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Dissertations / Theses on the topic 'Dystrophic muscle'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Laws, Nicola. "Characterisation and strategic treatment of dystrophic muscle." University of Southern Queensland, Faculty of Sciences, 2005. http://eprints.usq.edu.au/archive/00001457/.

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The mdx mouse is widely used as a model for Duchenne Muscular Dystrophy, a fatal X-linked disease caused by a deficiency of the sub-sarcolemmal protein, dystrophin. This dissertation reports characterisation of the features of dystrophy in the mdx mouse, including parameters such as electrophysiological and contractile properties of dystrophic cardiac tissue, quantitative evaluation of kyphosis throughout the mdx lifespan, and contractile properties of respiratory and paraspinal muscles. Following these characterisation studies, the efficacy of antisense oligonucleotides (AOs) to induce altern

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2

Wolff, Andrew. "Mechanical Properties of Maturing Dystrophic Skeletal Muscle." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/37922.

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The main goal for my research was to challenge the long held belief that the mechanical properties of maturing dystrophic compared to control skeletal muscle membranes are weaker, leading to onset of Duchenne muscular dystrophy (DMD). We built on a previous report from our lab that suggested sarcolemmal membranes from dystrophic mice are not more susceptible to damage early in maturation (i.e., age 9-12 days) and determined if and when muscle mechanical properties change as the mice mature. Across four studies, I have helped define the role of dystrophin-deficient skeletal muscle membranes i

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3

Morrison, Jamie Ian. "Factors affecting excessive collagen production in dystrophic muscle." Thesis, Imperial College London, 2002. http://hdl.handle.net/10044/1/7695.

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4

Dutton, Anna Louise. "An investigation into the effects of dystrophin on the lateral mobility of muscle membrane components." Thesis, Durham University, 1999. http://etheses.dur.ac.uk/4576/.

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Dystrophin is the product of the Duchenne Muscular Dystrophy gene locus, whose absence results in progressive skeletal muscle breakdown. Despite considerable work on the localisation of dystrophin and its associated complex, its role in muscle function remains unclear. In the light of the structural and mechanical instability of the dystrophic membrane, the idea was tested that dystrophin might impart membrane integrity and strength by anchoring membrane proteins and/or delineating the surface into specialised subcellular functional domains. Specifically, because dystrophin shows high sequence

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5

Rowe, K. A. "Quantitative microscopic studies of normal and dystrophic chicken muscle." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375318.

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6

Bryers, P. S. "Regeneration and differentiation of muscle from normal and dystrophic mice." Thesis, University of Newcastle Upon Tyne, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374843.

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7

Draper, Kati Elizabeth. "Increased structure-bound proteolytic activity in maturing dystrophic skeletal muscle." Thesis, Virginia Tech, 2004. http://hdl.handle.net/10919/31735.

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Duchenne Muscular Dystrophy (DMD) is a severe X-linked progressive muscle wasting disease resulting from the absence of the membrane-associated protein dystrophin and the secondary components of the dystrophin-glycoprotein complex. Although the genetic basis of the disease has been known for over 15 years, the onset mechanism of the disease is not yet known and no treatment is yet available to significantly increase the lifespan of DMD patients. Increased levels of intracellular calcium have been noted in dystrophic muscle (Turner et al., 1991) and increased intracellular levels of calcium

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8

Veal, Elizabeth Ann. "The role of proto-oncogenes in normal and dystrophic skeletal muscle." Thesis, University of Liverpool, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307666.

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9

Jarvis, Jonathan Charles. "The effects of electrical stimulation on normal and dystrophic avian muscle." Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/46382.

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10

Wang, Qiong. "The activity and content of calpains in maturing dystrophic muscle membranes." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/42729.

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Increased calcium-activated calpain proteolysis in the sarcolemma membrane is thought to be a primary mechanism in the pathophysiology of Duchenne Muscular Dystrophy (DMD). However, few studies have tested this possibility prior to the overt signs of the dystrophy. The purpose of this study was to test the hypothesis that there is greater calpain content and total relative calpain activity in membranes obtained from dystrophic (mdx; mdx:utrophin-deficient (mdx:utrn-/-)) compared to wildtype (wt) mouse skeletal muscles during maturation at ages 7- and 21-d,and at a post-maturation age of 35-d.

