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Journal articles on the topic 'Duchenne muscular dystrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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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2

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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3

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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4

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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5

Faqih, M. Izza Zulfana, Wahyu Tri Sudaryanto, and Salma Muazzaroh. "ACTIVE ASSISTED MOVEMENT DALAM MENJAGA KEMAMPUAN FUNGSIONAL PADA KONDISI DUCHENNE MUSCULAR DYSTROPHY." Journal of Innovation Research and Knowledge 3, no. 1 (2023): 5047–52. http://dx.doi.org/10.53625/jirk.v3i1.5990.

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Background: Duchenne muscular dystrophy which is a recessive x-linked disorder that often affects males. Duchenne muscular dystrophy is caused by mutations in the dystrophin gene at the Xp21 locus so that dystrophin protein is not produced or dystrophin deficiency and structural abnormalities occur. Dystrophinopathies are X-linked recessive disorders affecting 1 in 5,000 to 1 in 6,000 live male births. The prevalence of DMD is less than 10 cases per 100,000 males. Objective: Physiotherapy management in this case aims to determine the benefits of providing physiotherapy interventions in the for

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6

Jufan, Akhmad Yun, Djayanti Sari, and Karlina Mahardieni. "DUCHENNE MUSCULER DYSTROPHY." Jurnal Komplikasi Anestesi 3, no. 2 (2023): 47–53. http://dx.doi.org/10.22146/jka.v3i2.7242.

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Duchenne muscular dystrophy merupakan suatu kelainan otot yang sering ditemui. Penyakit ini terpaut pada kromosom X yang disebabkan oleh mutasi gen dystrophin. Gejalanya berupa kelemahan otot proksimal yang berat, bersifat degenerasi progresif dan infi ltrasi lemak ke otot. Efek duchenne muscular dystrophy terhadap otot respirasi dan berhubungan dengan kardio-miopati yang dapat mengarah ke kematian.Dilaporkan anak laki-laki usia 12 tahun dengan diagnosa duchenne muscular dystrophy dd/ Baker’s muscular dystrophy dilakukan prosedur biopsi. Pasien dinilai sebagai status fi sik ASA 2 yang dilakuka

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7

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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8

Assereto, Stefania, Silvia Stringara, Federica Sotgia, et al. "Pharmacological rescue of the dystrophin-glycoprotein complex in Duchenne and Becker skeletal muscle explants by proteasome inhibitor treatment." American Journal of Physiology-Cell Physiology 290, no. 2 (2006): C577—C582. http://dx.doi.org/10.1152/ajpcell.00434.2005.

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In this report, we have developed a novel method to identify compounds that rescue the dystrophin-glycoprotein complex (DGC) in patients with Duchenne or Becker muscular dystrophy. Briefly, freshly isolated skeletal muscle biopsies (termed skeletal muscle explants) from patients with Duchenne or Becker muscular dystrophy were maintained under defined cell culture conditions for a 24-h period in the absence or presence of a specific candidate compound. Using this approach, we have demonstrated that treatment with a well-characterized proteasome inhibitor, MG-132, is sufficient to rescue the exp

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9

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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10

Park, Eun-Woo, Ye-Jee Shim, Jung-Sook Ha, Jin-Hong Shin, Soyoung Lee, and Jang-Hyuk Cho. "Diagnosis of Duchenne Muscular Dystrophy in a Presymptomatic Infant Using Next-Generation Sequencing and Chromosomal Microarray Analysis: A Case Report." Children 8, no. 5 (2021): 377. http://dx.doi.org/10.3390/children8050377.

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Duchenne muscular dystrophy is a progressive and lethal X-linked recessive neuromuscular disease caused by mutations in the dystrophin gene. It has a high rate of diagnostic delay; early diagnosis and treatment are often not possible due to delayed recognition of muscle weakness and lack of effective treatments. Current treatments based on genetic therapy can improve clinical results, but treatment must begin as early as possible before significant muscle damage. Therefore, early diagnosis and rehabilitation of Duchenne muscular dystrophy are needed before symptom aggravation. Creatine kinase

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11

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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12

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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13

Soim, Aida, Bailey Wallace, Nedra Whitehead, et al. "Health Profile of Preterm Males With Duchenne Muscular Dystrophy." Journal of Child Neurology 36, no. 12 (2021): 1095–102. http://dx.doi.org/10.1177/08830738211047019.

