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Relevant bibliographies by topics / Genetics in muscular dystrophy

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Academic literature on the topic 'Genetics in muscular dystrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Genetics in muscular dystrophy"

1

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 (October 20, 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. In contrast, mdx mice, a dystrophin-deficient animal model for Duchenne muscular dystrophy, showed significant Evans blue accumulation in skeletal muscle fibers. We also studied Evans blue dispersion in transgenic mice bearing different dystrophin mutations, and we demonstrated that cytoskeletal and sarcolemmal attachment of dystrophin might be a necessary requirement to prevent serious fiber damage. The extent of dye incorporation in transgenic mice correlated with the phenotypic severity of similar dystrophin mutations in humans. We furthermore assessed Evans blue incorporation in skeletal muscle of the dystrophia muscularis (dy/dy) mouse and its milder allelic variant, the dy2J/dy2J mouse, animal models for congenital muscular dystrophy. Surprisingly, these mice, which have defects in the laminin α2-chain, an extracellular ligand of the DGC, showed little Evans blue accumulation in their skeletal muscles. Taken together, these results suggest that the pathogenic mechanisms in congenital muscular dystrophy are different from those in Duchenne muscular dystrophy, although the primary defects originate in two components associated with the same protein complex.

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Blake, Derek J., Andrew Weir, Sarah E. Newey, and Kay E. Davies. "Function and Genetics of Dystrophin and Dystrophin-Related Proteins in Muscle." Physiological Reviews 82, no. 2 (April 1, 2002): 291–329. http://dx.doi.org/10.1152/physrev.00028.2001.

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The X-linked muscle-wasting disease Duchenne muscular dystrophy is caused by mutations in the gene encoding dystrophin. There is currently no effective treatment for the disease; however, the complex molecular pathology of this disorder is now being unravelled. Dystrophin is located at the muscle sarcolemma in a membrane-spanning protein complex that connects the cytoskeleton to the basal lamina. Mutations in many components of the dystrophin protein complex cause other forms of autosomally inherited muscular dystrophy, indicating the importance of this complex in normal muscle function. Although the precise function of dystrophin is unknown, the lack of protein causes membrane destabilization and the activation of multiple pathophysiological processes, many of which converge on alterations in intracellular calcium handling. Dystrophin is also the prototype of a family of dystrophin-related proteins, many of which are found in muscle. This family includes utrophin and α-dystrobrevin, which are involved in the maintenance of the neuromuscular junction architecture and in muscle homeostasis. New insights into the pathophysiology of dystrophic muscle, the identification of compensating proteins, and the discovery of new binding partners are paving the way for novel therapeutic strategies to treat this fatal muscle disease. This review discusses the role of the dystrophin complex and protein family in muscle and describes the physiological processes that are affected in Duchenne muscular dystrophy.

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Sitzia, Clementina, Andrea Farini, Federica Colleoni, Francesco Fortunato, Paola Razini, Silvia Erratico, Alessandro Tavelli, et al. "Improvement of Endurance of DMD Animal Model Using Natural Polyphenols." BioMed Research International 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/680615.

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Duchenne muscular dystrophy (DMD), the most common form of muscular dystrophy, is characterized by muscular wasting caused by dystrophin deficiency that ultimately ends in force reduction and premature death. In addition to primary genetic defect, several mechanisms contribute to DMD pathogenesis. Recently, antioxidant supplementation was shown to be effective in the treatment of multiple diseases including muscular dystrophy. Different mechanisms were hypothesized such as reduced hydroxyl radicals, nuclear factor-κB deactivation, and NO protection from inactivation. Following these promising evidences, we investigated the effect of the administration of a mix of dietary natural polyphenols (ProAbe) on dystrophic mdx mice in terms of muscular architecture and functionality. We observed a reduction of muscle fibrosis deposition and myofiber necrosis together with an amelioration of vascularization. More importantly, the recovery of the morphological features of dystrophic muscle leads to an improvement of the endurance of treated dystrophic mice. Our data confirmed that ProAbe-based diet may represent a strategy to coadjuvate the treatment of DMD.

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Teramoto, Naomi, Hidetoshi Sugihara, Keitaro Yamanouchi, Katsuyuki Nakamura, Koichi Kimura, Tomoko Okano, Takanori Shiga, et al. "Pathological evaluation of rats carrying in-frame mutations in the dystrophin gene: a new model of Becker muscular dystrophy." Disease Models & Mechanisms 13, no. 9 (August 28, 2020): dmm044701. http://dx.doi.org/10.1242/dmm.044701.

