other participants: 300 women. Main Outcome Measures: Oral glucose tolerance test was performed twice along with adiponectin and leptin levels measured four times during pregnancy. Results: Circulating adiponectin was lower in mothers who gave birth to LGA offspring or had fetuses with high intrauterine abdominal circumference late in pregnancy. Adiponectin decreased most from early to late pregnancy in mothers who gave birth to LGA offspring, and the decrease was an independent predictor of birth weight. Adiponectin receptor 2 and system A amino acid transporter mRNA expression in placentas was negatively correlated with birth weight and was lower in placentas from LGA infants. Conclusions: Our findings suggest that maternal adiponectin may be an important predictor of fetal growth and birth weight, independent of body mass index and insulin resistance.
[Mh] Termos MeSH primário: Adiponectina/sangue
Peso ao Nascer
Desenvolvimento Fetal
Macrossomia Fetal/sangue
Resultado da Gravidez
Receptores de Adiponectina/metabolismo
[Mh] Termos MeSH secundário: Adulto
Estudos de Coortes
Feminino
Idade Gestacional
Teste de Tolerância a Glucose
Hospitais Universitários
Seres Humanos
Recém-Nascido
Resistência à Insulina/fisiologia
Leptina/sangue
Masculino
Gravidez
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOR2 protein, human); 0 (Adiponectin); 0 (Leptin); 0 (Receptors, Adiponectin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00289


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[PMID]:28454696
[Au] Autor:Ozmen A; Unek G; Korgun ET
[Ad] Endereço:Department of Histology and Embryology, Medical Faculty, Akdeniz University, 07070 Antalya, Turkey.
[Ti] Título:Effect of glucocorticoids on mechanisms of placental angiogenesis.
[So] Source:Placenta;52:41-48, 2017 Apr.
[Is] ISSN:1532-3102
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The benefits of antenatal glucocorticoid (GC) treatment to promote human fetal lung maturation are well established. However, reports have emerged indicating that maternal exposure to high concentrations of circulating GCs alters placental and fetal development. Because many adult-onset metabolic and cardiovascular disorders have their origins in utero, the importance of prenatal conditions should be considered in detail. Therefore, this review aims to present an overview of the GC effect on placental and fetal development, specifically with regard to mechanisms of placental angiogenesis. We assumed that GC overexposure affects fetal development by altering placental angiogenesis. Disturbances in the development of the villous tree and pathological changes in the villous vascular system with insufficient uteroplacental blood flow have been linked to the pathogenesis of intrauterine growth retardation. Moreover, low birth weight is a serious risk factor known to correlate with an increased risk of adult-onset diseases. Although there have been many circumstances in which maternal GCs are elevated, we focused on exogenous synthetic GCs that are applied for therapeutic reasons. However, some questions about the use of steroids remain unanswered, which will require further studies that lead us to review alterations in placental angiogenesis under the perspective of GC overexposure.
[Mh] Termos MeSH primário: Desenvolvimento Fetal/efeitos dos fármacos
Glucocorticoides/farmacologia
Neovascularização Patológica
Neovascularização Fisiológica/efeitos dos fármacos
Placenta/irrigação sanguínea
Placenta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucocorticoids)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:28454694
[Au] Autor:Jawerbaum A; White V
[Ad] Endereço:Laboratory of Reproduction and Metabolism, Center for Pharmacological and Botanical Studies, CEFyBO-CONICET, School of Medicine, University of Buenos Aires, Argentina. Electronic address: a.jawerbaum@gmail.com.
[Ti] Título:Review on intrauterine programming: Consequences in rodent models of mild diabetes and mild fat overfeeding are not mild.
[So] Source:Placenta;52:21-32, 2017 Apr.
[Is] ISSN:1532-3102
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:An adverse intrauterine programming occurs in diabetes and obesity as the consequence of an adverse maternal environment that affects the appropriate fetoplacental development and growth. Experimental models of diabetes and fat overfeeding have provided relevant tools to address putative mechanisms of the adverse intrauterine programming. The current knowledge far extends from the original thoughts of the resulting intrauterine programming of metabolic and cardiovascular diseases to a full range of alterations that affect multiple tissues, organs, and systems that will compromise the long-life health of the offspring. This review examines the postnatal effects of rodent models of mild diabetes and fat overfeeding, identifying the multiple organ derangements in the offspring resulting from mild maternal adverse conditions. In addition, the comparison of experimental models of severe diabetes and fat overfeeding and the crucial role of the placenta are discussed, providing an update of the actual scenario of the putative mechanisms and adverse consequences of maternal metabolic derangements.
