Evidence map›Paper›PMID 37272612›Full record

ArticleeLife2023

Quantitative trait and transcriptome analysis of genetic complexity underpinning cardiac interatrial septation in mice using an advanced intercross line.

Mahdi Moradi Marjaneh, Edwin P Kirk, Ralph Patrick, Dimuthu Alankarage, David T Humphreys, Gonzalo Del Monte-Nieto, Paola Cornejo-Paramo, Vaibhao Janbandhu, Tram B Doan, Sally L Dunwoodie and 5 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

15 authors at 3 institutions in 2 countries.

Mahdi Moradi Marjaneh *Victor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0002-9412-9029
Edwin P Kirk *Victor Chang Cardiac Research Institute, Sydney, Australia.
Ralph Patrick *Victor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0003-0956-1026
Dimuthu AlankarageVictor Chang Cardiac Research Institute, Sydney, Australia.
David T HumphreysVictor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0003-4140-0089
Gonzalo Del Monte-NietoVictor Chang Cardiac Research Institute, Sydney, Australia.
Paola Cornejo-ParamoVictor Chang Cardiac Research Institute, Sydney, Australia.
Vaibhao JanbandhuVictor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0002-3837-1865
Tram B DoanVictor Chang Cardiac Research Institute, Sydney, Australia.
Sally L DunwoodieVictor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0002-2069-7349
Emily S WongVictor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0003-0315-2942
Chris MoranSydney School of Veterinary Science, University of Sydney, Sydney, Australia.ORCID 0000-0003-4550-5101
Ian C A MartinSydney School of Veterinary Science, University of Sydney, Sydney, Australia.
Peter C ThomsonSydney School of Veterinary Science, University of Sydney, Sydney, Australia.ORCID 0000-0003-4428-444X
Richard P HarveyVictor Chang Cardiac Research Institute, Sydney, Australia.ORCID 0000-0002-9950-9792
Victor Chang Cardiac Research Institute · AUThe University of Sydney · AUNew South Wales Department of Health · AU

Funding

Genetic modifiers of congenital heart diseaseR01HL068885 · NHLBI · VICTOR CHANG CARDIAC RESEARCH INSTITUTE · PI HARVEY, RICHARD P · 2001 to 2005
$494k
NHLBI NIH HHS R01 HL068885
6 · The paper itself

Abstract

Unlike single-gene mutations leading to Mendelian conditions, common human diseases are likely to be emergent phenomena arising from multilayer, multiscale, and highly interconnected interactions. Atrial and ventricular septal defects are the most common forms of cardiac congenital anomalies in humans. Atrial septal defects (ASD) show an open communication between the left and right atria postnatally, potentially resulting in serious hemodynamic consequences if untreated. A milder form of atrial septal defect, patent

Indexed as

Brain IschemiaForamen Ovale, PatentHeart Defects, CongenitalStrokeAnimalsGene Expression ProfilingHumansMicePhenotypecardiac congenital defectsdevelopmental biologygeneticsgenomicsmousequantitative trait loci

Identifiers

PMID37272612
PMCPMC10284603
OpenAlexW4379376433

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.