Bibliografías temáticas / Duchenne Muscular Dystrophy (DMD)

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Literatura académica sobre el tema "Duchenne Muscular Dystrophy (DMD)"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 25 de julio de 2025

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Artículos de revistas sobre el tema "Duchenne Muscular Dystrophy (DMD)"

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Ibrahim Sory, P., T. Sidi, L. Guida, et al. "Dystrophie Musculaire de Duchenne: Aspects cliniques, biologiques et évolutifs à propos de cinq cas dans le service de Rhumatologie au CHU du Point G." Rhumatologie Africaine Francophone 6, no. 2 (2024): 18–23. http://dx.doi.org/10.62455/raf.v6i2.53.

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Résumé 
 La dystrophie musculaire de Duchenne (DMD) due à la non expression de la dystrophine est liée au chromosome X. Décrite au 19e siècle, est la plus courante dystrophie musculaire de l’enfant [1, 2]. L’incidence est estimée à 30 cas pour 100 000 naissances [1, 2].
 But- étudier les caractères cliniques, biologiques et évolutifs de la dystrophie musculaire de Duchenne.
 Patients et Méthodes :
 Il s’est agi d’une étude rétrospective portant sur 5 dossiers de DMD, colligés en 7 ans.
 Résultats
 Nous rapportons cinq dossiers de garçons colligés entre 2005 et 201
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lordlin, Dr R. T. J. R. Lordlin, and Dr Franklin Shaju. "PHYSIO IN DUCHENNE MUSCULAR DYSTROPHY (DMD)." IDC International Journal 8, no. 4 (2021): 1–4. http://dx.doi.org/10.47211/idcij.2021.v08i04.001.

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Duchenne muscular dystrophy is the most common and severe form of muscular dystrophy and is caused by mutations in the dystrophin gene. Dystrophin, together with several other protein components, is part of a complex known as the dystrophin glycoprotein complex (DGC). The DGC plays an essential role in maintaining the structural integrity of the muscle cell membrane by providing a link between the extracellular matrix and the cytoskeleton
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José, Juan Reyes Salazar, and Lazalde Medina Brissia. "Duchenne muscular dystrophy overview." GSC Advanced Research and Reviews 16, no. 1 (2023): 111–15. https://doi.org/10.5281/zenodo.8272022.

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This literature review addresses Duchenne muscular dystrophy (DMD), a serious muscle disease related to the X chromosome. DMD causes progressive loss of walking ability and dependence on wheelchairs in adolescence. Patients' quality of life and survival have been improved through the use of corticosteroids and a multidisciplinary approach to orthopaedic management. DMD is caused by partial or total absence of dystrophin protein due to specific mutations in the DMD gene (Xp21. 2 locus). The disease is characterized by progressive muscle weakness, deformities in the musculoskeletal system, p
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Dosani, Minaj, and Harish Kumar Singhal. "An Ayurvedic Approach in Muscular Dystrophy in Children." International Journal of Health Sciences and Research 14, no. 3 (2024): 105–16. http://dx.doi.org/10.52403/ijhsr.20240318.

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Duchenne muscular dystrophy stands out as the most prevalent and severe form of childhood muscular dystrophy, impacting approximately one in every 5200 male births. It results from dystrophin deficiency, a condition inherited through X-linked recessive traits due to a missing or altered dystrophin protein encoded by the DMD gene located on chromosome Xp21. Unfortunately, this myopathy is currently incurable, often leading to mortality between the ages of 20-25. The primary pharmaceutical intervention for Duchenne muscular dystrophy involves corticosteroids, though they come with long-term nega
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Sitzia, Clementina, Andrea Farini, Federica Colleoni, 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
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Spiro, Alfred J. "Muscular Dystrophy." Pediatrics In Review 16, no. 11 (1995): 437. http://dx.doi.org/10.1542/pir.16.11.437.

