Relevant bibliographies by topics / Dystrophic muscle

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Dystrophic muscle'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Dystrophic muscle"

1

Wehling, Michelle, Melissa J. Spencer, and James G. Tidball. "A nitric oxide synthase transgene ameliorates muscular dystrophy in mdx mice." Journal of Cell Biology 155, no. 1 (2001): 123–32. http://dx.doi.org/10.1083/jcb.200105110.

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Dystrophin-deficient muscles experience large reductions in expression of nitric oxide synthase (NOS), which suggests that NO deficiency may influence the dystrophic pathology. Because NO can function as an antiinflammatory and cytoprotective molecule, we propose that the loss of NOS from dystrophic muscle exacerbates muscle inflammation and fiber damage by inflammatory cells. Analysis of transgenic mdx mice that were null mutants for dystrophin, but expressed normal levels of NO in muscle, showed that the normalization of NO production caused large reductions in macrophage concentrations in t
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Spaulding, Hannah R., Tiffany Quindry, Kayleen Hammer, John C. Quindry, and Joshua T. Selsby. "Nutraceutical and pharmaceutical cocktails did not improve muscle function or reduce histological damage in D2-mdx mice." Journal of Applied Physiology 127, no. 4 (2019): 1058–66. http://dx.doi.org/10.1152/japplphysiol.00162.2019.

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Progressive muscle injury and weakness are hallmarks of Duchenne muscular dystrophy. We showed previously that quercetin (Q) partially protected dystrophic limb muscles from disease-related injury. As quercetin activates PGC-1α through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy; hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy. Lisinopril (Lis) protects skeletal muscle and improves cardiac function in dystrophin-deficient mice; therefore, it was included in this
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Spaulding, HR, C. Ballmann, JC Quindry, MB Hudson, and JT Selsby. "Autophagy in the heart is enhanced and independent of disease progression in mus musculus dystrophinopathy models." JRSM Cardiovascular Disease 8 (January 2019): 204800401987958. http://dx.doi.org/10.1177/2048004019879581.

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Background Duchenne muscular dystrophy is a muscle wasting disease caused by dystrophin gene mutations resulting in dysfunctional dystrophin protein. Autophagy, a proteolytic process, is impaired in dystrophic skeletal muscle though little is known about the effect of dystrophin deficiency on autophagy in cardiac muscle. We hypothesized that with disease progression autophagy would become increasingly dysfunctional based upon indirect autophagic markers. Methods Markers of autophagy were measured by western blot in 7-week-old and 17-month-old control (C57) and dystrophic (mdx) hearts. Results
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Whitehead, Nicholas P., Min Jeong Kim, Kenneth L. Bible, Marvin E. Adams, and Stanley C. Froehner. "A new therapeutic effect of simvastatin revealed by functional improvement in muscular dystrophy." Proceedings of the National Academy of Sciences 112, no. 41 (2015): 12864–69. http://dx.doi.org/10.1073/pnas.1509536112.

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Duchenne muscular dystrophy (DMD) is a lethal, degenerative muscle disease with no effective treatment. DMD muscle pathogenesis is characterized by chronic inflammation, oxidative stress, and fibrosis. Statins, cholesterol-lowering drugs, inhibit these deleterious processes in ischemic diseases affecting skeletal muscle, and therefore have potential to improve DMD. However, statins have not been considered for DMD, or other muscular dystrophies, principally because skeletal-muscle-related symptoms are rare, but widely publicized, side effects of these drugs. Here we show positive effects of st
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Ng, Rainer, Joseph M. Metzger, Dennis R. Claflin, and John A. Faulkner. "Poloxamer 188 reduces the contraction-induced force decline in lumbrical muscles from mdx mice." American Journal of Physiology-Cell Physiology 295, no. 1 (2008): C146—C150. http://dx.doi.org/10.1152/ajpcell.00017.2008.

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Duchenne Muscular Dystrophy is a genetic disease caused by the lack of the protein dystrophin. Dystrophic muscles are highly susceptible to contraction-induced injury, and following contractile activity, have disrupted plasma membranes that allow leakage of calcium ions into muscle fibers. Because of the direct relationship between increased intracellular calcium concentration and muscle dysfunction, therapeutic outcomes may be achieved through the identification and restriction of calcium influx pathways. Our purpose was to determine the contribution of sarcolemmal lesions to the force defici
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Watchko, Jon F., Terrence L. O'Day, and Eric P. Hoffman. "Functional characteristics of dystrophic skeletal muscle: insights from animal models." Journal of Applied Physiology 93, no. 2 (2002): 407–17. http://dx.doi.org/10.1152/japplphysiol.01242.2001.

