Evidence map›Paper›PMID 32563186›Full record

ArticlePediatric research2021

Troponin T amino acid mutation (ΔK210) knock-in mice as a neonatal dilated cardiomyopathy model.

Jun Tanihata, Teruyuki Fujii, Shunsuke Baba, Yoshitaka Fujimoto, Sachio Morimoto, Susumu Minamisawa

Abstract read
PubMed Publisher
In one paragraph

Article in Pediatric research, 2021. 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
0.3field-weighted citation impact, top 39% 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

6 authors at 2 institutions in 1 country.

Jun TanihataDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Teruyuki FujiiDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Shunsuke BabaDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Yoshitaka FujimotoDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Sachio MorimotoSchool of Health Science, International University of Health and Welfare, Fukuoka, Japan.
Susumu MinamisawaDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan. sminamis@jikei.ac.jp.
Jikei University School of Medicine · JPInternational University of Health and Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDilated cardiomyopathy (DCM) in children is often associated with poor morbidity and mortality and exhibits distinct pathological entities from those of adult DCM. Owing to the limited number of patients and the lack of a good animal model, the molecular mechanisms underlying pediatric DCM remain poorly understood. The purpose of this study is to establish an animal model of neonatal DCM and identify early progression factors.

methodsCardiac phenotypes and comprehensive gene expression profiles in homozygous ΔK210 knock-in (TNNT2

resultsImmediately after birth, the cardiac weight in TNNT2

conclusionsTNNT2 IMPACT: TNNT2

Indexed as

MutationAnimalsAnimals, NewbornCardiomyopathy, DilatedDisease Models, AnimalDown-RegulationEchocardiographyGene Expression ProfilingHeart VentriclesHomozygoteMiceMice, TransgenicOligonucleotide Array Sequence AnalysisPhenotypePrognosisTroponin TTroponin T

Identifiers

PMID32563186
OpenAlexW3036709333

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.