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Several varieties of muscular dystrophy can be distinguished on clinical, genetic, morphologic, and physiologic grounds. The classification includes Duchenne and Becker muscular dystrophies, both X-linked disorders; facioscapulohumeral muscular dystrophy, which is autosomal dominant; and limb-girdle muscular dystrophy, generally autosomal recessive. Duchenne muscular dystrophy (DMD), which occurs in approximately 1 in 3500 live male births, has no recognizable signs or symptoms at birth. However, markedly elevated serum creatine kinase always is demonstrable, even at birth. A molecular diagnos
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Danisovic, Lubos, Martina Culenova, and Maria Csobonyeiova. "Induced Pluripotent Stem Cells for Duchenne Muscular Dystrophy Modeling and Therapy." Cells 7, no. 12 (2018): 253. http://dx.doi.org/10.3390/cells7120253.

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Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder, caused by mutation of the DMD gene which encodes the protein dystrophin. This dystrophin defect leads to the progressive degeneration of skeletal and cardiac muscles. Currently, there is no effective therapy for this disorder. However, the technology of cell reprogramming, with subsequent controlled differentiation to skeletal muscle cells or cardiomyocytes, may provide a unique tool for the study, modeling, and treatment of Duchenne muscular dystrophy. In the present review, we describe current methods of induced pluripotent
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Steen, Michelle S., Marvin E. Adams, Yan Tesch, and Stanley C. Froehner. "Amelioration of Muscular Dystrophy by Transgenic Expression of Niemann-Pick C1." Molecular Biology of the Cell 20, no. 1 (2009): 146–52. http://dx.doi.org/10.1091/mbc.e08-08-0811.

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Duchenne muscular dystrophy (DMD) and other types of muscular dystrophies are caused by the loss or alteration of different members of the dystrophin protein complex. Understanding the molecular mechanisms by which dystrophin-associated protein abnormalities contribute to the onset of muscular dystrophy may identify new therapeutic approaches to these human disorders. By examining gene expression alterations in mouse skeletal muscle lacking α-dystrobrevin (Dtna−/−), we identified a highly significant reduction of the cholesterol trafficking protein, Niemann-Pick C1 (NPC1). Mutations in NPC1 ca
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Li, Xing-Chuan, Song Wang, Jia-Rui Zhu, Yu-Shan Yin, and Ni Zhang. "A Chinese boy with familial Duchenne muscular dystrophy owing to a novel hemizygous nonsense mutation (c.6283C>T) in an exon of the DMD gene." SAGE Open Medical Case Reports 10 (January 2022): 2050313X2211008. http://dx.doi.org/10.1177/2050313x221100881.

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Duchenne muscular dystrophy is a severe, X-linked, progressive neuromuscular disorder clinically characterised by muscle weakening and extremely high serum creatine kinase levels. A 1-year-old Chinese patient was diagnosed with early-onset Duchenne muscular dystrophy. Next-generation gene sequencing was conducted and the Sanger method was used to validate sequencing. We identified a novel nonsense mutation (c.6283C>T) in DMD that caused the replacement of native arginine at codon 2095 with a premature termination codon (p.R2095X), which may have had a pathogenic effect against dystrophin in
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Khatri, Ravi Shankar, Mridul Ranajan, and Shalini . "A COMPARATIVE AYURVEDIC REVIEW OF ETIOPATHOGENESIS OF DUCHENNE MUSCULAR DYSTROPHY (INHERITED DISORDER)." International Journal of Research in Ayurveda and Pharmacy 12, no. 1 (2021): 124–25. http://dx.doi.org/10.7897/2277-4343.120127.