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Muscular dystrophies are a clinically and genetically heterogeneous group of disorders that show myofiber degeneration and regeneration. Identification of animal models of muscular dystrophy has been instrumental in research on the pathogenesis, pathophysiology, and treatment of these disorders. We review our understanding of the functional status of dystrophic skeletal muscle from selected animal models with a focus on 1) the mdx mouse model of Duchenne muscular dystrophy, 2) the Bio 14.6 δ-sarcoglycan-deficient hamster model of limb-girdle muscular dystrophy, and 3) transgenic null mutant mu
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Reid, Andrea L., Yimin Wang, Adrienne Samani, et al. "DOCK3 is a dosage-sensitive regulator of skeletal muscle and Duchenne muscular dystrophy-associated pathologies." Human Molecular Genetics 29, no. 17 (2020): 2855–71. http://dx.doi.org/10.1093/hmg/ddaa173.

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Abstract DOCK3 is a member of the DOCK family of guanine nucleotide exchange factors that regulate cell migration, fusion and viability. Previously, we identified a dysregulated miR-486/DOCK3 signaling cascade in dystrophin-deficient muscle, which resulted in the overexpression of DOCK3; however, little is known about the role of DOCK3 in muscle. Here, we characterize the functional role of DOCK3 in normal and dystrophic skeletal muscle. Utilizing Dock3 global knockout (Dock3 KO) mice, we found that the haploinsufficiency of Dock3 in Duchenne muscular dystrophy mice improved dystrophic muscle
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Cui, Chang-Hao, Taro Uyama, Kenji Miyado, et al. "Menstrual Blood-derived Cells Confer Human Dystrophin Expression in the Murine Model of Duchenne Muscular Dystrophy via Cell Fusion and Myogenic Transdifferentiation." Molecular Biology of the Cell 18, no. 5 (2007): 1586–94. http://dx.doi.org/10.1091/mbc.e06-09-0872.

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Duchenne muscular dystrophy (DMD), the most common lethal genetic disorder in children, is an X-linked recessive muscle disease characterized by the absence of dystrophin at the sarcolemma of muscle fibers. We examined a putative endometrial progenitor obtained from endometrial tissue samples to determine whether these cells repair muscular degeneration in a murine mdx model of DMD. Implanted cells conferred human dystrophin in degenerated muscle of immunodeficient mdx mice. We then examined menstrual blood–derived cells to determine whether primarily cultured nontransformed cells also repair
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Straub, Volker, Jill A. Rafael, Jeffrey S. Chamberlain, and Kevin P. Campbell. "Animal Models for Muscular Dystrophy Show Different Patterns of Sarcolemmal Disruption." Journal of Cell Biology 139, no. 2 (1997): 375–85. http://dx.doi.org/10.1083/jcb.139.2.375.

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Genetic defects in a number of components of the dystrophin–glycoprotein complex (DGC) lead to distinct forms of muscular dystrophy. However, little is known about how alterations in the DGC are manifested in the pathophysiology present in dystrophic muscle tissue. One hypothesis is that the DGC protects the sarcolemma from contraction-induced damage. Using tracer molecules, we compared sarcolemmal integrity in animal models for muscular dystrophy and in muscular dystrophy patient samples. Evans blue, a low molecular weight diazo dye, does not cross into skeletal muscle fibers in normal mice.
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Reggio, Alessio, Marco Rosina, Natalie Krahmer, et al. "Metabolic reprogramming of fibro/adipogenic progenitors facilitates muscle regeneration." Life Science Alliance 3, no. 3 (2020): e202000646. http://dx.doi.org/10.26508/lsa.202000660.

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In Duchenne muscular dystrophy (DMD), the absence of the dystrophin protein causes a variety of poorly understood secondary effects. Notably, muscle fibers of dystrophic individuals are characterized by mitochondrial dysfunctions, as revealed by a reduced ATP production rate and by defective oxidative phosphorylation. Here, we show that in a mouse model of DMD (mdx), fibro/adipogenic progenitors (FAPs) are characterized by a dysfunctional mitochondrial metabolism which correlates with increased adipogenic potential. Using high-sensitivity mass spectrometry–based proteomics, we report that a sh
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Dissertations / Theses on the topic "Dystrophic muscle"

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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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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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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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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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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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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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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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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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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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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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Books on the topic "Dystrophic muscle"

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Yeung, Davy. Molecular and functional analysis of the purinergic P2X receptors in normal and dystrophic skeletal muscle: A thesis. University of Portsmouth, School of Pharmacy and Biomedical Sciences, 2004.

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Bestard, Jennifer. Dystrophin gene regulation in muscle. National Library of Canada, 2000.