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In this retrospective cohort study, we characterize the health profile of preterm males with Duchenne muscular dystrophy. Major clinical milestones (ambulation cessation, assisted ventilation use, and onset of left ventricular dysfunction) and corticosteroids use in males with Duchenne muscular dystrophy identified through a population-based surveillance system were analyzed using Kaplan-Meier survival curves and Cox proportional hazards modeling. The adjusted risk of receiving any respiratory intervention among preterm males with Duchenne muscular dystrophy was 87% higher than among the corre

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14

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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15

Heutinck, Lotte, Nadine van Kampen, Merel Jansen, and Imelda J. M. de Groot. "Physical Activity in Boys With Duchenne Muscular Dystrophy Is Lower and Less Demanding Compared to Healthy Boys." Journal of Child Neurology 32, no. 5 (2017): 450–57. http://dx.doi.org/10.1177/0883073816685506.

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This study describes the amount of physical activity and perception of physical activity in boys with Duchenne muscular dystrophy (DMD) compared to healthy boys. A questionnaire described 6 domains of physical activity. Four Duchenne muscular dystrophy subgroups were made: early and late ambulatory, nonambulatory with relative good, or limited arm function. Eighty-four boys with Duchenne muscular dystrophy (15.0 ± 6.4 years) and 198 healthy boys (14.0 ± 4.3 years) participated. Daily activities were more passive for boys with Duchenne muscular dystrophy. Physical activity was less and low dema

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16

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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17

Saad, Fawzy A., Gabriele Siciliano, and Corrado Angelini. "Advances in Dystrophinopathy Diagnosis and Therapy." Biomolecules 13, no. 9 (2023): 1319. http://dx.doi.org/10.3390/biom13091319.

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Dystrophinopathies are x-linked muscular disorders which emerge from mutations in the Dystrophin gene, including Duchenne and Becker muscular dystrophy, and dilated cardiomyopathy. However, Duchenne muscular dystrophy interconnects with bone loss and osteoporosis, which are exacerbated by glucocorticoids therapy. Procedures for diagnosing dystrophinopathies include creatine kinase assay, haplotype analysis, Southern blot analysis, immunological analysis, multiplex PCR, multiplex ligation-dependent probe amplification, Sanger DNA sequencing, and next generation DNA sequencing. Pharmacological t

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18

Biggar, W. D. "Duchenne Muscular Dystrophy." Pediatrics in Review 27, no. 3 (2006): 83–88. http://dx.doi.org/10.1542/pir.27-3-83.

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19

Juříková, Lenka, Zdeňka Bálintová, and Jana Haberlová. "Duchenne muscular dystrophy." Neurologie pro praxi 20, no. 3 (2019): 180–82. http://dx.doi.org/10.36290/neu.2019.111.

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20

Kornberg, AndrewJ, and EppieM Yiu. "Duchenne muscular dystrophy." Neurology India 56, no. 3 (2008): 236. http://dx.doi.org/10.4103/0028-3886.43441.

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21

Sussman, Michael. "Duchenne Muscular Dystrophy." Journal of the American Academy of Orthopaedic Surgeons 10, no. 2 (2002): 138–51. http://dx.doi.org/10.5435/00124635-200203000-00009.

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22

Millichap, J. Gordon. "Duchenne Muscular Dystrophy." Pediatric Neurology Briefs 3, no. 5 (1989): 40. http://dx.doi.org/10.15844/pedneurbriefs-3-5-11.

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23

Biggar, W. Douglas. "Duchenne Muscular Dystrophy." Pediatrics In Review 27, no. 3 (2006): 83–88. http://dx.doi.org/10.1542/pir.27.3.83.

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24

Bushby, K. "Duchenne Muscular Dystrophy." Journal of Medical Genetics 31, no. 6 (1994): 506. http://dx.doi.org/10.1136/jmg.31.6.506.

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25

Bundey, S. "Duchenne Muscular Dystrophy." Journal of Medical Genetics 25, no. 2 (1988): 140. http://dx.doi.org/10.1136/jmg.25.2.140.

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26

Bundey, S. "Duchenne Muscular Dystrophy." Journal of Medical Genetics 26, no. 6 (1989): 416. http://dx.doi.org/10.1136/jmg.26.6.416.

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27

Heckmatt, J. Z. "Duchenne Muscular Dystrophy." Archives of Disease in Childhood 64, no. 5 (1989): 767. http://dx.doi.org/10.1136/adc.64.5.767.

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28

McDonald, Craig M., Richard T. Abresch, Gregory T. Carter, et al. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 74, Supplement 1 (1995): S70—S92. http://dx.doi.org/10.1097/00002060-199509001-00003.

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29

Gomez-Merino, Elia, and John R. Bach. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 81, no. 6 (2002): 411–15. http://dx.doi.org/10.1097/00002060-200206000-00003.