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Duchenne muscular dystrophy (DMD) is an inherited disorder with severe progressive muscle weakness. In Ayurveda, Adibala Pravritta Vyadhi are also known as inherited diseases that caused by Matruja beeja dushti (Shonita) and Pitruja beeja dushti (Shukra). Duchenne muscular dystrophy (DMD) has been classified under Adibala Pravritta Vyadhi as per Ayurveda. The main objective of this article is to describe the various aspect of etiopathogenesis of Duchenne muscular dystrophy (DMD) as per Ayurvedic literature. This article will be helpful to making the Nidana (Diagnosis) as per Ayurveda and also
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Tesis sobre el tema "Duchenne Muscular Dystrophy (DMD)"

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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 con
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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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Taylor, Peter John Medical Sciences Faculty of Medicine UNSW. "Molecular genetic analysis of a New South Wales muscular dystrophy cohort." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/43309.

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Duchenne muscular dystrophy (DMD) is an X-linked lethal condition associated with high morbidity and mortality. There is currently no cure for this disease. Several gene-based therapeutic approaches for treating DMD are currently under development but all are dependent on the knowledge of the causative dystrophin gene mutation. A combined mutation detection approach consisting of a quantitative PCR based analysis and DNA sequencing of the dystrophin gene resulted in a mutation etection rate of 96% in the New South Wales (NSW) DMD cohort. The proportion of exon duplication mutations was twice
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Sharma, Dishant. "Development of tolerogenic plasmid vectors for gene therapy of Duchenne muscular dystrophy (DMD)." Thesis, University of Portsmouth, 2017. https://researchportal.port.ac.uk/portal/en/theses/development-of-tolerogenic-plasmid-vectors-for-gene-therapy-of-duchenne-muscular-dystrophy-dmd(55b88eaa-5f23-4ae6-83e7-baed45f82d00).html.

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This project focused on the development of an effective gene replacement therapy for the Duchenne muscular dystrophy (DMD) in its mouse models [(X-linked muscular dystrophy, mdx) and mdx-βgeo mice]. Earlier studies on the DMD replacement therapy (usually using mini-dystrophin) were largely not successful because dystrophin is being recognised as an antigen upon re-expression in dystrophic muscles and initiates the specific immune response. This leads to a short-lived or no expression of mini-dystrophin as was found in both human clinical trials and in animal models. It had been shown that the
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Heller, Kristin Noreen. "Alternative to Gene Replacement for Duchenne Muscular Dystrophy using Human Alpha7 Integrin (ITGA7)." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1388401639.

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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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Humbertclaude, Véronique. "Variabilité phénotypique et corrélations génotype – phénotype des dystrophinopathies : contribution des banques de données." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T028/document.

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L'objectif de ce travail est de développer la partie clinique de la banque de données du gène DMD, afin d'étudier l'histoire naturelle des dystrophinopathies et les corrélations génotype–phénotype, et de faciliter la sélection des patients pour les futurs essais thérapeutiques. La méthodologie créée pour le gène DMD peut être généralisée et utilisée pour d'autres banques de données dédiées à des maladies génétiques. La collecte de 70 000 données cliniques chez 600 patients avec un suivi longitudinal moyen de 12 ans permet de décrire l'histoire naturelle des dystrophies musculaires de Duchenne
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Thaker, Rajsi Y. "Potential drug treatment for Duchenne muscular dystrophy which could be through upregulation of lipin1." Wright State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1629996330644397.

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Papadopoulou, Georgia. "Cognitive profile in advanced Duchenne Muscular Dystrophy (DMD) and the effects of hypoventilation on cognition." Thesis, University of Hull, 2010. http://hydra.hull.ac.uk/resources/hull:3471.

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The portfolio has three parts.Part One is a systematic literature review concerning the nature and severity of the psychological distress experienced by carers (primarily parents) of people with Muscular Dystrophy. Quantitative and qualitative studies investigating distress in these carers have been reviewed and critically evaluated to draw conclusions and implications for clinical practice. Part Two is an empirical paper aimed at creating a cognitive profile for people suffering from Duchenne Muscular Dystrophy in the advanced stages of the illness. The focus of this cross-sectional study is
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Zatti, Susi. "Micro-engineered skeletal and cardiac muscle for Duchenne muscular dystrophy in vitro models." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422953.