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ABSTRACTDystrophin, encoded by the DMD gene on the X chromosome, stabilizes the sarcolemma by linking the actin cytoskeleton with the dystrophin-glycoprotein complex (DGC). In-frame mutations in DMD cause a milder form of X-linked muscular dystrophy, called Becker muscular dystrophy (BMD), characterized by the reduced expression of truncated dystrophin. So far, no animal model with in-frame mutations in Dmd has been established. As a result, the effect of in-frame mutations on the dystrophin expression profile and disease progression of BMD remains unclear. In this study, we established a novel rat model carrying in-frame Dmd gene mutations (IF rats) and evaluated the pathology. We found that IF rats exhibited reduced expression of truncated dystrophin in a proteasome-independent manner. This abnormal dystrophin expression caused dystrophic changes in muscle tissues but did not lead to functional deficiency. We also found that the expression of additional dystrophin named dpX, which forms the DGC in the sarcolemma, was associated with the appearance of truncated dystrophin. In conclusion, the outcomes of this study contribute to the further understanding of BMD pathology and help elucidate the efficiency of dystrophin recovery treatments in Duchenne muscular dystrophy, a more severe form of X-linked muscular dystrophy.

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Nogami, Ken'ichiro, Yusuke Maruyama, Fusako Sakai-Takemura, Norio Motohashi, Ahmed Elhussieny, Michihiro Imamura, Satoshi Miyashita, et al. "Pharmacological activation of SERCA ameliorates dystrophic phenotypes in dystrophin-deficient mdx mice." Human Molecular Genetics 30, no. 11 (April 5, 2021): 1006–19. http://dx.doi.org/10.1093/hmg/ddab100.

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Abstract Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder characterized by progressive muscular weakness because of the loss of dystrophin. Extracellular Ca2+ flows into the cytoplasm through membrane tears in dystrophin-deficient myofibers, which leads to muscle contracture and necrosis. Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) takes up cytosolic Ca2+ into the sarcoplasmic reticulum, but its activity is decreased in dystrophic muscle. Here, we show that an allosteric SERCA activator, CDN1163, ameliorates dystrophic phenotypes in dystrophin-deficient mdx mice. The administration of CDN1163 prevented exercise-induced muscular damage and restored mitochondrial function. In addition, treatment with CDN1163 for 7 weeks enhanced muscular strength and reduced muscular degeneration and fibrosis in mdx mice. Our findings provide preclinical proof-of-concept evidence that pharmacological activation of SERCA could be a promising therapeutic strategy for DMD. Moreover, CDN1163 improved muscular strength surprisingly in wild-type mice, which may pave the new way for the treatment of muscular dysfunction.

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Sun, Chengmei, Luoan Shen, Zheng Zhang, and Xin Xie. "Therapeutic Strategies for Duchenne Muscular Dystrophy: An Update." Genes 11, no. 8 (July 23, 2020): 837. http://dx.doi.org/10.3390/genes11080837.

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Neuromuscular disorders encompass a heterogeneous group of conditions that impair the function of muscles, motor neurons, peripheral nerves, and neuromuscular junctions. Being the most common and most severe type of muscular dystrophy, Duchenne muscular dystrophy (DMD), is caused by mutations in the X-linked dystrophin gene. Loss of dystrophin protein leads to recurrent myofiber damage, chronic inflammation, progressive fibrosis, and dysfunction of muscle stem cells. Over the last few years, there has been considerable development of diagnosis and therapeutics for DMD, but current treatments do not cure the disease. Here, we review the current status of DMD pathogenesis and therapy, focusing on mutational spectrum, diagnosis tools, clinical trials, and therapeutic approaches including dystrophin restoration, gene therapy, and myogenic cell transplantation. Furthermore, we present the clinical potential of advanced strategies combining gene editing, cell-based therapy with tissue engineering for the treatment of muscular dystrophy.

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Foncuberta, M., F. Lubieniecki, L. Gravina, L. González Quereda, P. Gallano, L. Chertkoff, and S. Monges. "DUCHENNE MUSCULAR DYSTROPHY - GENETICS." Neuromuscular Disorders 28 (October 2018): S96—S97. http://dx.doi.org/10.1016/j.nmd.2018.06.260.

