Evidence map›Paper›PMID 24966941›Full record

ArticleInternational journal of clinical and experimental pathology2014

Differential expressions of BMPR1α, ACTN4α and FABP7 in Hirschsprung disease.

Weilin Wang, Zhenwei Su, Dong Chen, Jie Mi, Hong Gao

Open access · greenAbstract readComparative Study
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. 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 40% 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, 1 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

5 authors at 2 institutions in 1 country.

Weilin WangKey Laboratory of Health Ministry for Congenital Malformations, Shengjing Hospital of China Medical University 36 Sanhao Street Heping District, Shenyang, Liaoning, 110004, The People's Republic of China.
Zhenwei SuDepartment of Pediatric Surgery, Women and Children Hospital Dandong City Liaoning 118002, The People's Republic of China.
Dong ChenKey Laboratory of Health Ministry for Congenital Malformations, Shengjing Hospital of China Medical University 36 Sanhao Street Heping District, Shenyang, Liaoning, 110004, The People's Republic of China.
Jie MiKey Laboratory of Health Ministry for Congenital Malformations, Shengjing Hospital of China Medical University 36 Sanhao Street Heping District, Shenyang, Liaoning, 110004, The People's Republic of China.
Hong GaoKey Laboratory of Health Ministry for Congenital Malformations, Shengjing Hospital of China Medical University 36 Sanhao Street Heping District, Shenyang, Liaoning, 110004, The People's Republic of China.
China Medical University · CNFujian Women and Children Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hirschsprung disease (HSCR) is characterized by the absence of intramural ganglion cells in the nerve plexuses of the distal gut. Recent studies have shown that the bone morphogenetic protein receptor-type IA (BMPR1α), actinin-alpha 4 (ACTN4α) and fatty acid binding protein 7 (FABP7) play important roles in the differentiation and development of neurons. The aganglionic (stenotic) and the ganglionic (normal) colon segment tissues of 60 HSCR patients were collected to investigate the expression pattern of BMPR1α, ACTININ-4α and FABP7 using RT-PCR, quantitative real-time RT-PCR (qRT-PCR) and immunohistochemical staining. The mRNA and protein expressions of BMPR1α and ACTN4α were higher in the stenotic colon segment tissue than those in the normal colon segment tissue. However, the mRNA and protein expressions of FABP7 were lower in the stenotic colon segment tissue than those in the normal colon segment tissue. The study in HSCR patients, findings in mRNA and protein alterations to expecting provide more information to in order to find some clue for the pathomechanism of HSCR disease.

Indexed as

ActininBiopsyBone Morphogenetic Protein Receptors, Type ICarrier ProteinsChild, PreschoolColonConstriction, PathologicFatty Acid-Binding Protein 7FemaleGene Expression RegulationHirschsprung DiseaseHumansImmunohistochemistryInfantMaleReal-Time Polymerase Chain ReactionActininACTN4 protein, humanBMPR1A protein, humanBone Morphogenetic Protein Receptors, Type ICarrier ProteinsFABP7 protein, humanFatty Acid-Binding Protein 7RNA, MessengerTumor Suppressor ProteinsACTININ-4α and FABP7aganglionic (stenotic) colon segmentBMPR1αganglionic (normal) colon segmentHirschsprung disease (HSCR)

Identifiers

PMID24966941
PMCPMC4069943
OpenAlexW254245393

What OpenQuestion holds

Textmetadata
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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.