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Duchenne muscular dystrophy (DMD) is the most common and severe genetic neuromuscular disorder affecting both skeletal and cardiac muscle functionality. More than twenty years have passed since the identification of the dystrophin gene, which mutations cause the disease. Many progresses have been made in understanding the pathogenesis and different experimental strategies has been tested both in vitro, on bench-top cell cultures, and in vivo, on different animal models. So far, despite some promising outcomes coming from recent clinical trials, this has not resulted in an effective and definit
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Libros sobre el tema "Duchenne Muscular Dystrophy (DMD)"

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Bernardini, Camilla, ed. Duchenne Muscular Dystrophy. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7374-3.

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S, Chamberlain Jeffrey, and Rando Thomas A, eds. Duchenne muscular dystrophy: Advances in therapeutics. Taylor & Francis, 2005.

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Kate, Stone, ed. Occupational therapy and Duchenne muscular dystrophy. John Wiley & Sons, 2007.

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1932-, Kakulas Byron A., Mastaglia Frank L, and Neuromuscular Foundation of Western Australia., eds. Pathogenesis and therapy of Duchenne and Becker muscular dystrophy. Raven Press, 1990.

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

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

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

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1932-, Kakulas Byron A., Howell J. McC, and Roses Allen D, eds. Duchenne muscular dystrophy: Animal models and genetic manipulation. Raven Press, 1992.

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Bergman, Thomas. Precious time: Children living with muscular dystrophy. Gareth Stevens Pub., 1996.

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

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Capítulos de libros sobre el tema "Duchenne Muscular Dystrophy (DMD)"

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Alavanda, Ceren. "Duchenne Muscular Dystrophy: Clinical Characteristics, Molecular Mechanisms and Management." In Molecular Approaches in Medicine. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359524.9.

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The dystrophinopathies encompass a range of X-linked muscle disorders varying from mild to severe, including Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD), and DMD-associated dilated cardiomyopathy (DCM). DMD typically manifests in early childhood and progresses rapidly, with affected children becoming wheelchair-dependent by the age of 12. Increased serum CK levels are detected in almost all DMD patients. Pathogenic variants in the DMD gene affect dystrophin expression, leading to DMD. More than four thousand pathogenic variants have been identified in the DMD gene. delet
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Srivastava, Niraj Kumar, Ramakant Yadav, and Deepak Sharma. "Aging: Influence on Duchenne Muscular Dystrophy (DMD) and Becker Muscular Dystrophy (BMD)." In Models, Molecules and Mechanisms in Biogerontology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3585-3_8.

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Lu-Nguyen, Ngoc, Alberto Malerba, and Linda Popplewell. "Use of Small Animal Models for Duchenne and Parameters to Assess Efficiency upon Antisense Treatment." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_20.

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AbstractDuchenne muscular dystrophy (DMD) is a rare genetic disease affecting 1 in 5000 newborn boys. It is caused by mutations in the DMD gene with a consequent lack of dystrophin protein that leads to deterioration of myofibers and their replacement with fibro-adipogenic tissue. Using antisense oligonucleotides (AONs) to modify out-of-frame mutations in the DMD gene, named exon skipping, is currently considered among the most promising treatments for DMD patients. The development of this strategy is rapidly moving forward, and AONs designed to skip exons 51 and 53 have received accelerated a
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Goossens, Remko, and Annemieke Aartsma-Rus. "In Vitro Delivery of PMOs in Myoblasts by Electroporation." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_12.

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AbstractAntisense oligonucleotides (AONs) are small synthetic molecules of therapeutic interest for a variety of human disease. Their ability to bind mRNA and affect its splicing gives AONs potential use for exon skipping therapies aimed at restoring the dystrophin transcript reading frame for Duchenne muscular dystrophy (DMD) patients. The neutrally charged phosphorodiamidate morpholino oligomers (PMOs) are a stable and relatively nontoxic AON modification. To assess exon skipping efficiency in vitro, it is important to deliver them to target cells. Here, we describe a method for the delivery
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López-Martínez, Andrea, Patricia Soblechero-Martín, and Virginia Arechavala-Gomeza. "Evaluation of Exon Skipping and Dystrophin Restoration in In Vitro Models of Duchenne Muscular Dystrophy." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_14.