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Neri, M., A. Mauro, F. Gualandi, C. Bruno, F. Santorelli, S. Tedeschi, A. D'Amico, et al. "DUCHENNE MUSCULAR DYSTROPHY - GENETICS." Neuromuscular Disorders 28 (October 2018): S97. http://dx.doi.org/10.1016/j.nmd.2018.06.261.

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Lara, S., V. Saez, P. Santander, G. Fariña, M. Troncoso, and G. Legaza. "DUCHENNE MUSCULAR DYSTROPHY - GENETICS." Neuromuscular Disorders 28 (October 2018): S97. http://dx.doi.org/10.1016/j.nmd.2018.06.262.

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Schottlaender, L., J. Domingos, L. D'Argenzio, I. Zaharieva, P. Ala, A. Manzur, J. Bourke, J. Morgan, and F. Muntoni. "DUCHENNE MUSCULAR DYSTROPHY - GENETICS." Neuromuscular Disorders 28 (October 2018): S97. http://dx.doi.org/10.1016/j.nmd.2018.06.263.

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Dissertations / Theses on the topic "Genetics in muscular dystrophy"

1

Hodgson, Shirley V. "Genetic studies in Duchenne muscular dystrophy." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235878.

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Smith, T. J. "Molecular analysis of Duchenne muscular dystrophy." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233559.

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Messaed, Christiane. "Investigation of molecular mechanisms underlying Oculopharyngeal Muscular Dystrophy (OPMD)." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111879.

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Oculopharyngeal Muscular Dystrophy (OPMD) is a late-onset dominant/recessive myopathy caused by the expansion of a polyalanine repeat in exon 1 of the PABPN1 gene. The expression of expanded PABPN1 (expPABPN1) triggers the formation of insoluble nuclear aggregates within muscle fiber nuclei of OPMD patients. These aggregates are enriched in poly(A)RNA and sequester molecular chaperones, ubiquitin and proteasome subunits. In addition to these cellular components, we first identified two novel PABPN1 interacting partners, hnRNPA1 and hnRNPA/B that also localized to the insoluble expPABPN1 aggregates. However, only hnRNPA1 was observed in inclusions of OPMD patients' muscle fiber nuclei. Following this finding, we next established the involvement of the ubiquitin-proteasome pathway in the clearance of misfolded expPABPN1 and provided more insights into the beneficial role of molecular chaperones in OPMD. The inhibition of proteasome correlated with an increase in the aggregation of expPABPN1, suggesting a possible proteasome impairment in OPMD. Conversely, the overexpression of Hsp70 and Hsp40 coincided with a decrease in nuclear aggregates concomitant with a reduced cellular toxicity, suggesting the therapeutic potential of manipulating molecular chaperones levels. Finally, we demonstrated that soluble forms of expPABPN1 are the primary toxic species in OPMD. In the presence of endogenous HSPs, a decrease in expPABPN1 aggregation correlated with an increased cellular toxicity. A defect in polyadenylation or ubiquitination significantly increased expPABPN1 solubility and cell death. Using live-cell imaging, we observed that nuclear aggregates prolonged the survival of expPABPN1-expressing cells, which led us to speculate that protein aggregates are subnuclear structures that preserve cellular homeostasis by depleting the expPABPN1 from the nuclear soluble pool. We propose that the polyalanine expansion in expPABPN1 could enable aberrant protein-protein interactions that would compromise the cellular function of nuclear factors and the expression of genes essential for muscle integrity and differentiation. For instance, expPABPN1 might compromise the function of hnRNP proteins and lead to altered mRNA processing and nucleocytoplasmic export, which can be detrimental to the cell.

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Clapp, Jannine. "Investigating the molecular genetics of FSH muscular dystrophy." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435765.

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Bia, Britta Lydia. "Cardiomyopathy in mouse models of Duchenne muscular dystrophy." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301799.

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Cockburn, David James. "Analysis of DMD translocations." Thesis, University of Oxford, 1991. http://ora.ox.ac.uk/objects/uuid:ab53825b-b18e-4f60-954a-4ea9e0435126.