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11

van, Erp Christel. "Modifying function and fibrosis of cardiac and skeletal muscle from mdx mice." University of Southern Queensland, Faculty of Sciences, 2005. http://eprints.usq.edu.au/archive/00001521/.

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Duchenne Muscular Dystrophy (DMD) is a fatal condition occurring in approximately 1 in 3500 male births and is due to the lack of a protein called dystrophin. Initially DMD was considered a skeletal myopathy, but the pathology and consequences of cardiomyopathy are being increasingly recognised. Fibrosis, resulting from continual cycles of degeneration of the muscle tissues followed by inadequate regeneration of the muscles, is progressive in both cardiac and skeletal dystrophic muscle. In the heart fibrosis interferes with contractility and rhythm whereas it affects contractile function and c

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12

Turner, Sally Ann. "Analysis of dystrophic mdx muscle following the implantation of normal dermal fibroblasts." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271623.

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13

Fisher, Ivan Brian. "Glucocorticoid-induced changes in the skeletal muscle of the dystrophic MDX mouse." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407223.

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14

Coenen-Stass, Anna. "Investigation of extracellular microRNAs and Serum Protein Biomarkers in dystrophic Muscle Disease." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:66d50b2b-b8b5-4604-a8ef-6b08de3d06b6.

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15

Gerhalter, Teresa. "Characterization of the dystrophic muscle by ²³Na NMR and ¹H NMR T₂ spectrum." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS219/document.

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Le but de la thèse était d'étudier la sensibilité de nouveaux biomarqueurs RMN visant à quantifier les changements pathologiques dans le muscle dystrophique. La dystrophie musculaire (DM) désigne un groupe hétérogène de maladies avec une atrophie musculaire progressive associée à un état de faiblesse. Elle est caractérisée par des degrés variables de nécrose, de régénération, de troubles de l'homéostasie ionique, d'inflammation chronique et finalement par le remplacement des muscles par du tissu fibro-graisseux. Mon objectif était d’évaluer la RMN du ²³Na et les techniques avancées de mesure d

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16

Johnson, Marjorie Isabelle. "Alterations in fast and slow-twitch muscles of genetically dystrophic mice with special reference to parvalbumin." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/27358.

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Muscular dystrophy is a genetic disease which affects the morphology, physiology and biochemical nature of the muscle fiber. This study was designed to examine the progressive effects of muscular dystrophy on the differentiation process of skeletal muscle. Chapter 1 examines the neonatal development of muscle spindles and their intrafusal fibers in the soleus and extensor digitorum longus (EDL) of genetically dystrophic mice according to histochemical, quantitative, and ultrastructural parameters. Despite alterations in the surrounding extrafusal fibers, muscle spindles and their intrafusal fi

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17

Joseph, Sarah. "The potential role of toll-like receptor 2 in dystrophic- deficient skeletal muscle." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86855.

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The mdx mouse is the genetic homologue of Duchenne Muscular Dystrophy (DMD). In this model, repeated cycles of muscle fiber necrosis occur within the diaphragm and other muscles. It has been reported that molecules associated with tissue damage, such as extracellular matrix breakdown products, can act as endogenous ligands for Toll-Like receptors (TLRs). However, the role of TLRs and endogenous ligands released from damaged skeletal muscle has not been examined. The goals of this study were to determine whether genes associated with TLR function are abnormally regulated in mdx diaphragm an

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18

Marrone, Anna Filomena. "Retinoblastoma (Rb) regulation and programmed cell death (PCD) in dystrophic (mdx) skeletal muscle." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621356.

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19

Doreste, Gonzalez Bruno. "The effect of modulating the dystrophic skeletal muscle environment on satellite cell engraftment." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10051216/.