[Mh] Termos MeSH primário: Diabetes Mellitus/metabolismo
Desenvolvimento Fetal/fisiologia
Placenta/metabolismo
Efeitos Tardios da Exposição Pré-Natal/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus/patologia
Modelos Animais de Doenças
Feminino
Placenta/patologia
Gravidez
Efeitos Tardios da Exposição Pré-Natal/patologia
Roedores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:28463237
[Au] Autor:Weber-Stadlbauer U
[Ad] Endereço:Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.
[Ti] Título:Epigenetic and transgenerational mechanisms in infection-mediated neurodevelopmental disorders.
[So] Source:Transl Psychiatry;7(5):e1113, 2017 May 02.
[Is] ISSN:2158-3188
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prenatal infection is an environmental risk factor for various brain disorders with neurodevelopmental components, including autism spectrum disorder and schizophrenia. Modeling this association in animals shows that maternal immune activation negatively affects fetal brain development and leads to the emergence of behavioral disturbances later in life. Recent discoveries in these preclinical models suggest that epigenetic modifications may be a critical molecular mechanism by which prenatal immune activation can mediate changes in brain development and functions, even across generations. This review discusses the potential epigenetic mechanisms underlying the effects of prenatal infections, thereby highlighting how infection-mediated epigenetic reprogramming may contribute to the transgenerational transmission of pathological traits. The identification of epigenetic and transgenerational mechanisms in infection-mediated neurodevelopmental disorders appears relevant to brain disorders independently of existing diagnostic classifications and may help identifying complex patterns of transgenerational disease transmission beyond genetic inheritance. The consideration of ancestral infectious histories may be of great clinical interest and may be pivotal for developing new preventive treatment strategies against infection-mediated neurodevelopmental disorders.
[Mh] Termos MeSH primário: Encéfalo/fisiopatologia
Epigênese Genética/imunologia
Transtornos do Neurodesenvolvimento/imunologia
Efeitos Tardios da Exposição Pré-Natal/imunologia
[Mh] Termos MeSH secundário: Animais
Transtorno do Espectro Autista
Encéfalo/crescimento & desenvolvimento
Modelos Animais de Doenças
Exposição Ambiental/efeitos adversos
Epigenômica
Feminino
Desenvolvimento Fetal/imunologia
Desenvolvimento Fetal/fisiologia
Seres Humanos
Transmissão Vertical de Doença Infecciosa/prevenção & controle
Transtornos do Neurodesenvolvimento/prevenção & controle
Fenótipo
Gravidez
Efeitos Tardios da Exposição Pré-Natal/epidemiologia
Efeitos Tardios da Exposição Pré-Natal/patologia
Fatores de Risco
Esquizofrenia/imunologia
Esquizofrenia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1038/tp.2017.78


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[PMID]:29343712
[Au] Autor:Hirsch AJ; Roberts VHJ; Grigsby PL; Haese N; Schabel MC; Wang X; Lo JO; Liu Z; Kroenke CD; Smith JL; Kelleher M; Broeckel R; Kreklywich CN; Parkins CJ; Denton M; Smith P; DeFilippis V; Messer W; Nelson JA; Hennebold JD; Grafe M; Colgin L; Lewis A; Ducore R; Swanson T; Legasse AW; Axthelm MK; MacAllister R; Moses AV; Morgan TK; Frias AE; Streblow DN
[Ad] Endereço:The Vaccine & Gene Institute, Oregon Health and Science University (OHSU), 505 NW 185th Ave, Beaverton, 97006, USA. hirschal@ohsu.edu.
[Ti] Título:Zika virus infection in pregnant rhesus macaques causes placental dysfunction and immunopathology.