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30

Harper, P. "Duchenne Muscular Dystrophy." Journal of Neurology, Neurosurgery & Psychiatry 50, no. 9 (1987): 1249. http://dx.doi.org/10.1136/jnnp.50.9.1249.

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31

Scott, Oona M. "Duchenne Muscular Dystrophy." Physiotherapy 76, no. 3 (1990): 138. http://dx.doi.org/10.1016/s0031-9406(10)62140-2.

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32

Villanova, Marcello, Beatrice Brancalion, and Anokhi D. Mehta. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 93, no. 7 (2014): 595–99. http://dx.doi.org/10.1097/phm.0000000000000074.

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33

Shieh, Perry B. "Duchenne muscular dystrophy." Current Opinion in Neurology 28, no. 5 (2015): 542–46. http://dx.doi.org/10.1097/wco.0000000000000243.

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34

Roper, Helen P. "Duchenne muscular dystrophy." Neuromuscular Disorders 14, no. 5 (2004): 346–47. http://dx.doi.org/10.1016/j.nmd.2004.02.001.

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35

Davies, Kay E. "Duchenne muscular dystrophy." Trends in Genetics 3 (January 1987): 231–32. http://dx.doi.org/10.1016/0168-9525(87)90244-7.

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36

Topaloglu, Haluk. "Duchenne Muscular Dystrophy." European Journal of Paediatric Neurology 8, no. 5 (2004): 269. http://dx.doi.org/10.1016/j.ejpn.2004.05.004.

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37

Bolhuis, P. A. "Duchenne muscular dystrophy." Journal of the Neurological Sciences 80, no. 1 (1987): 118–19. http://dx.doi.org/10.1016/0022-510x(87)90230-9.

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38

Bolhuis, P. A. "Duchenne muscular dystrophy." Journal of the Neurological Sciences 90, no. 3 (1989): 348. http://dx.doi.org/10.1016/0022-510x(89)90125-1.

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39

Samson, Kurt. "DUCHENNE MUSCULAR DYSTROPHY." Neurology Today 3, no. 9 (2003): 1. http://dx.doi.org/10.1097/00132985-200309000-00001.

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40

Casademont, Jordi. "Duchenne Muscular Dystrophy." Clinical Neurophysiology 115, no. 10 (2004): 2426. http://dx.doi.org/10.1016/j.clinph.2004.05.006.

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41

Bach, John R., Daniel Martinez, and Bilal Saulat. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 89, no. 8 (2010): 620–24. http://dx.doi.org/10.1097/phm.0b013e3181e72207.

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42

Spies, S., K. Schipper, F. Nollet, and T. A. Abma. "Duchenne muscular dystrophy." BMJ 341, sep07 1 (2010): c4364. http://dx.doi.org/10.1136/bmj.c4364.

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43

Behera, V., M. K. Behera, R. Chauhan, and V. Nair. "Duchenne muscular dystrophy." Case Reports 2014, jun10 1 (2014): bcr2014205296. http://dx.doi.org/10.1136/bcr-2014-205296.

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44

ISHIKAWA, Y., J. R. BACH;, and A. K. SIMONDS. "Duchenne muscular dystrophy." Thorax 54, no. 6 (1999): 562. http://dx.doi.org/10.1136/thx.54.6.562c.

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45

Yiu, Eppie M., and Andrew J. Kornberg. "Duchenne muscular dystrophy." Journal of Paediatrics and Child Health 51, no. 8 (2015): 759–64. http://dx.doi.org/10.1111/jpc.12868.

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46

Chamberlain, Jeffrey S. "Duchenne muscular dystrophy." Current Opinion in Genetics & Development 1, no. 1 (1991): 11–14. http://dx.doi.org/10.1016/0959-437x(91)80033-i.

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47

Iannaccone, Susan T., and Zohair Nanjiani. "Duchenne muscular dystrophy." Current Treatment Options in Neurology 3, no. 2 (2001): 105–17. http://dx.doi.org/10.1007/s11940-001-0045-2.

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48

Lankester, Benedict J. A., Michael R. Whitehouse, and Martin F. Gargan. "Duchenne muscular dystrophy." Current Orthopaedics 21, no. 4 (2007): 298–300. http://dx.doi.org/10.1016/j.cuor.2007.07.001.

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49

Rifai, Z. "Duchenne Muscular Dystrophy." Archives of Neurology 51, no. 9 (1994): 846. http://dx.doi.org/10.1001/archneur.1994.00540210016003.

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50

Hyser, C. "Duchenne Muscular Dystrophy." Archives of Neurology 45, no. 4 (1988): 369. http://dx.doi.org/10.1001/archneur.1988.00520280011003.

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