Evidence map›Paper›PMID 27891608›Full record

ArticleThe Journal of physiology2017

Compensatory axon sprouting for very slow axonal die-back in a transgenic model of spinal muscular atrophy type III.

Esther Udina, Charles T Putman, Luke R Harris, Neil Tyreman, Victoria E Cook, Tessa Gordon

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

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-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

7 citing papers in PubMed, 12 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 2 institutions in 2 countries.

Esther UdinaNeuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada, T6G 2S2.
Charles T PutmanNeuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada, T6G 2S2.
Luke R HarrisNeuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada, T6G 2S2.ORCID 0000-0001-6771-1200
Neil TyremanNeuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada, T6G 2S2.
Victoria E CookNeuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada, T6G 2S2.
Tessa GordonNeuroscience and Mental Health Institute, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada, T6G 2S2.
University of Alberta · CAUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsSmn ABSTRACT: Spinal muscular atrophy (SMA) is a common autosomal recessive disorder in humans and is the leading genetic cause of infantile death. Patients lack the SMN1 gene with the severity of the disease depending on the number of copies of the highly homologous SMN2 gene. Although motoneuron death in the Smn

Indexed as

AnimalsAxonsFemoral NerveHindlimbMice, Inbred C57BLMice, TransgenicMotor NeuronsMuscle Fibers, Fast-TwitchMuscle Fibers, Slow-TwitchMuscular Atrophy, SpinalSciatic NerveSurvival of Motor Neuron 1 ProteinSmn1 protein, mouseSurvival of Motor Neuron 1 Proteinmotoneuron countsmotor unitsSmn+/− III transgenic micespinal muscular atrophy

Identifiers

PMID27891608
PMCPMC5330916
OpenAlexW2558825915

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.