[So] Source:Nat Commun;9(1):263, 2018 01 17.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Zika virus (ZIKV) infection during pregnancy leads to an increased risk of fetal growth restriction and fetal central nervous system malformations, which are outcomes broadly referred to as the Congenital Zika Syndrome (CZS). Here we infect pregnant rhesus macaques and investigate the impact of persistent ZIKV infection on uteroplacental pathology, blood flow, and fetal growth and development. Despite seemingly normal fetal growth and persistent fetal-placenta-maternal infection, advanced non-invasive in vivo imaging studies reveal dramatic effects on placental oxygen reserve accompanied by significantly decreased oxygen permeability of the placental villi. The observation of abnormal oxygen transport within the placenta appears to be a consequence of uterine vasculitis and placental villous damage in ZIKV cases. In addition, we demonstrate a robust maternal-placental-fetal inflammatory response following ZIKV infection. This animal model reveals a potential relationship between ZIKV infection and uteroplacental pathology that appears to affect oxygen delivery to the fetus during development.
[Mh] Termos MeSH primário: Placenta/metabolismo
Circulação Placentária
Complicações Infecciosas na Gravidez/imunologia
Infecção pelo Zika virus/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Encéfalo/embriologia
Encéfalo/patologia
Citocinas/sangue
Modelos Animais de Doenças
Feminino
Desenvolvimento Fetal
Feto/patologia
Imunidade Inata
Macaca mulatta
Imagem por Ressonância Magnética
Oxigênio/metabolismo
Permeabilidade
Placenta/imunologia
Placenta/patologia
Placenta/virologia
Gravidez
Complicações Infecciosas na Gravidez/metabolismo
Complicações Infecciosas na Gravidez/patologia
Complicações Infecciosas na Gravidez/fisiopatologia
Carga Viral
Infecção pelo Zika virus/metabolismo
Infecção pelo Zika virus/patologia
Infecção pelo Zika virus/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); S88TT14065 (Oxygen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02499-9


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[PMID]:29390471
[Au] Autor:Niu G; Yuan LJ; Gong FQ; Yang J; Zhu CX; Shen HW
[Ad] Endereço:Department of Gynecology and Obstetrics.
[Ti] Título:Early pregnancy following multidrug regimen chemotherapy in a gestational trophoblastic neoplasia patient: A case report.
[So] Source:Medicine (Baltimore);96(51):e9221, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Gestational trophoblastic neoplasia is a group of rare tumors that can be cured using chemotherapy. The use of artificial contraception for at least 1 year is recommended not only due to the high recurrence rate in the first year after treatment, but also because of the unclear genetic toxic effects of multidrug regimen chemotherapy on reproductive cells. There is no consensus about the contraception duration, but most patients want to have children. PATIENT CONCERNS: This case involved a 33-year-old female suffering from gestational trophoblastic neoplasia and 5-fluorouracil + actinomycin-D chemotherapy. She became pregnant 1 month after finishing the chemotherapy. DIAGNOSIS: Gestational trophoblastic neoplasia. INTERVENTIONS: No treatment during pregnancy. OUTCOMES: The patient had a full-term normal delivery, and the baby showed normal development and growth after a follow-up of 48 months. LESSONS: Pregnancy soon after chemotherapy can be viable with rigorous prenatal care.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Doença Trofoblástica Gestacional/tratamento farmacológico
Complicações Neoplásicas na Gravidez/tratamento farmacológico
Resultado da Gravidez
[Mh] Termos MeSH secundário: Adulto
Gonadotropina Coriônica/sangue
Dactinomicina/administração & dosagem
Relação Dose-Resposta a Droga
Esquema de Medicação
Feminino
Desenvolvimento Fetal/fisiologia
Fluoruracila/administração & dosagem
Idade Gestacional
Doença Trofoblástica Gestacional/diagnóstico
Seres Humanos
Saúde do Lactente
Recém-Nascido
Masculino
Gravidez
Complicações Neoplásicas na Gravidez/diagnóstico
Cuidado Pré-Natal/métodos
Nascimento a Termo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chorionic Gonadotropin); 1CC1JFE158 (Dactinomycin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009221


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[PMID]:29382640
[Au] Autor:Braillon A; Bewley S
[Ad] Endereço:University Hospital, 80000 Amiens, France.
[Ti] Título:Healthcare professionals must demand action on the social determinants of preventable low fetal growth and preterm birth.