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1934-, Ozawa Eijirō, Masaki Tomoh, and Nabeshima Yoichi, eds. Frontiers in muscle research: Myogenesis, muscle contraction, and muscle dystrophy : proceedings of the Uehara Memorial Foundation Symposium on Frontiers in Muscle Research, Tokyo, 15-19 July 1990. Excerpta Medica, 1991.

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C, Strohman Richard, Wolf Stewart 1914-, and Muscular Dystrophy Association, eds. Gene expression in muscle. Plenum Press, 1985.

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Duan, Dongsheng. Muscle gene therapy. Springer, 2010.

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Myoblast transfer: Gene therapy for muscular dystrophy. R.G. Landes, 1994.

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Manchev, Ivan. Systematic hereditary degenerative and dystrophic diseases of the nervous and muscular system. AuthorHouse, 2007.

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International Symposium on Oculopharyngeal Muscular Dystrophy (1st 1995 Québec). Oculopharyngeal muscular dystrophy: Proceedings of the First International Symposium on Oculopharyngeal Muscular Dystrophy, Québec, 22-23 September 1995. Edited by Bouchard Jean Pierre, Brais Bernard, and Tomé Fernando. Pergamon, 1997.

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Muscle gene therapy: Methods and protocols. Humana, 2011.

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Charles, Emerson, Hoffmann-La Roche inc, and University of California, Los Angeles., eds. Molecular biology of muscle development: Proceedings of a Roche-UCLA Symposium, held in Park City, Utah, March 15-22, 1985. A.R. Liss, 1986.

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Book chapters on the topic "Dystrophic muscle"

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Lewis, Caroline, Philip Doran, and Kay Ohlendieck. "Proteomic Analysis of Dystrophic Muscle." In Methods in Molecular Biology. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-343-1_20.

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Wells, Kim E., Jill McMahon, Helen Foster, Aurora Ferrer, and Dominic J. Wells. "Gene Delivery to Dystrophic Muscle." In Methods in Molecular Biology. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-194-9_33.

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Allen, Milton J., and Gwendolyn Geffert. "The Electronic Properties of Dystrophic Muscle Membrane Systems." In Charge and Field Effects in Biosystems—2. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0557-6_12.

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Bandman, Everett. "Distribution of Slow Myosin in Dystrophic Chicken Muscle." In Advances in Experimental Medicine and Biology. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4907-5_5.

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Schultz, Edward. "Satellite Cells in Normal, Regenerating and Dystrophic Muscle." In Advances in Experimental Medicine and Biology. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4907-5_6.

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Pratt, Stephen J. P., Shama R. Iyer, Sameer B. Shah, and Richard M. Lovering. "Imaging Analysis of the Neuromuscular Junction in Dystrophic Muscle." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7374-3_5.

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Pessina, Patrizia, and Pura Muñoz-Cánoves. "Fibrosis-Inducing Strategies in Regenerating Dystrophic and Normal Skeletal Muscle." In Methods in Molecular Biology. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3810-0_7.

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Matsuda, Ryoichi, and Richard C. Strohman. "Myotrophic Factor(s) in Normal and Dystrophic Chicken Skeletal Muscle." In Advances in Experimental Medicine and Biology. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4907-5_11.

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Di Foggia, Valentina, and Lesley Robson. "Isolation of Satellite Cells from Single Muscle Fibers from Young, Aged, or Dystrophic Muscles." In Methods in Molecular Biology. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-980-8_1.

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Kastenschmidt, Jenna M., Ileen Avetyan, and S. A. Villalta. "Characterization of the Inflammatory Response in Dystrophic Muscle Using Flow Cytometry." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7374-3_4.

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Conference papers on the topic "Dystrophic muscle"

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Cassino, Theresa R., Masaho Okada, Lauren M. Drowley, Joseph Feduska, Johnny Huard, and Philip R. LeDuc. "Using Mechanical Environment to Enhance Stem Cell Transplantation in Muscle Regeneration." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176545.

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Muscle-derived stem cell (MDSC) transplantation has shown potential as a therapy for cardiac and skeletal muscle dysfunction in diseases such as Duchenne muscular dystrophy (DMD). In this study we explore mechanical environment and its effects on MDSCs engraftment into cardiac and skeletal muscle in mdx mice and neoangiogenesis within the engraftment area. We first looked at transplantation of the same number of MDSCs into the heart and gastrocnemius (GN) muscle of dystrophic mice and the resulting dystrophin expression. We then explored neoangiogenesis within the engraftments through quantifi
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Cassino, Theresa R., Masaho Okada, Lauren Drowley, Johnny Huard, and Philip R. LeDuc. "Mechanical Stimulation Improves Muscle-Derived Stem Cell Transplantation for Cardiac Repair." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192941.