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Satellite cells derived from normal donor mice contribute to muscle regeneration and restore dystrophin expression when transplanted into dystrophin-deficient mice (mdxnu/nu). However, unless the local host muscle environment has been modulated with high doses of gamma-radiation to incapacitate host satellite cells, but maintaining a functional niche, donor satellite cell engraftment is negligible. This work aimed to determine the cells and pathway(s) within host muscle which are responsible for mediating the radiation-induced effect. I first investigated whether this effect was mediated by ap

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20

Rittler, Matthew Robert. "Sarcoplasmic Reticulum Calcium Handling in Maturing Skeletal Muscle From Two Models of Dystrophic Mice." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/35619.

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<p>Duchenne's muscular dystrophy (DMD) is a debilitating disease that affects approximately 1 in 3500 boys, with many DMD patients dying before the age of 20 due to cardio-respiratory complications. DMD is the result of defects in the gene that encodes dystrophin, an integral muscle membrane protein. Although the genetic defect has been identified, the relation between the absence of expressed dystrophin and the mechanisms leading to its onset are still unclear. One possibility is that disrupted calcium (Ca<sup>2+</sup>) handling by the sarcoplasmic reticulum (SR) leads to an increased cytoso

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21

Russell, Paul. "Membrane properties and calcium ion activity in skeletal muscle fibres of the dystrophic mouse." Thesis, University of Central Lancashire, 1993. http://clok.uclan.ac.uk/20630/.

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The ReJI29 murine model of muscular dystrophy was employed to investigate the properties of skeletal muscle plasmalemma and calcium ion movements during muscle wastage, with the intention of determining the route of calcium influx, and the efficacy of calcium ion blockers in preventing this influx. Electrophysiological parameters (Resting membrane potential [RMP] and input resistance) reached adult magnitude in normal soleus and extensor digitorum longus (EDL) by 4 weeks and 3 weeks respectively. Electrophysiological parameters in dystrophic soleus developed in a similar maimer to normal muscl

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22

Penton, Christopher. "In Vitro Differentiation of Muscle Side Population Cells from Dystrophic Muscle Reveals Absence of Myogenesis and Implications for Hedgehog Signaling." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385397533.

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23

Al-Rewashdy, Hasanen. "Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31470.

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Duchenne Muscular Dystrophy (DMD) results from the absence of a functional dystrophin protein. Among its possible therapeutic options is the upregulation of dystrophin’s autosomal analogue, utrophin A. This can be achieved by a pharmacologically induced shift towards a slower, more oxidative skeletal muscle phenotype, which has been shown to confer morphological and functional improvements on models of DMD. Whether these improvements are a result of the utrophin A upregulation or other beneficial adaptations associated with the slow, oxidative phenotype, such as improved autophagy, has not bee

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24

Gerhalter, Teresa [Verfasser]. "Characterization of the dystrophic muscle by 23Na NMR and 1H NMR T2 spectrum / Teresa Gerhalter." Berlin : Freie Universität Berlin, 2018. http://d-nb.info/118099423X/34.

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25

Maffioletti, S. M. "Generation of biocompatible human 3D skeletal muscle tissue from healthy and dystrophic pluripotent stem cells." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1556255/.

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Skeletal muscle is a tissue with remarkable regenerative abilities but a wide range of disorders can impair its functions. At present, there is no effective therapy for most of these pathologies and this represents a significant unmet medical need. The pursuit of therapeutic strategies has led to the development of different encouraging approaches. Importantly, tissue engineering is also emerging as a promising discipline for the establishment of new platforms with therapeutic relevance for muscle disorders. Generating human artificial skeletal muscles in vitro would indeed provide an invaluab

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26

Gainer, Thomas Gregory. "Immune Response Markers are Prevalent in the mRNA Expression Profile of Maturing Dystrophic Murine Skeletal Muscle." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/33263.

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Duchenne muscular dystrophy (DMD) is a severe and fatal muscle wasting disease characterized by a high mutation rate in the gene that encodes the membrane-associated protein dystrophin that results in absence of expressed protein. Although the primary genetic defect for DMD is known, the mechanisms that initiate the onset of DMD are not currently understood. This study tested the hypothesis that pathophysiological processes involved in DMD could be identified by the global expression of mRNA in maturing dystrophin- and utrophin-deficient mouse (mdx:utrn-/-) muscles. Two potential dystrophic o

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27

Moulay, Gilles. "APPROCHES DE THÉRAPIES GÉNIQUES POUR DES MALADIES NEUROMUSCULAIRES." Phd thesis, Université d'Evry-Val d'Essonne, 2010. http://tel.archives-ouvertes.fr/tel-00507450.

