Evidence map›Paper›PMID 29157190›Full record

ArticleVeterinary pathology2018

Mucopolysaccharidosis Type VI in a Great Dane Caused by a Nonsense Mutation in the ARSB Gene.

Ping Wang, Carol Margolis, Gloria Lin, Elizabeth L Buza, Scott Quick, Karthik Raj, Rachel Han, Urs Giger

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in Veterinary pathology, 2018. 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 30% 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, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. A HomozygousGenes · 2023
    Article
  4. Article
  5. Mucopolysaccharidosis Type VI, an Updated Overview of the Disease.International journal of molecular sciences · 2021
    Review
  6. 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

8 authors at 1 institution in 1 country.

Ping Wang1 Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Carol Margolis1 Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Gloria Lin1 Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Elizabeth L Buza2 Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Scott Quick3 Quality Pet Care, LLC, Monticello, NY, USA.
Karthik Raj1 Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Rachel Han1 Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Urs Giger1 Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
University of Pennsylvania · US

Funding

Referral Ctr-Animal models of human genetic diseaseP40OD010939 · OD · UNIVERSITY OF PENNSYLVANIA · PI CASAL, MARGRET L · 2012 to 2023
$7.9M
NIH HHS P40 OD010939
6 · The paper itself

Abstract

Mucopolysaccharidoses are inherited metabolic disorders that result from a deficiency of lysosomal enzymes required for the catabolism of glycosaminoglycans. Lysosomal glycosaminoglycan accumulation results in cell and organ dysfunction. This study characterized the phenotype and genotype of mucopolysaccharidosis VI in a Great Dane puppy with clinical signs of stunted growth, facial dysmorphia, skeletal deformities, corneal opacities, and increased respiratory sounds. Clinical and pathologic evaluations, urine glycosaminoglycan analyses, lysosomal enzyme assays, and ARSB sequencing were performed. The urine mucopolysaccharide spot test was strongly positive predominantly due to the accumulation of dermatan sulfate. Enzyme assays in leukocytes and tissues indicated a deficiency of arylsulfatase B (ARSB) activity. Histologic examination revealed cytoplasmic vacuoles in many tissues. Analysis of the exonic ARSB DNA sequences from the affected puppy compared to the published canine genome sequence revealed a homozygous nonsense mutation (c.295C>T) in exon 1, replacing glutamine with a premature stop codon (p.Gln99*), predicting no enzyme synthesis. A polymerase chain reaction-based restriction fragment length polymorphism test was established to assist with the clinical diagnosis and breeding of Great Danes. This genotyping test revealed that the clinically healthy parents and some other relatives of the puppy were heterozygous for the mutant allele, but all 200 clinically healthy dogs screened including 15 Great Danes were homozygous for the normal allele. This ARSB mutation is the fourth identified genetic variant causing canine mucopolysaccharidosis VI. Mucopolysaccharidosis VI is the first lysosomal storage disorder described in Great Danes but does not appear to be widespread in this breed.

Indexed as

AnimalsCodon, NonsenseDog DiseasesDogsMaleMucopolysaccharidosis VIN-Acetylgalactosamine-4-SulfataseSequence Analysis, DNACodon, NonsenseN-Acetylgalactosamine-4-Sulfatasearylsulfatase Bdogsgenetic diseaseshereditary diseaselysosomal storage diseaseskeletal deformity

Identifiers

PMID29157190
PMCPMC7879606
OpenAlexW2768724720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.