Evidence map›Paper›PMID 32210824›Full record

ReviewFrontiers in pharmacology2020

The Role of Fibroblast Growth Factor 10 Signaling in Duodenal Atresia.

Matthew L M Jones, Gulcan Sarila, Pierre Chapuis, John M Hutson, Sebastian K King, Warwick J Teague

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2020. 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
1.0field-weighted citation impact, top 24% 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, 11 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

6 authors at 4 institutions in 1 country.

Matthew L M JonesF. Douglas Stephens Surgical Research Laboratory, Murdoch Children's Research Institute, Melbourne, VIC, Australia.
Gulcan SarilaF. Douglas Stephens Surgical Research Laboratory, Murdoch Children's Research Institute, Melbourne, VIC, Australia.
Pierre ChapuisDiscipline of Surgery, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia.
John M HutsonF. Douglas Stephens Surgical Research Laboratory, Murdoch Children's Research Institute, Melbourne, VIC, Australia.
Sebastian K KingF. Douglas Stephens Surgical Research Laboratory, Murdoch Children's Research Institute, Melbourne, VIC, Australia.
Warwick J TeagueF. Douglas Stephens Surgical Research Laboratory, Murdoch Children's Research Institute, Melbourne, VIC, Australia.
Murdoch Children's Research Institute · AUUniversity of Sydney · AURoyal Children's Hospital · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDuodenal atresia (DA) is a congenital bowel obstruction requiring major surgery in the first week of life. Three morphological phenotypes are described, reflecting increasing degrees of obstruction and discontinuity of the duodenum. The cause of DA is not known. Tandler's original "solid cord" hypothesis conflicts with recent biological evidence, and is unable to account for differing DA types. In humans, a genetic etiology is supported by the association between Trisomy 21 and DA, and reports of familial inheritance patterns. Interruption of FGF10/FGFR2b signaling is the best demonstrated genetic link to DA in mice, with 35-75% of homozygous knockout embryos developing DA. PURPOSE: This review examines the current evidence surrounding the etiology of DA. We focus on research regarding FGF10/FGFR2b signaling and its role in duodenal and other intestinal atresia. Further, we outline planned future research in this area, that we consider necessary to validate and better understand this murine model in order to successfully translate this research into clinical practice.

conclusionDetermining the etiology of DA in humans is a clinical and scientific imperative.

Indexed as

congenital intestinal atresiaduodenal obstructionfibroblast growth factor 10fibroblast growth factor receptor 2bmorphogenesis

Identifiers

PMID32210824
PMCPMC7076179
OpenAlexW3011402677

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.