[So] Source:BMJ;360:k399, 2018 01 30.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Desenvolvimento Fetal
Nascimento Prematuro
[Mh] Termos MeSH secundário: Feminino
Retardo do Crescimento Fetal
Idade Gestacional
Seres Humanos
Renda
Recém-Nascido
Gravidez
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k399


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[PMID]:27777362
[Au] Autor:Petry CJ; Sanz Marcos N; Pimentel G; Hayes MG; Nodzenski M; Scholtens DM; Hughes IA; Acerini CL; Ong KK; Lowe WL; Dunger DB
[Ad] Endereço:From the Department of Paediatrics (C.J.P., N.S.M., G.P., I.A.H., C.L.A., K.K.O., D.B.D.), Medical Research Council Epidemiology Unit (K.K.O.), and Institute of Metabolic Science (D.B.D.), University of Cambridge, United Kingdom; Hospital Sant Joan de Déu, Servicio de Pediatría, Barcelona, Spain (N.
[Ti] Título:Associations Between Fetal Imprinted Genes and Maternal Blood Pressure in Pregnancy.
[So] Source:Hypertension;68(6):1459-1466, 2016 12.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In addition to maternal genes and environmental exposures, variation in fetal imprinted genes could also affect maternal blood pressure during pregnancy. Our objective was to test the associations between polymorphic variants in 16 imprinted genes and maternal mean arterial blood pressures in 1160 DNA trios from 2 established birth cohorts (the Cambridge Baby Growth and Wellbeing Studies) and seek replication in 1367 Hyperglycemia and Adverse Pregnancy Outcome Study participants. Significant univariate associations, all independent of fetal sex, were observed in the Cambridge cohorts, including FAM99A rs1489945 transmitted from the mother (P=2×10 ), DLK1 rs10139403 (mother; P=9×10 ), DLK1 rs12147008 (mother; P=1×10 ), H19 rs217222 (father; P=1×10 ), SNRPN rs1453556 (father; P=1×10 ), IGF2 rs6356 (father; P=1×10 ), and NNAT rs6066671 (father; P=1×10 ). In meta-analysis including additional independent Hyperglycemia and Adverse Pregnancy Outcome Study data, the association with maternally transmitted fetal DLK1 rs10139403 reached genome-wide significance (P=6.3×10 ). With the exception of fetal rs1489945 and rs217222, all of other associations were unidirectional and most were statistically significant. To further explore the significance of these relationships, we developed an allele score based on the univariate findings. The score was strongly associated with maternal blood pressure at 31 weeks (P=4.1×10 ; adjusted r =5.6%) and 37 weeks of pregnancy (P=1.1×10 ; r =3.6%), and during the last 2 weeks before parturition (P=1.1×10 ; r =8.7%). It was also associated with gestational hypertension (odds ratio, 1.54 [range, 1.14-2.09] per allele; P=0.005; 45 cases and 549 controls). These data support the concept that fetal imprinted genes are related to the development of gestational hypertension.
[Mh] Termos MeSH primário: Pressão Sanguínea/genética
Desenvolvimento Fetal/genética
Hipertensão Induzida pela Gravidez/genética
Peptídeos e Proteínas de Sinalização Intercelular/genética
Proteínas de Membrana/genética
Resultado da Gravidez
[Mh] Termos MeSH secundário: Adulto
Alelos
Análise de Variância
Pressão Sanguínea/fisiologia
Determinação da Pressão Arterial
Estudos de Coortes
Metilação de DNA/genética
Feminino
Estudos de Associação Genética
Idade Gestacional
Seres Humanos
Hipertensão Induzida pela Gravidez/fisiopatologia
Recém-Nascido
Estudos Longitudinais
Masculino
Razão de Chances
Gravidez
Proteínas da Gravidez/genética
Estudos Prospectivos
RNA Longo não Codificante/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; META-ANALYSIS; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DLK1 protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Pregnancy Proteins); 0 (RNA, Long Noncoding)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29262349
[Au] Autor:Fu B; Zhou Y; Ni X; Tong X; Xu X; Dong Z; Sun R; Tian Z; Wei H
[Ad] Endereço:Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Te
[Ti] Título:Natural Killer Cells Promote Fetal Development through the Secretion of Growth-Promoting Factors.