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Muscle-derived stem cells (MDSCs) have been successfully transplanted into both skeletal (1) and cardiac muscle (2) of dystrophin-deficient (mdx) mice, and show potential for improving cardiac and skeletal dysfunction in diseases like Duchenne muscular dystrophy (DMD). Our previous study explored the regeneration of dystrophin-expressing myocytes following MDSC transplantation into environments with distinct blood flow and chemical/mechanical stimulation attributes. After MDSC transplantation within left ventricular myocardium and gastrocnemius (GN) muscles of the same mdx mice, significantly
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Wagner, Hallie, Dawn Lowe, and Victor Barocas. "Reduced Compliance in Patellar Tendons From a Mouse Model of Muscular Dystrophy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80762.

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Muscular dystrophies are degenerative diseases that affect primarily skeletal muscles. Most studies of muscular dystrophy focus on muscles, but tendons are an important part of the musculotendon complex that transmits forces from muscles to bones. As the disease progresses, tendon shortening occurs, and some patients require tendon release or cord lengthening surgery to increase tendon length [1]. Despite the prevalence of these surgeries, very little is known about the mechanical properties of tendons in muscular dystrophy patients, or how they change as the tendon remodels or compensate in r
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Moore, Christopher J., Stephanie Montgomery, Juan Prieto, et al. "Computational Texture Features and Mechanical Anisotropy Reflect Structure and Composition of Dystrophic Canine Skeletal Muscle." In 2018 IEEE International Ultrasonics Symposium (IUS). IEEE, 2018. http://dx.doi.org/10.1109/ultsym.2018.8579898.

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Selzo, Mallory R., Joe N. Kornegay, Kathy A. Spaulding, et al. "VisR ultrasound evaluation of dystrophic muscle degeneration in a dog cross-section and comparison to histology and MRI." In 2015 IEEE International Ultrasonics Symposium (IUS). IEEE, 2015. http://dx.doi.org/10.1109/ultsym.2015.0473.

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Liang, F., G. Danialou, A. Maniakas, S. Yim, J. Bourdon, and BJ Petrof. "Genetic Ablation of CC Family Chemokine Receptor 2 (CCR2) Mitigates Muscle Dysfunction in the Dystrophic (Mdx) Mouse Diaphragm." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6132.

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Wallace, K. D., J. N. Marsh, S. L. Baldwin, et al. "1K-4 Differentiation of Dystrophic and Normal Skeletal Muscle Tissues with Energy and Entropy Images Acquired In Vivo from the Biceps of mdx and Wild-Type Mice." In 2006 IEEE Ultrasonics Symposium. IEEE, 2006. http://dx.doi.org/10.1109/ultsym.2006.280.

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Rizzuto, E., A. Musarò, A. Catizone, and Z. Del Prete. "Morpho-Functional Interaction Between Muscle and Tendon in Hypertrophic MLC/mIGF-1 Mice." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19332.

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Tendons and ligaments are uniaxial viscoelastic connective tissues and, during normal activity, tendons transmit forces from muscles to bones, while ligaments stabilize the joints. Many experiments have been carried out to study ligaments and tendons mechanical properties [1], and the effects of training protocols [2] or specific pathologies. Recently, different transgenic mice models have been proposed as a new way to study in depth tendons’ function and development [3]. Within this context, we made use of pathological and transgenic animal models to investigate the morpho-functional interact
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Omairi, Saleh, Antonios Matsakas, Silvia Torelli, and Ketan Patel. "Muscle-specific Expression of Erry in the Myostatin Null Background Leads to the Development of Hypertrophied Oxidative Muscle." In Congenital Dystrophies - Neuromuscular Disorders Precision Medicine: Genomics to Care and Cure. Hamad bin Khalifa University Press (HBKU Press), 2020. http://dx.doi.org/10.5339/qproc.2020.nmd.26.

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Nowlan, Niamh C., Paula Murphy, and Patrick J. Prendergast. "Mechanical Stimuli Resulting From Embryonic Muscle Contractions Promote Avian Periosteal Bone Collar Formation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-172077.

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Mechanical forces due to muscle contractions play an essential role in embryonic skeletal development. In neuromuscular conditions such as congenital myotonic dystrophy, where movement of the fetus in utero is reduced or absent, the bones and joints of the newborn often show malformations [1]. In this paper, we examine the effect of muscle contractions on embryonic bone development. We propose the hypothesis that mechanical loading due to muscle contractions promotes periosteal ossification and we test this hypothesis using computational and experimental methods. A set of FE analyses were perf
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Reports on the topic "Dystrophic muscle"

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Gonzalez-Cadavid, Nestor F. Modulation of Stem Cell Differentiation and Myostatin as an Approach to Counteract Fibrosis in Muscle Dystrophy and Regeneration After Injury. Addendum. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada586854.

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