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La thérapie génique de myopathies telles que la dystrophie musculaire de Duchenne nécessite une approche systémique afin de traiter l'ensemble de la musculature. Le vecteur AAV est actuellement le plus efficace pour transduire le muscle. Nous montrons que la biodistribution du vecteur AAV administré par voie veineuse peut être modifiée en utilisant diverses stratégies adjuvantes chez la souris saine. La pré-injection de polymères permet ainsi d'améliorer la transduction des muscles par le vecteur AAV, ou encore de baisser la réponse immune neutralisante induite par l'injection intraveineuse du

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28

Fair, Jeanette L. "Effects of compensatory hypertrophy on dystrophic (Bio 14.6) hamster muscle : changes in collagen and myofibrillar protein content." Virtual Press, 1987. http://liblink.bsu.edu/uhtbin/catkey/494971.

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Compensatory hypertrophy was induced on the plantaris (PL) and soleus (SOL) muscles of five week old normal and dystrophic (strain 14.6) hamsters. This was done to indicate whether submaximal exercise would be beneficial in reducing the progression of the muscular dystrophy (i.e., by causing muscle hypertrophy, reducing the total collagen content, and increasing the total protein content of the diseased muscle to approximate that of normal tissue).The hamsters were divided into four groups: 1) dystrophic overload (DO), 2) dystrophic control (DC), 3) normal overload (NO), and 4) normal control

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29

Nahirney, Patrick Charles. "Morphological quantitative and ultracytochemical studies on the internal membrane systems of normal and mdx-dystrophic murine skeletal muscle fibers." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/NQ48681.pdf.

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30

Acharyya, Swarnali. "Elucidating molecular mechanisms of muscle wasting in chronic diseases." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1180096565.

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31

Pasalic, Dario. "No Calpain, No Gain: Newly Developed Procedures for the Separation and Characterization of The Calpain Family of Proteins in Human Dystrophic and Non-dystophic Muscle." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146022.

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Muscular dystrophy is a disease which gradually deteriorates skeletal muscle cells, leading to the eventual death of such cells and the surrounding tissue. Calpains are Ca2+- dependent proteases and together with the Ca2+-dependent specific inhibitor of calpains, calpastatin, are widely distributed in eukaryotic cells. It has been suggested that part of the enhanced deterioration in the dystrophic state is due to enhanced calpain activity; therefore analysis of normal and dystrophic muscle was essential. Conventional techniques for the isolation and characterization of calpain and calpastatin

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32

Dias, Wilson Vinicius. "Adaptations du métabolisme musculaire en réponse à l’exercice et à une supplémentation en antioxydants chez des patients atteints de Dystrophie Fascioscapulohumérale." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT030.

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La dystrophie FacioScapuloHumérale (FSHD), décrite pour la première fois en 1885 par Landouzy Dejerine, est la première dystrophie musculaire de l’adulte en France affectant entre 4000 et 5000 personnes. La destruction progressive des fibres musculaires entraîne une atrophie et une faiblesse musculaires s’aggravant progressivement, avec cependant une grande variabilité intra-familiale du degré des atteintes. Une caractéristique de l’atteinte musculaire est généralement son asymétrie. Les premières manifestations concernent souvent les muscles du visage, les muscles de l’omoplate et des muscles

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33

Lekan, Jaimy Marie. "Exercise-induced mechanisms of muscle adaptation in mdx mice." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379.

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34

Deol, Jatinderpal. "Development of helper-dependent adenovirus for gene expression in muscle." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33745.