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AbstractSeveral exon skipping antisense oligonucleotides (eteplirsen, golodirsen, viltolarsen, and casimersen) have been approved for the treatment of Duchenne muscular dystrophy, but many more are in development targeting an array of different DMD exons. Preclinical screening of the new oligonucleotide sequences is routinely performed using patient-derived cell cultures, and evaluation of their efficacy may be performed at RNA and/or protein level. While several methods to assess exon skipping and dystrophin expression in cell culture have been developed, the choice of methodology often depen
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Meregalli, Mirella, Andrea Farini, and Yvan Torrente. "Duchenne Muscular Dystrophy: Isolation of CD133-Expressing Myogenic Progenitors from Blood and Muscle of DMD Patients." In Stem Cells and Cancer Stem Cells,Volume 3. Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2415-0_28.

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Law, Peter K., Danlin M. Law, Ping Lu, Ming Zhang Ao, and Long Jiang Yu. "Twenty-Year Life Prolongation Achieved through Muscle Regeneration by Implanting 50-Billion Allogeneic Myoblasts into Duchenne Muscular Dystrophy (DMD) Boys." In Handbook of Regenerative Medicine. CRC Press, 2025. https://doi.org/10.1201/9781003464594-18.

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Adhikary, Joy, and Sriyankar Acharyya. "Identification of Biologically Relevant Biclusters from Gene Expression Dataset of Duchenne Muscular Dystrophy (DMD) Disease Using Elephant Swarm Water Search Algorithm." In Advances in Intelligent Systems and Computing. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-9927-9_15.

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Srivastava, Niraj Kumar. "Proton Nuclear Magnetic Resonance (1H NMR) Spectroscopy-Based Analysis of Lipid Components in Serum/Plasma of Patients with Duchenne Muscular Dystrophy (DMD)." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7374-3_14.

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Johannesmeyer, David, and Reed Estes. "Duchenne Muscular Dystrophy." In Orthopedic Surgery Clerkship. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52567-9_122.

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Actas de conferencias sobre el tema "Duchenne Muscular Dystrophy (DMD)"

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Rossoni, Tainara Emanuele, Ranieri Alvin Stroher Junior, and Bruna Hoeller. "Duchenne Muscular Dystrophy - Case Report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.129.

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Context: Duchenne Muscular Dystrophy (DMD) is an inherited recessive disease linked to the X chromosome, it is a progressive neuromuscular disease most prevalent in the world, affecting 1/3600 male births. It is associated with mutations that lead to loss of dystrophin protein expression, loss of severe muscle, respiratory and cardiac failure. At birth, the signs are generally nonspecific. At 3 years of age there is the appearance of specific changes, starting with muscle weakness, which occurs in an ascending, symmetrical and bilateral manner, becoming evident at around 5 years of age, with d
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Lima, Karlla Danielle Ferreira, Pedro Henrique Marte Arruda Sampaio, Marco Antonio Veloso Albuquerque, and Edmar Zanoteli. "Evaluation of lung function and respiratory muscles in Duchenne muscular dystrophy." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.695.

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Introduction: Duchenne muscular Dystrophy (DMD) is a genetic disease of recessive inheritance linked to the X chromosome, caused by a mutation in the dystrophin gene. This mutation will result in absence of the dystrophin protein, leading to the degeneration of muscle skeletal. The disease is the most common childhood-onset form of muscular dystrophy and affects males almost exclusively. DMD symptoms onset occurs in early childhood, usually between the ages of three and five years, with progressive muscle weakness and loss of gait in adolescence, progressive cardiomyopathy, and respiratory fai
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Miyata, Marcela Misao, Mariana Rabelo de Brito, Anamarli Nucci, and Marcondes Cavalcante França Jr. "Metabolic syndrome in patients with Duchenne muscular dystrophy." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.512.

