Evidence map›Paper›PMID 25254322›Full record

ArticleChest2015

Platelet count mediates the contribution of a genetic variant in LRRC16A to ARDS risk.

Yongyue Wei, Zhaoxi Wang, Li Su, Feng Chen, Paula Tejera, Ednan K Bajwa, Mark M Wurfel, Xihong Lin, David C Christiani

Open access · bronzeAbstract read
In one paragraph

Article in Chest, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Yongyue WeiDepartment of Environmental Health, Department of Epidemiology and Biostatistics, Ministry of Education Key Laboratory for Modern Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China.
Zhaoxi WangDepartment of Environmental Health, Harvard School of Public Health, Boston, MA.
Li SuDepartment of Environmental Health, Harvard School of Public Health, Boston, MA.
Feng ChenDepartment of Epidemiology and Biostatistics, Ministry of Education Key Laboratory for Modern Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China.
Paula TejeraDepartment of Environmental Health, Harvard School of Public Health, Boston, MA.
Ednan K BajwaDepartment of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Mark M WurfelDivision of Pulmonary and Critical Care Medicine, University of Washington, Harborview Medical Center, Seattle, WA.
Xihong LinDepartment of Biostatistics, Harvard School of Public Health, Boston, MA.
David C ChristianiDepartment of Environmental Health, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA. Electronic address: dchris@hsph.harvard.edu.
Massachusetts General Hospital · USNanjing Medical University · CNHarvard University · USUniversity of Washington · US

Funding

MOLECULAR EPIDEMIOLOGY OF ARDSR01HL060710 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI CHRISTIANI, DAVID C · 2000 to 2015
$8.4M
NHLBI NIH HHS R01 HL060710NHLBI NIH HHS R01HL060710
6 · The paper itself

Abstract

backgroundPlatelets are believed to be critical in pulmonary-origin ARDS as mediators of endothelial damage through their interactions with fibrinogen and multiple signal transduction pathways. A prior meta-analysis identified five loci for platelet count (PLT): BAD, LRRC16A, CD36, JMJD1C, and SLMO2. This study aims to validate the quantitative trait loci (QTLs) of PLT within BAD, LRRC16A, CD36, JMJD1C, and SLMO2 among critically ill patients and to investigate the associations of these QTLs with ARDS risk that may be mediated through PLT.

methodsARDS cases and at-risk control subjects were recruited from the intensive care unit of the Massachusetts General Hospital. Exome-wide genotyping data of 629 ARDS cases and 1,026 at-risk control subjects and genome-wide gene expression profiles of 18 at-risk control subjects were generated for analysis.

resultsSingle-nucleotide polymorphism (SNP) rs7766874 within LRRC16A was a significant locus for PLT among at-risk control subjects (β = -13.00; 95% CI, -23.22 to -2.77; P = .013). This association was validated using LRRC16A gene expression data from at-risk control subjects (β = 77.03 per 1 SD increase of log2-transformed expression; 95% CI, 27.26-126.80; P = .005). Further, rs7766874 was associated with ARDS risk conditioned on PLT (OR = 0.68; 95% CI, 0.51-0.90; P = .007), interacting with PLT (OR = 1.15 per effect allele per 100 × 103/μL of PLT; 95% CI, 1.03-1.30; P = .015), and mediated through PLT (indirect OR = 1.045; 95% CI, 1.007-1.085; P = .021).

conclusionsOur findings support the role of LRRC16A in platelet formation and suggest the importance of LRRC16A in ARDS pathophysiology by interacting with, and being mediated through, platelets.

Indexed as

Platelet CountAdolescentAdultAgedAged, 80 and overCase-Control StudiesCritical IllnessEndothelium, VascularFemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeHumansMaleMicrofilament ProteinsMiddle AgedCARMIL1 protein, humanMicrofilament Proteins

Identifiers

PMID25254322
PMCPMC4347530
OpenAlexW2001315007

What OpenQuestion holds

Textmetadata
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.