Publications by authors named "Harron R"

Article Synopsis
  • Duchenne muscular dystrophy (DMD) is a severe condition resulting from mutations in the dystrophin gene, and DE50-MD dogs serve as a model to test new therapies for this disease.
  • * Researchers aimed to find stable microRNA (miR) references for normalizing expression data across different ages and muscle groups in both healthy (WT) and DMD-affected dogs.
  • * The study identified four stable miRs (miR-191, let-7b, miR-125a, and miR-15a) that can be used to accurately normalize the expression levels of other miRs in muscle, indicating differences in miR levels between DE50-MD and WT dogs.
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Objective assessment of activity via accelerometry can provide valuable insights into dog health and welfare. Common activity metrics involve using acceleration cut-points to group data into intensity categories and reporting the time spent in each category. Lack of consistency and transparency in cut-point derivation makes it difficult to compare findings between studies.

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Duchenne muscular dystrophy (DMD), caused by mutations in the dystrophin (DMD) gene, is associated with fatal muscle degeneration and atrophy. Patients with DMD have progressive reductions in skeletal muscle strength and resistance to eccentric muscle stretch. Using the DE50-MD dog model of DMD, we assessed tibiotarsal joint (TTJ) flexor and extensor force dynamics, and the resistance of dystrophic muscle to eccentric stretch.

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Article Synopsis
  • - The DE50-MD dog model helps scientists study Duchenne muscular dystrophy (DMD) because these dogs show similar muscle problems as humans do, unlike mice models.
  • - Researchers took muscle samples from DE50-MD dogs and healthy dogs every three months to track the disease and find ways to test new treatments more effectively.
  • - They found that DE50-MD dogs experience muscle damage and inflammation, especially in their first year, and discovered biomarkers that can help measure the disease's progress.
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Duchenne muscular dystrophy (DMD) is a fatal muscle-wasting disease, caused by mutations in the dystrophin gene, characterised by cycles of muscle degeneration, inflammation and regeneration. Recently, there has been renewed interest specifically in drugs that ameliorate muscle inflammation in DMD patients. The DE50-MD dog is a model of DMD that closely mimics the human DMD phenotype.

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Duchenne muscular dystrophy (DMD) is a fatal muscle wasting disease caused by mutations in the dystrophin gene. Due to their phenotypic similarity to human patients, large animal models are invaluable tools for pre-clinical trials. The DE50-MD dog is a relatively new model of DMD, and carries a therapeutically-tractable mutation lying within the hotspot for human patients, making it especially valuable.

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The DE50-MD canine model of Duchenne muscular dystrophy (DMD) has a dystrophin gene splice site mutation causing deletion of exon 50, an out-of-frame transcript and absence of dystrophin expression in striated muscles. We hypothesized that the musculoskeletal phenotype of DE50-MD dogs could be detected using Magnetic Resonance Imaging (MRI), that it would progress with age and that it would reflect those in other canine models and DMD patients. 15 DE50-MD and 10 age-matched littermate wild type (WT) male dogs underwent MRI every 3 months from 3 to 18 months of age.

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The dystrophin gene has multiple isoforms: full-length dystrophin (dp427) is principally known for its expression in skeletal and cardiac muscle, but is also expressed in the brain, and several internal promoters give rise to shorter, N-terminally truncated isoforms with wider tissue expression patterns (dp260 in the retina, dp140 in the brain and dp71 in many tissues). These isoforms are believed to play unique cellular roles both during embryogenesis and in adulthood, but their shared sequence identity at both mRNA and protein levels makes study of distinct isoforms challenging by conventional methods. RNAscope is a novel hybridisation technique that offers single-transcript resolution and the ability to multiplex, with different target sequences assigned to distinct fluorophores.

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Background: Erosion of the distal catheter into lung parenchyma is an extremely rare complication of ventriculopleural shunt placement.

Case Description: We report a 51-year-old woman with a history of parasagittal meningioma invading the sagittal sinus who presented with recurrent pneumonia after placement of a ventriculopleural shunt. A nuclear study revealed accumulation of radiotracer material sequentially in the right hemithorax, trachea, mainstem bronchi, stomach, and bowel.

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Mutations in the gene encoding dystrophin, a protein that maintains muscle integrity and function, cause Duchenne muscular dystrophy (DMD). The deltaE50-MD dog model of DMD harbors a mutation corresponding to a mutational "hotspot" in the human gene. We used adeno-associated viruses to deliver CRISPR gene editing components to four dogs and examined dystrophin protein expression 6 weeks after intramuscular delivery ( = 2) or 8 weeks after systemic delivery ( = 2).

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A study was conducted to evaluate the effects of a long-acting trace mineral rumen bolus (TMB) supplement on the productive performance, metabolic profiles, and trace mineral status of growing camels under natural grazing conditions. Fifteen 6-month-old growing male camels (average bodyweight 139.51 ± 26.

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