Evidence map›Paper›PMID 34854126›Full record

ArticleJournal of veterinary internal medicine2022

Congenital muscular dystrophy in a dog with a LAMA2 gene deletion.

G Diane Shelton, Katie M Minor, Stephanie Thomovsky, Ling T Guo, Steven G Friedenberg, Jonah N Cullen, James R Mickelson

Open access · goldAbstract readCase Reports
In one paragraph

Article in Journal of veterinary internal medicine, 2022. 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 35% 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, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Congenital muscular dystrophy in a dog with a LAMA2 gene deletion.Journal of veterinary internal medicine · 2022
    Article
  6. Genes · 2021
    Article
  7. 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

7 authors at 3 institutions in 1 country.

G Diane SheltonDepartment of Pathology, School of Medicine, University of California San Diego, La Jolla, California, USA.ORCID https://orcid.org/0000-0002-3332-1359
Katie M MinorDepartment of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, Minnesota, USA.ORCID https://orcid.org/0000-0002-5472-5088
Stephanie ThomovskyDepartment of Veterinary Clinical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, Indiana, USA.
Ling T GuoDepartment of Pathology, School of Medicine, University of California San Diego, La Jolla, California, USA.ORCID https://orcid.org/0000-0002-2935-2646
Steven G FriedenbergDepartment of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, Minnesota, USA.ORCID https://orcid.org/0000-0002-7510-2322
Jonah N CullenDepartment of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, Minnesota, USA.
James R MickelsonDepartment of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, Minnesota, USA.ORCID https://orcid.org/0000-0001-6951-0234
University of Minnesota · USUniversity of California San Diego · USPurdue University West Lafayette · US

Funding

Immunological Basis of Autoimmune Addison's Disease in a Novel Canine Model SystemK01OD027058 · OD · UNIVERSITY OF MINNESOTA · PI FRIEDENBERG, STEVEN GENE · 2019 to 2023
$724k
NIH HHS K01 OD027058ODCDC CDC HHS K01 OD027058
6 · The paper itself

Abstract

A 2-year-old female spayed dog was presented with a chronic history of short-strided gait and inability to completely open the jaw. Clinical signs were present since the dog was adopted from a humane society at a few months of age. Serum creatine kinase activity was abnormally high. Neurological examination, electromyography, muscle biopsies with immunofluorescent staining, and whole genome sequencing (WGS) were performed. A dystrophic phenotype was identified histologically in muscle biopsies, deficiency of laminin α2 protein was confirmed by immunofluorescent staining, and a deletion in the LAMA2 gene was identified by analysis of the WGS data. Congenital muscular dystrophy associated with a disease variant in LAMA2 was identified.

Indexed as

Dog DiseasesMuscular DystrophiesAnimalsBiopsyDogsFemaleGene DeletionLamininMuscle, SkeletalPhenotypeLamininlaminin α2musclemyopathywhole genome sequencing

Identifiers

PMID34854126
PMCPMC8783360
OpenAlexW3216658853

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.