Evidence map›Paper›PMID 28881463›Full record

ArticlePaediatric and perinatal epidemiology2018

A Family Based Study of Carbon Monoxide and Nitric Oxide Signalling Genes and Preeclampsia.

Anna E Bauer, Christy L Avery, Min Shi, Clarice R Weinberg, Andrew F Olshan, Quaker E Harmon, Jingchun Luo, Jenny Yang, Tracy A Manuck, Michael C Wu and 7 more

Open access · greenAbstract read
In one paragraph

Article in Paediatric and perinatal epidemiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 6 institutions in 3 countries.

Anna E BauerDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.ORCID 0000-0002-7771-930X
Christy L AveryDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
Min ShiBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Clarice R WeinbergBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Andrew F OlshanDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
Quaker E HarmonEpidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Jingchun LuoLineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
Jenny YangDepartment of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
Tracy A ManuckDivision of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of North Carolina, School of Medicine, Chapel Hill, NC, USA.
Michael C WuBiostatistics and Biomathematics Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Nicholas WilliamsWellcome Trust Sanger Institute, Hinxton, Cambridge, UK.
Ralph McGinnisWellcome Trust Sanger Institute, Hinxton, Cambridge, UK.
Linda MorganSchool of Life Sciences, University of Nottingham, Nottingham, UK.
Kari KlungsøyrNorwegian Institute of Public Health, Oslo, Norway.
Lill TrogstadNorwegian Institute of Public Health, Oslo, Norway.
Per MagnusNorwegian Institute of Public Health, Oslo, Norway.
Stephanie M EngelDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
University of North Carolina at Chapel Hill · USNational Institute of Environmental Health Sciences · USNorwegian Institute of Public Health · NOWellcome Sanger Institute · GBFred Hutch Cancer Center · USUniversity of Nottingham · GB

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
Gene-Environment Interactions in an Autism Birth CohortU01NS047537 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIPKIN, W. IAN · 2003 to 2013
$27.0M
Training Program in Reproductive, Perinatal, and Pediatric EpidemiologyT32HD052468 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Julie L Daniels · 2008 to 2026
$3.8M
Prenatal Smoking, Maternal & Fetal Genetic Variation & Risk of PreeclampsiaR01HD058008 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ENGEL, STEPHANIE · 2008 to 2012
$2.7M
Applications of methods in collaborative scienceZIAES103086 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WEINBERG, CLARICE · 2012 to 2025
$986k
British Heart Foundation RG/99006NICHD NIH HHS R01 HD058008NICHD NIH HHS T32 HD052468NIEHS NIH HHS N01 ES075558NIEHS NIH HHS P30 ES010126NINDS NIH HHS U01 NS047537Wellcome TrustWellcome Trust 076113Wellcome Trust 083948/Z/07/ZWellcome Trust 088841/Z/09/Z
6 · The paper itself

Abstract

backgroundPreeclampsia is thought to originate during placentation, with incomplete remodelling and perfusion of the spiral arteries leading to reduced placental vascular capacity. Nitric oxide (NO) and carbon monoxide (CO) are powerful vasodilators that play a role in the placental vascular system. Although family clustering of preeclampsia has been observed, the existing genetic literature is limited by a failure to consider both mother and child.

methodsWe conducted a nested case-control study within the Norwegian Mother and Child Birth Cohort of 1545 case-pairs and 995 control-pairs from 2540 validated dyads (2011 complete pairs, 529 missing mother or child genotype). We selected 1518 single-nucleotide polymorphisms (SNPs) with minor allele frequency >5% in NO and CO signalling pathways. We used log-linear Poisson regression models and likelihood ratio tests to assess maternal and child effects.

resultsOne SNP met criteria for a false discovery rate Q-value <0.05. The child variant, rs12547243 in adenylate cyclase 8 (ADCY8), was associated with an increased risk (relative risk [RR] 1.42, 95% confidence interval [CI] 1.20, 1.69 for AG vs. GG, RR 2.14, 95% CI 1.47, 3.11 for AA vs. GG, Q = 0.03). The maternal variant, rs30593 in PDE1C was associated with a decreased risk for the subtype of preeclampsia accompanied by early delivery (RR 0.45, 95% CI 0.27, 0.75 for TC vs. CC; Q = 0.02). None of the associations were replicated after correction for multiple testing.

conclusionsThis study uses a novel approach to disentangle maternal and child genotypic effects of NO and CO signalling genes on preeclampsia.

Indexed as

AdultCarbon MonoxideCase-Control StudiesFemaleGene FrequencyGenesGenetic Predisposition to DiseaseGenotyping TechniquesHumansInfant, NewbornNitric OxideNorwayPoisson DistributionPolymorphism, Single NucleotidePre-EclampsiaPregnancyCarbon MonoxideNitric Oxidecase-controlfamily based designgenetic epidemiologyMoBamother-child dyadNorwegian Mother and Child Cohort Studypreeclampsia

Identifiers

PMID28881463
PMCPMC5771849
OpenAlexW2750634979

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.