Evidence map›Paper›PMID 25574480›Full record

ArticleAnnals of clinical and translational neurology2014

Laing distal myopathy pathologically resembling inclusion body myositis.

Ricardo H Roda, Alice B Schindler, Craig Blackstone, Andrew L Mammen, Andrea M Corse, Thomas E Lloyd

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  3. Review
  4. 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 4 institutions in 1 country.

Ricardo H RodaNeuromuscular Disorders and Neurogenetics Divisions, Department of Neurology, New York University Langone Medical Center New York, New York ; Cell Biology Section, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, Maryland.
Alice B SchindlerHereditary Neurological Diseases Section, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, Maryland.
Craig BlackstoneCell Biology Section, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, Maryland.
Andrew L MammenDepartment of Neurology, Johns Hopkins University School of Medicine Baltimore, Maryland ; Department of Medicine, Johns Hopkins University School of Medicine Baltimore, Maryland ; Muscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulation, National Institutes of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health Bethesda, Maryland.
Andrea M CorseDepartment of Neurology, Johns Hopkins University School of Medicine Baltimore, Maryland.
Thomas E LloydDepartment of Neurology, Johns Hopkins University School of Medicine Baltimore, Maryland ; Department of Neuroscience, Johns Hopkins University School of Medicine Baltimore, Maryland.
Johns Hopkins University · USNational Institutes of Health · USNational Institute of Neurological Disorders and Stroke · USNYU Langone Health · US

Funding

Regulation of Mitochondrial Fission and FusionZIANS003025 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI BLACKSTONE, CRAIG · 2009 to 2021
$2.4M
Dynactin function in axons, synapses, and neurodegenerative diseaseR01NS082563 · NINDS · JOHNS HOPKINS UNIVERSITY · PI LLOYD, THOMAS E. · 2013 to 2017
$1.8M
NINDS NIH HHS R01 NS082563
6 · The paper itself

Abstract

Mutations in MYH7 cause autosomal dominant Laing distal myopathy. We present a family with a previously reported deletion (c.5186_5188delAGA, p.K1729del). Muscle pathology in one family member was characterized by an inflammatory myopathy with rimmed vacuoles, increased MHC Class I expression, and perivascular and endomysial muscle inflammation comprising CD3(+), CD4(+), CD8(+), and CD68(+) inflammatory cells. Interestingly, this biopsy specimen contained TDP-43, p62, and SMI-31-positive protein aggregates typical of inclusion body myositis. These findings should alert physicians to the possibility that patients with MYH7 mutations may have muscle biopsies showing pathologic findings similar to inclusion body myositis.

Identifiers

PMID25574480
PMCPMC4284131
OpenAlexW2075324861

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.