Evidence map›Paper›PMID 21573030›Full record

ArticlePloS one2011

An NFKB1 promoter insertion/deletion polymorphism influences risk and outcome in acute respiratory distress syndrome among Caucasians.

Ednan K Bajwa, Paul C Cremer, Michelle N Gong, Rihong Zhai, Li Su, B Taylor Thompson, David C Christiani

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The promoter polymorphism ofJournal of exercise rehabilitation · 2018
    Article
  5. Review
  6. Article
  7. Review
  8. Functional genomic assessment of phosgene-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2013
    Article
  9. Article
  10. Integrative assessment of chlorine-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2012
    Article
  11. 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

7 authors at 3 institutions in 1 country.

Ednan K BajwaPulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Paul C Cremer
Michelle N Gong
Rihong Zhai
Li Su
B Taylor Thompson
David C Christiani
Harvard University · USMassachusetts General Hospital · USAlbert Einstein College of Medicine · US

Funding

Translational Research Support CoreP30ES000002 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI Marc G Weisskopf · 1985 to 2026
$44.6M
MOLECULAR EPIDEMIOLOGY OF ARDSR01HL060710 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI CHRISTIANI, DAVID C · 2000 to 2015
$8.4M
TRAINING GRANT IN LUNG CELL &MOLECULAR BIOLOGYT32HL007874 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEDOFF, BENJAMIN DAVID · 1997 to 2011
$4.1M
Molecular Epidemiology of ARDS and Septic ShockK23HL067197 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GONG, MICHELLE NG · 2001 to 2005
$650k
NHLBI NIH HHS HL07874NHLBI NIH HHS HL60710NHLBI NIH HHS HL67197NHLBI NIH HHS K23 HL067197NHLBI NIH HHS R01 HL060710NHLBI NIH HHS T32 HL007874NIEHS NIH HHS ES0002NIEHS NIH HHS P30 ES000002
6 · The paper itself

Abstract

backgroundNuclear factor-κB (NF-κB) is required for transcription of many pro-inflammatory genes and has been implicated in the pathogenesis of acute respiratory distress syndrome (ARDS). We hypothesized that a known functional polymorphism in the promoter of the NFKB1 gene may affect susceptibility to and outcome from ARDS.

methodsA case control study was conducted among a cohort of patients admitted to the intensive care unit (ICU) with risk factors for the development of ARDS. 379 patients with ARDS and 793 at-risk controls were studied. Patients were followed for 60 days with development of ARDS as a primary outcome; ARDS-related mortality and organ dysfunction were secondary outcomes.

resultsPatients homozygous for the 4 base pair deletion in the promoter of NFKB1 (del/del) did not have an increased odds ratio (OR) of developing ARDS in unadjusted analysis but were more likely to develop ARDS in the presence of a significant interaction between the del/del genotype and age (OR 5.21, 95% CI 1.35-20.0). In multivariate analysis, patients with ARDS and the del/del genotype also had increased 60 day mortality (HR 1.54, 95% CI 1.01-2.36) and more severe daily organ dysfunction (P<.001) when compared to ARDS patients with other genotypes.

conclusionThe del/del genotype is associated with an age-dependent increase in odds of developing ARDS. Patients with the del/del genotype and ARDS also have increased hazard of 60 day mortality and more organ failure.

Indexed as

AgedAged, 80 and overCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedNF-kappa B p50 SubunitPolymorphism, GeneticRespiratory Distress SyndromeWhite PeopleNF-kappa B p50 SubunitNFKB1 protein, human

Identifiers

PMID21573030
PMCPMC3090449
OpenAlexW2041715016

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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.