Q3166698 (Q3166698): Difference between revisions
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(Created claim: summary (P836): Objectives: Evaluate gestational venous hypertension (GVH) as a risk factor for hypoxia and placental insufficiency with an impact on fetal growth, and identify and characterise biomarkers of hypoxic damage. Methodology: Design: Case-control study nested in a cohort. Population: Pregnant women who attend the usual control in the third trimester (32-35 weeks) of two hospital centers (HGUGM and huCD). Estimated a sample of 503 patients. Variable...) |
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Objectives: Evaluate gestational venous hypertension (GVH) as a risk factor for hypoxia and placental insufficiency with an impact on fetal growth, and identify and characterise biomarkers of hypoxic damage. Methodology: Design: Case-control study nested in a cohort. Population: Pregnant women who attend the usual control in the third trimester (32-35 weeks) of two hospital centers (HGUGM and huCD). Estimated a sample of 503 patients. Variables: Clinical characteristics of pregnant women with and without venous hypertension. Presence of markers of hypoxia in placenta, maternal blood and cord using histopathological, genomic and metabolomic studies to determine: Hypoxic phenotype: HIF-1alfa, HIF-2alfa, HIF-3alfa, KDM3A, SLC2A1, EGLN-3, CDKN1C and PHLDA2; Cell transduction activation: PI3K/Akt/mTOR; Eritopoyesis: EPO; Angiogenesis: VEGF; Glucolitic phenotype: PGK1, ALDA and GLUT-1 and Apoptosis: Bax/Bcl-2, Caspasas, BNIP3 and PARP-1. Perinatal results recorded on a regular basis. Statistical analysis: A descriptive analysis of the variables collected will be performed from both the cohort and the case-control study. The association measures and their confidence intervals will be estimated. Finally, multivariate models will be generated to adjust for possible confounding factors, describing the interactions found. (English) | |||||||||||||||
| Property / summary: Objectives: Evaluate gestational venous hypertension (GVH) as a risk factor for hypoxia and placental insufficiency with an impact on fetal growth, and identify and characterise biomarkers of hypoxic damage. Methodology: Design: Case-control study nested in a cohort. Population: Pregnant women who attend the usual control in the third trimester (32-35 weeks) of two hospital centers (HGUGM and huCD). Estimated a sample of 503 patients. Variables: Clinical characteristics of pregnant women with and without venous hypertension. Presence of markers of hypoxia in placenta, maternal blood and cord using histopathological, genomic and metabolomic studies to determine: Hypoxic phenotype: HIF-1alfa, HIF-2alfa, HIF-3alfa, KDM3A, SLC2A1, EGLN-3, CDKN1C and PHLDA2; Cell transduction activation: PI3K/Akt/mTOR; Eritopoyesis: EPO; Angiogenesis: VEGF; Glucolitic phenotype: PGK1, ALDA and GLUT-1 and Apoptosis: Bax/Bcl-2, Caspasas, BNIP3 and PARP-1. Perinatal results recorded on a regular basis. Statistical analysis: A descriptive analysis of the variables collected will be performed from both the cohort and the case-control study. The association measures and their confidence intervals will be estimated. Finally, multivariate models will be generated to adjust for possible confounding factors, describing the interactions found. (English) / rank | |||||||||||||||
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| Property / summary: Objectives: Evaluate gestational venous hypertension (GVH) as a risk factor for hypoxia and placental insufficiency with an impact on fetal growth, and identify and characterise biomarkers of hypoxic damage. Methodology: Design: Case-control study nested in a cohort. Population: Pregnant women who attend the usual control in the third trimester (32-35 weeks) of two hospital centers (HGUGM and huCD). Estimated a sample of 503 patients. Variables: Clinical characteristics of pregnant women with and without venous hypertension. Presence of markers of hypoxia in placenta, maternal blood and cord using histopathological, genomic and metabolomic studies to determine: Hypoxic phenotype: HIF-1alfa, HIF-2alfa, HIF-3alfa, KDM3A, SLC2A1, EGLN-3, CDKN1C and PHLDA2; Cell transduction activation: PI3K/Akt/mTOR; Eritopoyesis: EPO; Angiogenesis: VEGF; Glucolitic phenotype: PGK1, ALDA and GLUT-1 and Apoptosis: Bax/Bcl-2, Caspasas, BNIP3 and PARP-1. Perinatal results recorded on a regular basis. Statistical analysis: A descriptive analysis of the variables collected will be performed from both the cohort and the case-control study. The association measures and their confidence intervals will be estimated. Finally, multivariate models will be generated to adjust for possible confounding factors, describing the interactions found. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