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Introduction: Duchenne muscular dystrophy (DMD) is the most frequent muscle dystrophy in children. It is an X-linked condition caused by loss of function variants in the DMD gene. During disease course, affected patients lose lean body mass, become severely motor disabled and are often treated with long term steroids. All these factors pose them at increased risk for developing metabolic syndrome (MS), even as children. Surprisingly, there are few studies addressing this aspect in DMD cohorts, particularly in Brazil. Objectives: To estimate the frequency and risk factors for DMD-related MS in
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Oliveira, Marco Antônio Rodrigues Gomes de, and Isaura Maria Mesquita Prado. "Evidence and affects in Duchenne muscular dystrophy in children and Golden Retriever dogs." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.302.

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Introduction: Progressive muscular dystrophies differ in different ways due to their age of manifestation, the distribution of muscle weakness and the association of heart, central nervous system and peripheral nervous system. The most severe and common form of muscular dystrophies is Duchenne muscular dystrophy (DMD). Its involvement is 1/3500 male babies born alive and is attributed to 80% of cases of dystrophinopathies. The impairment of the dystrophin-glycoprotein complex in Becker and Duchenne dystrophies, in most congenital and girdle dystrophies, destruction of the sarcolemmal muscle fi
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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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Lomauro, Antonella, Marianna Romei, Maria Grazia D'Angelo, and Andrea Aliverti. "The natural course of lung volumes in Duchenne Muscular Dystrophy (DMD)." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3331.

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Rummey, Christian, Shabir Hasham, and Oscar Mayer. "Effects of idebenone on pulmonary morbidity in Duchenne muscular dystrophy (DMD)." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa2927.

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Connolly, M., A. Fallon, R. O’Hanlon, and D. Waterhouse. "1 Pictorial evolution of focal myocardial fibrosis in duchenne muscular dystrophy (DMD)." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 4th – Saturday October 6th 2018, Galway Bay Hotel, Galway, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-ics.1.

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Nogueira, Cristiana Bello Dultra, João Gustavo dos Anjos Morais Oliveira, and Alexandre Martins Lopes Filho. "The use of biomarkers in Duchenne muscular dystrophy – a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.330.

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Background: Biomarkers are indicators associated with a disease, used for diagnosis, monitoring progression and prognosis. In Duchenne Muscular Dystrophy (DMD), they are very important. Although the literature describes various types of biomarkers for it, there is no consensus of their appropriate use. Objective: Describe the use of biomarkers associated with DMD. Methods: This literature review used articles searched in PubMed using the formula: (“Duchenne Muscular Dystrophy”) AND (“Biomarkers”). Those that corroborate with the objective of this review were included. Model’s studies and studi
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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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Informes sobre el tema "Duchenne Muscular Dystrophy (DMD)"

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

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Kumar, Manish, and Shilpa Singh. Antisense Oligonucleotides for Duchenne Muscular Dystrophy: Rapid Systematic Review of Phase 3 Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2024. http://dx.doi.org/10.37766/inplasy2024.7.0031.

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

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C. Uy, Genevieve, Raymond L. Rosales, and Satish Khadilkar. Myopathies in Clinical Care: A Focus on Treatable Causes. Progress in Neurobiology, 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.01.

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Myopathies present a wide range of clinical symptoms that affect the skeletal muscles, including weakness, fatigue, and pain. While acquired myopathies receive significant attention due to the availability of treatment options, it is important to note that some inherited myopathies can also be effectively managed. These myopathies can be classified based on their underlying causes, such as infectious agents, autoimmune disorders leading to muscle inflammation, granulomatous inflammation, metabolic abnormalities within the muscle cells, skeletal muscle channel dysfunctions, prolonged ICU stay,
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