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Duchenne and Becker muscular dystrophies (DMD, BMD) are allelic X-linked diseases which affect approximately one in 3500 male newborns. They are caused by mutations in a gene positioned on the short arm of the X chromosome at Xp21. The first indication of the location of this gene was the description of rare females expressing DMD and who were found to have constitutional X;autosome translocations with an X chromosome breakpoint at this site. There are now 24 such females known worldwide. They express DMD as a consequence of preferential inactivation of the normal X chromosome. In order to contribute to the understanding of the aetiology of mutations causing DMD and the aetiology of constitutional translocations, two types of study have been performed here. Firstly, the detailed mapping of the X chromosome breakpoints of DMD-associated X;autosome translocations has been investigated. The results of this study have been compared with data on the physical distribution of mutations causing DMD in male patients. Secondly, one translocation, an X;l translocation with an autosomal breakpoint at Ip34, has been selected for more detailed investigation and the DNA sequence has been determined at the site of the rearrangement. Translocation breakpoint mapping studies were performed by somatic cell hybrid analysis. Hybrids were karyotyped and this information was used to construct a hybrid panel for the purpose of determining the autosomal localisations of anonymous DNA probes. The mapping of seven probes using this panel is described. The work described in this thesis revealed that the distribution of translocation breakpoints within the DMD gene appears to be random and may differ from the distribution of mutations in male patients. The X;l translocation whose breakpoints are cloned and sequenced was found to involve two expressed loci, one coding for dystrophin on the X chromosome and one for the leukocyte antigen related protein on chromosome 1. Sequence data revealed that a deletion of four to seven nucleotides from the X chromosome and a duplication of two to five nucleotides are associated with the translocation. The possible involvement of trinucleotides adjacent to the breakpoints, and of a LINE, a SINE and a stretch of potential Z-DNA within 1 kb of the X chromosome or the chromosome 1 breakpoint, is discussed.

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Brais, Bernard. "Oculopharyngeal muscular dystrophy : from phenotype to genotype." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0002/NQ44369.pdf.

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Van, der Merwe Annelize. "Genetic heterogeneity in South African facioscapulohumeral muscular dystrophy (FSHD) families." Pretoria : [s.n.], 2006. http://upetd.up.ac.za/thesis/available/etd-10262005-110841/.

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Kaspar, Rita Wen. "Genotype-Phenotype Association Analysis of Dilated Cardiomyopathy in Becker Muscular Dystrophy." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243469474.

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Montanaro, Federica. "The role of dystroglycan in muscular dystrophy and synaptogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ55361.pdf.

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Books on the topic "Genetics in muscular dystrophy"

1

Emery, Alan E. H. The history of a genetic disease: Duchenne muscular dystrophy or Meryon's disease. London: Royal Society of Medicne Press, 1995.

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Herrmann, Falko H. X-linked muscular dystrophies (Duchenne and Becker): A bibliography. Jena: Universitaẗsbibliothek, 1985.

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Herrmann, Falko H. X-linked muscular dystrophies (Duchenne and Becker): A bibliography. Jena: Universita tsbibliothek, 1985.

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Herrmann, Falko H. X-linked muscular dystrophies (Duchenne and Becker): A bibliography. Jena: Universitätsbibliothek, 1985.

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H, Emery Marcia L., ed. The history of a genetic disease: Duchenne muscular dystrophy or Meryon's disease. 2nd ed. Oxford [England]: Oxford University Press, 2011.

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

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Group), Ozawahan (Research. Kin-jisutorofī-shō no hasshō ni kansuru saibō seibutsugakuteki kiso kenkyū: Heisei 2-nendo kenkyū hōkokusho. [Tokyo: Kōseishō], 1991.

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group), Nonomurahan (Research. Kin-jisutorofī-shō no hasshō ni kansuru idenshi kōgakuteki kiso kenkyū: Shōwa 63-nendo kenkyū hōkokusho. [Tokyo: Kōseishō], 1989.

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Nonomura, Yoshiaki. Kin-jisutorofī-shō no hasshō ni kansuru idenshi kōgakuteki kiso kenkyū: BShōwa 62-nendo kenkyū hōkokusho. [Tokyo: Kōseishō], 1988.

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International Symposium on Facioscapulohumeral Muscular Dystrophy (1995 Kyoto, Japan). Clinical and molecular genetic aspects of the disease: Kyoto, Japan, July 10, 1994, Kyoto International Congress Hall. Edited by Sugita Hideo and Arahata Kiichi. New York: Wiley, 1995.

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Book chapters on the topic "Genetics in muscular dystrophy"

1

Mah, Jean K. "Duchenne and Becker Muscular Dystrophies: Underlying Genetic and Molecular Mechanisms." In Muscular Dystrophy, 21–35. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17362-7_4.

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Mah, Jean K. "An Overview of the Other Muscular Dystrophies: Underlying Genetic and Molecular Mechanisms." In Muscular Dystrophy, 37–53. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17362-7_5.