[So] Source:Immunity;47(6):1100-1113.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are present in large populations at the maternal-fetal interface during early pregnancy. However, the role of NK cells in fetal growth is unclear. Here, we have identified a CD49a Eomes subset of NK cells that secreted growth-promoting factors (GPFs), including pleiotrophin and osteoglycin, in both humans and mice. The crosstalk between HLA-G and ILT2 served as a stimulus for GPF-secreting function of this NK cell subset. Decreases in this GPF-secreting NK cell subset impaired fetal development, resulting in fetal growth restriction. The transcription factor Nfil3, but not T-bet, affected the function and the number of this decidual NK cell subset. Adoptive transfer of induced CD49a Eomes NK cells reversed impaired fetal growth and rebuilt an appropriate local microenvironment. These findings reveal properties of NK cells in promoting fetal growth. In addition, this research proposes approaches for therapeutic administration of NK cells in order to reverse restricted nourishments within the uterine microenvironment during early pregnancy.
[Mh] Termos MeSH primário: Aborto Habitual/imunologia
Transferência Adotiva
Proteínas de Transporte/secreção
Citocinas/secreção
Desenvolvimento Fetal/imunologia
Retardo do Crescimento Fetal/prevenção & controle
Peptídeos e Proteínas de Sinalização Intercelular/secreção
Células Matadoras Naturais/transplante
[Mh] Termos MeSH secundário: Aborto Habitual/genética
Aborto Habitual/patologia
Adulto
Animais
Antígenos CD/genética
Antígenos CD/imunologia
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/imunologia
Proteínas de Transporte/genética
Proteínas de Transporte/imunologia
Microambiente Celular
Citocinas/genética
Citocinas/imunologia
Decídua/imunologia
Decídua/patologia
Feminino
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/imunologia
Retardo do Crescimento Fetal/patologia
Feto
Regulação da Expressão Gênica no Desenvolvimento
Antígenos HLA-G/genética
Antígenos HLA-G/imunologia
Seres Humanos
Integrina alfa1/genética
Integrina alfa1/imunologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/imunologia
Células Matadoras Naturais/citologia
Células Matadoras Naturais/imunologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/genética
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Gravidez
Transdução de Sinais
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Carrier Proteins); 0 (Cytokines); 0 (EOMES protein, human); 0 (HLA-G Antigens); 0 (Integrin alpha1); 0 (Intercellular Signaling Peptides and Proteins); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (NFIL3 protein, human); 0 (OGN protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 134034-50-7 (pleiotrophin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28934257
[Au] Autor:Simic M; Stephansson O; Petersson G; Cnattingius S; Wikström AK
[Ad] Endereço:Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska University Hospital and Institutet, Stockholm, Sweden.
[Ti] Título:Slow fetal growth between first and early second trimester ultrasound scans and risk of small for gestational age (SGA) birth.
[So] Source:PLoS One;12(9):e0184853, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To investigate the association between fetal growth between first and early second trimester ultrasound scan and the risk of severe small for gestational age (SGA) birth. METHODS: This cohort study included 69 550 singleton pregnancies with first trimester dating and an early second trimester growth scan in Stockholm and Gotland Counties, Sweden between 2008 and 2014. Exposure was difference in biparietal diameter growth between observed and expected at the second trimester scan, calculated by z-scores. Risk of birth of a severe SGA infant (birth weight for gestational age by fetal sex less than the 3rd centile) was calculated using multivariable logistic regression analysis and presented as adjusted odds ratio (aOR). RESULTS: Parietal growth less than 2.5 percentile between first and second trimester ultrasound examination was associated with elevated risk of being born severe SGA. (aOR 1.67; 95% Confidence Interval 1.28-2.18). The risks of preterm severe SGA (birth before 37 weeks) and term severe SGA (birth 37 weeks or later) were at similar levels, and risk of severe SGA were also elevated in the absence of preeclampsia, hypertensive diseases or gestational diabetes. CONCLUSIONS: Fetuses with slow growth of biparietal diameter at ultrasound examination in early second trimester exhibit increased risk of being born SGA independent of gestational age at birth and presence of maternal hypertensive diseases or diabetes mellitus.
[Mh] Termos MeSH primário: Desenvolvimento Fetal
Recém-Nascido Pequeno para a Idade Gestacional
Ultrassonografia Pré-Natal
[Mh] Termos MeSH secundário: Adulto
Estudos de Coortes
Feminino
Seres Humanos
Modelos Logísticos
Masculino
Análise Multivariada
Gravidez
Segundo Trimestre da Gravidez
Terceiro Trimestre da Gravidez
Risco
Suécia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184853



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