Evidence map›Paper›PMID 27748330›Full record

ArticleChinese medical journal2016

Zhao-Ru Ju, Hui-Jun Wang, Xiao-Jing Ma, Duan Ma, Guo-Ying Huang

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

Article in Chinese medical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. 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

5 authors at 1 institution in 1 country.

Zhao-Ru JuPediatric Cardiovascular Center, Children's Hospital of Fudan University, Shanghai 201102, China.
Hui-Jun WangPediatric Cardiovascular Center, Children's Hospital of Fudan University, Shanghai 201102; Laboratory of Congenital Heart Disease, Shanghai Key Laboratory of Birth Defects, Shanghai 201102, China.
Xiao-Jing MaPediatric Cardiovascular Center, Children's Hospital of Fudan University, Shanghai 201102; Laboratory of Congenital Heart Disease, Shanghai Key Laboratory of Birth Defects, Shanghai 201102, China.
Duan MaLaboratory of Congenital Heart Disease, Shanghai Key Laboratory of Birth Defects, Shanghai 201102, China.
Guo-Ying HuangPediatric Cardiovascular Center, Children's Hospital of Fudan University, Shanghai 201102; Laboratory of Congenital Heart Disease, Shanghai Key Laboratory of Birth Defects, Shanghai 201102, China.
Children's Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe most typical cardiac abnormality is conotruncal defects (CTDs) in patients with 22q11 deletion syndrome (22q11DS). HIRA (histone cell cycle regulator) gene, as one of the candidate genes located at the critical region of 22q11DS, was reported as possibly relevant to CTD in animal models. This study aimed to analyze the level of expression of the HIRA gene in tetralogy of Fallot (TOF) patients and the potential DNA sequence variations in the promoter region.

methodsThe messenger RNA (mRNA) expression was examined with quantitative real-time polymerase chain reaction in 39 myocardial tissues of the right ventricular outflow tract (RVOT) from TOF patients and 4 myocardial tissues of RVOT from noncardiac death children. The protein expression was detected using immunohistochemistry in 12 TOF patients and 4 controls. A total of 100 TOF cases and 200 healthy controls were recruited for DNA sequencing.

resultsThe mRNA and protein expressions of the HIRA gene in the myocardium of the TOF patients were both significantly lower as compared to the controls (P < 0.05). Five single nucleotide polymorphisms (SNPs), including g.4111A>G (rs1128399), g.4265C>A (rs4585115), g.4369T>G (rs2277837), g.4371C>A (rs148516780), and g.4543T>C (rs111802956), were found in the promoter region of the HIRA gene. There were no significant differences of frequencies in these SNPs between the TOF patients and the controls (P > 0.05).

conclusionThe abnormal lower expression of the HIRA gene in the myocardium may participate in the pathogenesis of TOF.

Indexed as

AllelesCell Cycle ProteinsFemaleGenotypeHistone ChaperonesHumansImmunohistochemistryIn Vitro TechniquesMaleMyocardiumPolymorphism, Single NucleotideReal-Time Polymerase Chain ReactionRNA, MessengerTetralogy of FallotTranscription FactorsCell Cycle ProteinsHIRA protein, humanHistone ChaperonesRNA, MessengerTranscription Factors

Identifiers

PMID27748330
PMCPMC5072250
OpenAlexW2531506713

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.