Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse

Research output: ResearchDoctoral Thesis

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Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse. / Crabb, Hannah.

2010.

Research output: ResearchDoctoral Thesis

Harvard

Crabb, H 2010, 'Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse', Doctor of Philosophy.

APA

Crabb, H. (2010). Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse

Vancouver

Crabb H. Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse. 2010.

Author

Crabb, Hannah. / Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse. 2010.

Bibtex

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@phdthesis{1c5e00b55c2e4023b297663a84d0c853,
title = "Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse",
abstract = "[Truncated abstract] Duchenne Muscular Dystrophy (DMD) is a lethal X-linked muscle wasting disease resulting from defects in the myofibre subsarcolemmal protein dystrophin. The lack of functional dystrophin protein leads to myofibre membrane fragility, repeated cycles of myofibre necrosis and regeneration, and the eventual replacement of skeletal muscle by fatty and fibrous connective tissue. DMD is characterised by progressive muscle weakness and wasting with a limited life expectancy of approximately 20 years in humans. Myofibre necrosis is the fundamental destructive process in DMD although the exact mechanism by which the absence of dystrophin leads to myofibre necrosis is unknown; inflammation, oxidative stress, metabolic abnormality, mislocalisation of nNOS and increased intracellular calcium are all heavily implicated in the process.",
keywords = "Duchene muscular dystrophy, Mdx mouse, Exercise, Therapeutic interventions, Anti-inflammatory, Skeletal muscle",
author = "Hannah Crabb",
year = "2010",

}

RIS

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TY - THES

T1 - Therapeutic interventions for Duchenne Muscular Dystrophy - studies in the mdx mouse

AU - Crabb,Hannah

PY - 2010

Y1 - 2010

N2 - [Truncated abstract] Duchenne Muscular Dystrophy (DMD) is a lethal X-linked muscle wasting disease resulting from defects in the myofibre subsarcolemmal protein dystrophin. The lack of functional dystrophin protein leads to myofibre membrane fragility, repeated cycles of myofibre necrosis and regeneration, and the eventual replacement of skeletal muscle by fatty and fibrous connective tissue. DMD is characterised by progressive muscle weakness and wasting with a limited life expectancy of approximately 20 years in humans. Myofibre necrosis is the fundamental destructive process in DMD although the exact mechanism by which the absence of dystrophin leads to myofibre necrosis is unknown; inflammation, oxidative stress, metabolic abnormality, mislocalisation of nNOS and increased intracellular calcium are all heavily implicated in the process.

AB - [Truncated abstract] Duchenne Muscular Dystrophy (DMD) is a lethal X-linked muscle wasting disease resulting from defects in the myofibre subsarcolemmal protein dystrophin. The lack of functional dystrophin protein leads to myofibre membrane fragility, repeated cycles of myofibre necrosis and regeneration, and the eventual replacement of skeletal muscle by fatty and fibrous connective tissue. DMD is characterised by progressive muscle weakness and wasting with a limited life expectancy of approximately 20 years in humans. Myofibre necrosis is the fundamental destructive process in DMD although the exact mechanism by which the absence of dystrophin leads to myofibre necrosis is unknown; inflammation, oxidative stress, metabolic abnormality, mislocalisation of nNOS and increased intracellular calcium are all heavily implicated in the process.

KW - Duchene muscular dystrophy

KW - Mdx mouse

KW - Exercise

KW - Therapeutic interventions

KW - Anti-inflammatory

KW - Skeletal muscle

M3 - Doctoral Thesis

ER -

ID: 3367537