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Duchenne muscular dystrophy (DMD) is characterized by necrosis and progressive loss of muscle fibers. DMD patients have a mutation in the gene encoding dystrophin, a large membrane-associated cytoskeletal protein on the cytoplasmic side of the sarcolemma. Gene therapy using fully deleted adenoviral vectors shows great potential for the eventual treatment of DMD and other genetic diseases. These vectors are less immunogenic than their predecessors and have the capacity to carry large DNA inserts such as the full-length dystrophin (12 kb). However, the lack of viral genes results in a weakened a

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35

Judge, Luke Milburn. "Dissecting the signaling and mechanical functions of the dystrophin-glycoprotein complex in skeletal muscle /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/4989.

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36

Chevron, Marie-Pierre. "Dystrophine et utrophine dans les dystrophies musculaires et au cours du développemnt des muscles squelettique, cardiaque et lisse humains." Montpellier 1, 1994. http://www.theses.fr/1994MON1T023.

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37

Johnson, Eric K. "A new model for the dystrophin associated protein complex in striated muscles." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354554580.

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38

Lecroisey-Leroy, Claire. "Caractérisation moléculaire et cellulaire de la dégénérescence musculaire dépendante de la dystrophine chez le nématode Cænorhabditis elegans." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10152.

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La Dystrophie Musculaire de Duchenne (DMD) est la plus fréquente et la plus sévère des maladies dégénératives du muscle. Elle se caractérise par une dégénérescence progressive des fibres musculaires due à l’absence de dystrophine fonctionnelle dans les muscles. Actuellement, le rôle physiologique de la dystrophine n’est pas clairement établi et il n’existe pas encore de traitement curatif pour cette maladie. La difficulté de mettre en évidence la fonction de la dystrophine et la physiopathologie de la DMD est en partie expliquée par la complexité moléculaire et cellulaire du muscle des modèles

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39

Chassagne, Julie. "Mécanismes moléculaires impliqués dans l’efficacité de transduction des vecteurs AAV dans le muscle dystrophique." Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS514.pdf.

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La Dystrophie Musculaire de Duchenne (DMD) est une maladie génétique causée par l’absence de dystrophine et provoquant une dégénérescence musculaire sévère. Aucun traitement curatif n’existe aujourd’hui mais la thérapie génique par vecteur AAV est l’une des stratégies les plus prometteuses pour traiter la DMD. Malgré l’efficacité bien établie de l’AAV de sérotype 8 (AAV8) pour le transfert de gène dans le muscle, de fortes doses de vecteurs sont nécessaires pour obtenir une efficacité thérapeutique dans des modèles animaux de la DMD. Dans ce contexte, j’ai étudié les mécanismes qui peuvent lim

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40

Bestard, Jennifer. "Dystrophin gene regulation in muscle." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0016/MQ54086.pdf.

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41

Woolf, Peter James. "Cardiac calcium handling in the mouse model of Duchenne Muscular Dystrophy." University of Southern Queensland, Faculty of Sciences, 2003. http://eprints.usq.edu.au/archive/00001525/.

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The dystrophinopathies are a group of disorders characterised by cellular absence of the membrane stabilising protein, dystrophin. Duchenne muscular dystrophy is the most severe disorder clinically. The deficiency of dystrophin, in the muscular dystrophy X-linked (mdx) mouse causes an elevation in intracellular calcium in cardiac myocytes. Potential mechanisms contributing to increased calcium include enhanced influx, sarcoplasmic reticular calcium release and\or reduced sequestration or sarcolemmal efflux. This dissertation examined the potential mechanisms that may contribute to an intracell

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Sperringer, Justin Edward. "Chronic Dietary Supplementation of Branched-Chain Amino Acids Does Not Attenuate Muscle Torque Loss in a Mouse Model of Duchenne Muscular Dystrophy." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/93577.

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Duchenne Muscular Dystrophy (DMD) is an X-linked recessive, progressive muscle-wasting disease characterized by mutations in the dystrophin gene. Duchenne muscular dystrophy is the most common and most severe form of inherited muscle diseases, with an incidence of 1 in 3,500 male births1,2. Mutations in the dystrophin gene result in non-functional dystrophin or the complete absence of the protein dystrophin, resulting in necrosis and fibrosis in the muscle, loss of ambulation, cardiomyopathies, inadequate or failure of respiratory function, and decreased lifespan. Although there has been littl

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43

Barthélémy, Florian. "La modularité de la dysferline peut-elle permettre le développement d'approches thérapeutiques?" Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5035.

