Evidence map›Paper›PMID 34678164›Full record

ArticleJornal de pediatria

Possible association between a polymorphism of EPAS1 gene and persistent pulmonary hypertension of the newborn: a case-control study.

Narongsak Nakwan, Surakameth Mahasirimongkol, Nusara Satproedprai, Tassamonwan Chaiyasung, Punna Kunhapan, Cheep Charoenlap, Kamonnut Singkhamanan, Chariyawan Charalsawadi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Jornal de pediatria. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Narongsak NakwanPrince of Songkla University, Faculty of Medicine, Department of Biomedical Sciences, Hat Yai, Thailand; Hat Yai Hospital, Hat Yai Medical Education Center, Department of Pediatrics, Hat Yai, Thailand.
Surakameth MahasirimongkolMinistry of Public Heath, Department of Medical Sciences, Division of Genomic Medicine and Innovation Support, Medical Genetics Center, Nonthaburi, Thailand.
Nusara SatproedpraiMinistry of Public Heath, Department of Medical Sciences, Division of Genomic Medicine and Innovation Support, Medical Genetics Center, Nonthaburi, Thailand.
Tassamonwan ChaiyasungMinistry of Public Heath, Department of Medical Sciences, Division of Genomic Medicine and Innovation Support, Medical Genetics Center, Nonthaburi, Thailand.
Punna KunhapanMinistry of Public Heath, Department of Medical Sciences, Division of Genomic Medicine and Innovation Support, Medical Genetics Center, Nonthaburi, Thailand.
Cheep CharoenlapHat Yai Hospital, Hat Yai Medical Education Center, Department of Anatomical Pathology, Hat Yai, Thailand.
Kamonnut SingkhamananPrince of Songkla University, Faculty of Medicine, Department of Biomedical Sciences, Hat Yai, Thailand.
Chariyawan CharalsawadiPrince of Songkla University, Faculty of Medicine, Department of Pathology, Hat Yai, Thailand. Electronic address: cchariya@medicine.psu.ac.th.
Department of Medical Sciences · THPrince of Songkla University · THHatyai Hospital · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore possible genes related to the development of persistent pulmonary hypertension of the newborn (PPHN).

methodsThe authors identified 285 single nucleotide polymorphisms (SNPs) of 11 candidate genes (BMPR2, EPAS1, PDE3A, VEGFA, ENG, NOTCH3, SOD3, CPS1, ABCA3, ACVRL1, and SMAD9), using an Illumina Asian Screening Array-24 v1.0 BeadChip Array. The FastLmmC and R package was used for statistical analyses. The chi-square test and Cochrane-Armitage trend test were used to compare the allele and genotype frequencies between the groups and to test the genetic models, respectively.

resultsA total of 45 PPHN infants and 294 control subjects were analyzed. The most common cause of PPHN was meconium aspiration syndrome. Among the 285 SNPs, 17 SNPs from 6 candidate genes (BMPR2, EPAS1, PDE3A, VEGFA, ENG, and NOTCH3) were significantly associated with PPHN (P < 0.05). After using the Bonferroni correction (P < 0.00018), only the rs17034984 SNP located in intron 1 of the EPAS1 gene remained significantly different between the PPHN and control subjects (P = 0.00014). The frequency of the TC/TT genotype of rs17034984 in the gene with the dominant model was significant in the patients with PPHN (OR = 5.38, 95% CI: 2.15-13.49). The T allele frequency of rs17034984 in the gene showed a significant difference compared with the control subjects (OR = 4.89, 95% CI: 2.03-11.82).

conclusionsThe present study suggests that the rs17034984 variant of EPAS1 gene is associated with PPHN.

Indexed as

Basic Helix-Loop-Helix ProteinsHypertension, PulmonaryMeconium Aspiration SyndromePersistent Fetal Circulation SyndromeCase-Control StudiesEndothelial PAS Domain-Containing Protein 1FemaleHumansInfant, NewbornPolymorphism, Single NucleotideBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Association studyEPAS1 genePolymorphismPPHNSNP

Identifiers

PMID34678164
PMCPMC9432230
OpenAlexW3207198503

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.