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Angelini, Corrado. "Duchenne Muscular Dystrophy." In Genetic Neuromuscular Disorders, 3–7. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56454-8_1.

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Angelini, Corrado. "Becker Muscular Dystrophy." In Genetic Neuromuscular Disorders, 13–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56454-8_3.

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Angelini, Corrado. "Oculopharyngeal Muscular Dystrophy." In Genetic Neuromuscular Disorders, 133–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56454-8_34.

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Angelini, Corrado. "Duchenne Muscular Dystrophy." In Genetic Neuromuscular Disorders, 3–7. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07500-6_1.

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Angelini, Corrado. "Becker Muscular Dystrophy." In Genetic Neuromuscular Disorders, 13–17. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07500-6_3.

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Chen, Harold. "Congenital Muscular Dystrophy." In Atlas of Genetic Diagnosis and Counseling, 617–26. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-2401-1_55.

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Chen, Harold. "Facioscapulohumeral Muscular Dystrophy." In Atlas of Genetic Diagnosis and Counseling, 993–1004. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-2401-1_84.

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Chen, Harold. "Congenital Muscular Dystrophy." In Atlas of Genetic Diagnosis and Counseling, 1–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6430-3_55-2.

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Conference papers on the topic "Genetics in muscular dystrophy"

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Ali, Rehab. "Duchenne Muscular Dystrophy, Clinical and Genetic Spectrum in Qatar." 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.15.

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Fiorentino, Giuseppe, Anna Annunziata, Maria Antonietta Mazza, Rosa Cauteruccio, Gianfranco Scotto di Frega, and Anna Michela Gaeta. "Mouthpiece ventilation in Duchenne muscular dystrophy." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2166.

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Cavache, Alina, Diana Zaharia, Raluca Ioana Teleanu, Diana Anamaria Epure, Dana Vasile, Magdalena Sandu, Ioana Adriana Ghiorghiu, and Doina Anca Plesca. "P315 Electrocardiographic changes in duchenne muscular dystrophy." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.403.

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Dell'Acqua, Guido, and Filippo Castiglione. "A Mathematical Model of Duchenne Muscular Dystrophy." In Selected Contributions from the 9th SIMAI Conference. WORLD SCIENTIFIC, 2009. http://dx.doi.org/10.1142/9789814280303_0028.

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Grinio, L. "A new hypothesis of duchenne muscular dystrophy." In Scientific achievements of the third millennium. SPC "LJournal", 2021. http://dx.doi.org/10.18411/scienceconf-03-2021-41.

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Abdel Aleem, Alice. "Congenital Muscular Dystrophy and Neuromuscular Disorders: An Overview." 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.2.

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Nair, Vidya, Mahmoud Elsaid, Rana Al Shami, Noora ElMudehki, Khalid Mohamed, Khalid Ibrahim, and Alice AbdelAleem. "COL6A Mutations in Patients with Congenital Muscular Dystrophy." 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.25.

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Koppaka, Sisir, Matthew W. Gilbertson, Jim S. Wu, Seward B. Rutkove, and Brian W. Anthony. "Assessing duchenne muscular dystrophy with force-controlled ultrasound." In 2014 IEEE 11th International Symposium on Biomedical Imaging (ISBI 2014). IEEE, 2014. http://dx.doi.org/10.1109/isbi.2014.6867965.

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"Mutations in Duchenne and Becker Muscular Dystrophy Patients." In AEBMS-2017, ICCET-2017, BBMPS-17, UPACEE-17, LHESS-17, TBFIS-2017, IC4E-2017, AMLIS-2017 & BEFM-2017. Higher Education and Innovation Group (HEAIG), 2018. http://dx.doi.org/10.15242/heaig.c1217230.

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Gushue, C. A., and R. Shell. "Effectiveness of Airway Clearance in Duchenne Muscular Dystrophy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3679.

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Reports on the topic "Genetics in muscular dystrophy"

1

Cox, Gregory A. Translational Research for Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada609750.

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Cox, Gregory A. Translational Research for Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada564543.

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Huard, Johnny, Eric Hoffman, John Day, Kevin Campbell, Xiao Xiao, and Paula Clemens. New Advanced Technology for Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada536121.

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Martin, Paul T. Translational Studies of GALGT2 Gene Therapy for Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613577.

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Martin, Paul T. Translational Studies of GALGT2 Gene Therapy for Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598203.

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Byrne, Barry J. Advanced Gene Therapy for Treatment of Cardiomyopathy and Respiratory Insufficiency in Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613171.

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