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Durant ma thèse, mes recherches se sont principalement portées sur l'identification des propriétés modulaires de la dysferline, une protéine impliquée dans des dystrophies musculaires, afin d'identifier les approches thérapeutiques les plus prometteuses. Mon travail s’est donc orienté selon deux axes de recherche, une approche par « mini-protéines » et une approche par «saut d’exon », toutes deux basées sur des preuves de principe obtenues chez des patients. Nous avons tout d'abord testé une approche de saut d'exon pour l'exon 32 de DYSF. Nous avons pu établir la fonctionnalité de cette protéi

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44

Brouilly, Nicolas. "Dégénérescence musculaire chez Caenorhabditis elegans : caractérisation morphologique et étude de suppresseurs." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10143/document.

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Les dystrpohies musculaires sont des maladies génétiques rares qui se caractérisent par une dégénérescence musculaire progressive. la Dystrophie Musculaire de Duchenne (DMD) qui est la plus sévère d'entre elles est due à des mutations dans le gène de la dystrophine. Les mécanismes cellulaires impliqués dans le processus de dégénérescence des muscles restent peu compris et aucun traitement efficace n'existe à ce jour. Notre équipe a développé un modèle de la DMD chez le nématode C. elegans qui présente une dégénérescence musculaire progressive. Pendant ma thèse, j'ai caractérisé le processus de

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45

Sommer, Barbara. "Changes of skeletal muscle in adult dystrophin-deficient cats /." [S.l.] : [s.n.], 2000. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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46

Guibinga, Ghiabe H. "Molecular therapeutic interventioan for dystrophin-deficient muscles." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36945.

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Duchenne muscular dystrophy (DMD) is common and fatal X-linked genetic disorder. The overall objective of this thesis was to carry out a prospective study for dystrophin gene therapy in dystrophic muscles, using the X-linked muscular dystrophy (mdx) mouse model. Recombinant adenovirus (AdV) is presently the vehicle of choice for gene therapy for a number of diseases including DMD. However AdV possess two major limitations when utilized as vectors in skeletal muscles: (i) the maturation-dependency of AdV-infectivity in skeletal muscles, (ii) the host immune response against adenoviral proteins

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47

Wang, Yu Xin. "Molecular Regulation of Muscle Stem Cell Self-Renewal." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35207.

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Muscle stem cells self-renew to maintain the long-term capacity for skeletal muscles to regenerate. However, the homeostatic regulation of muscle stem cell self-renewal is poorly understood. By utilizing high-throughput screening and transcriptomic approaches, we identify the critical function of dystrophin, the epidermal growth factor receptor (EGFR), and fibronectin in the establishment of cell polarity and in determining symmetric and asymmetric modes of muscle stem cell self-renewal. These findings reveal an orchestrated network of paracrine signaling that regulate muscle stem cell homeost

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48

Guiraud, Simon. "Evaluation de régulateurs positifs de la croissance musculaire chez un modèle dystrophique murin." Thesis, Evry-Val d'Essonne, 2011. http://www.theses.fr/2011EVRY0014/document.

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En 1997, le caractère culard, un phénotype hypermusclé chez le bovin, est attribué à des mutations dans le gène de la myostatine (MSTN). Depuis, il a été confirmé qu’une baisse de l’activité de la MSTN conduisait à une augmentation de la masse musculaire chez d’autres espèces, y compris chez l’Homme. L’identification de ce facteur et des conséquences de son invalidation sur le développement musculaire ouvre de nombreuses perspectives en médecine humaine comme, par exemple, chez des personnes ayant eu une fonte musculaire importante suite à une immobilisation prolongée ou en conséquence du viei

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49

Piper, Tony Andrew. "A study of the transfer of recombinant dystrophin genes into skeletal muscle cells." Thesis, Royal Holloway, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286683.

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McArdle, Anne. "Mechanisms skeletal muscle damage in the dystrophin-deficient MDX mouse." Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385144.

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