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Revision as of 17:05, 12 October 2021
Project Q3166698 in Spain
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | No label defined |
Project Q3166698 in Spain |
Statements
66,000.0 Euro
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132,000.0 Euro
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50.0 percent
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1 January 2019
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31 March 2022
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FUNDACION INVESTIGACION BIOMEDICA HOSPITAL RAMON Y CAJAL
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40°25'0.12"N, 3°42'12.89"W
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28079
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Objetivos: Evaluar la hipertensión venosa gestacional (HTVG) como factor de riesgo de hipoxia e insuficiencia placentaria con repercusión en el crecimiento fetal, e identificar y caracterizar biomarcadores de daño hipóxico. Metodología: Diseño: Estudio de casos-control anidado en una cohorte. Población: Gestantes que acudan al control habitual en el tercer trimestre (32-35 semanas) de dos centros hospitalarios (HGUGM y HUCD). Estimado una muestra de 503 pacientes. Variables: Características clínicas de las gestantes con y sin hipertensión venosa. Presencia de marcadores de hipoxia en placenta, sangre materna y cordón mediante estudios histopatológico, genómicos y metabolómicos para determinación de: Fenótipo hipóxico: HIF-1alfa, HIF-2alfa, HIF-3alfa, KDM3A, SLC2A1, EGLN-3, CDKN1C y PHLDA2; Activación de transducción celular: PI3K/Akt/mTOR; Eritopoyesis: EPO; Angiogenésis: VEGF; Fenotipo glucolitico: PGK1, ALDA y GLUT-1 y Apoptosis: Bax/Bcl-2, Caspasas, BNIP3 y PARP-1. Resultados perinatales registrados de forma habitual. Análisis estadístico: Se realizará, tanto de la cohorte como del estudio de casos-control, un análisis descriptivo de las variables recogidas, se estimaran las medidas de asociación y sus intervalos de confianza. Finalmente, se generarán los modelos multivariantes para ajustar por los posibles factores de confusión, describiendo las interacciones encontradas. (Spanish)
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Objectives: Evaluate gestational venous hypertension (GVH) as a risk factor for hypoxia and placental insufficiency with an impact on fetal growth, and identify and characterise biomarkers of hypoxic damage. Methodology: Design: Case-control study nested in a cohort. Population: Pregnant women who attend the usual control in the third trimester (32-35 weeks) of two hospital centers (HGUGM and huCD). Estimated a sample of 503 patients. Variables: Clinical characteristics of pregnant women with and without venous hypertension. Presence of markers of hypoxia in placenta, maternal blood and cord using histopathological, genomic and metabolomic studies to determine: Hypoxic phenotype: HIF-1alfa, HIF-2alfa, HIF-3alfa, KDM3A, SLC2A1, EGLN-3, CDKN1C and PHLDA2; Cell transduction activation: PI3K/Akt/mTOR; Eritopoyesis: EPO; Angiogenesis: VEGF; Glucolitic phenotype: PGK1, ALDA and GLUT-1 and Apoptosis: Bax/Bcl-2, Caspasas, BNIP3 and PARP-1. Perinatal results recorded on a regular basis. Statistical analysis: A descriptive analysis of the variables collected will be performed from both the cohort and the case-control study. The association measures and their confidence intervals will be estimated. Finally, multivariate models will be generated to adjust for possible confounding factors, describing the interactions found. (English)
12 October 2021
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Madrid
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Identifiers
PI18_00912
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