Literatura académica sobre el tema "D2-mdx"
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Artículos de revistas sobre el tema "D2-mdx"
De Giorgio, Daria, Deborah Novelli, Francesca Motta, Marianna Cerrato, Davide Olivari, Annasimon Salama, Francesca Fumagalli et al. "Characterization of the Cardiac Structure and Function of Conscious D2.B10-Dmdmdx/J (D2-mdx) mice from 16–17 to 24–25 Weeks of Age". International Journal of Molecular Sciences 24, n.º 14 (22 de julio de 2023): 11805. http://dx.doi.org/10.3390/ijms241411805.
Texto completoHassani, Medhi, Dylan Moutachi, Mégane Lemaitre, Alexis Boulinguiez, Denis Furling, Onnik Agbulut y Arnaud Ferry. "Beneficial effects of resistance training on both mild and severe mouse dystrophic muscle function as a preclinical option for Duchenne muscular dystrophy". PLOS ONE 19, n.º 3 (8 de marzo de 2024): e0295700. http://dx.doi.org/10.1371/journal.pone.0295700.
Texto completoHayes, Holly M., Julie Angerosa, Adam T. Piers, Jason D. White, Jane Koleff, Madeline Thurgood, Jessica Moody, Michael M. Cheung y Salvatore Pepe. "Preserved Left Ventricular Function despite Myocardial Fibrosis and Myopathy in the Dystrophin-Deficient D2.B10-Dmdmdx/J Mouse". Oxidative Medicine and Cellular Longevity 2022 (16 de marzo de 2022): 1–19. http://dx.doi.org/10.1155/2022/5362115.
Texto completoKrishna, Swathy, Tiffany Quindry, Matthew B. Hudson, John C. Quindry y Joshua T. Selsby. "Defective Autophagic Degradation in Aged D2‐mdx Diaphragms". FASEB Journal 34, S1 (abril de 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.04955.
Texto completoYarlagadda, Sai, Christina Kulis, Peter G. Noakes y Mark L. Smythe. "Hematopoietic Prostaglandin D Synthase Inhibitor PK007 Decreases Muscle Necrosis in DMD mdx Model Mice". Life 11, n.º 9 (21 de septiembre de 2021): 994. http://dx.doi.org/10.3390/life11090994.
Texto completoSpaulding, Hannah R., Tiffany Quindry, Kayleen Hammer, John C. Quindry y 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, n.º 4 (1 de octubre de 2019): 1058–66. http://dx.doi.org/10.1152/japplphysiol.00162.2019.
Texto completoMartins-Bach, A., E. Araujo, B. Matot, Y. Fromes, P. Baudin, I. Richard y P. Carlier. "Nuclear magnetic resonance relaxometry characterization of D2-mdx mice". Neuromuscular Disorders 27 (octubre de 2017): S124. http://dx.doi.org/10.1016/j.nmd.2017.06.120.
Texto completoWard, Christopher W., Frederick Sachs, Ernest D. Bush y Thomas M. Suchyna. "GsMTx4-D provides protection to the D2.mdx mouse". Neuromuscular Disorders 28, n.º 10 (octubre de 2018): 868–77. http://dx.doi.org/10.1016/j.nmd.2018.07.005.
Texto completoPandeya, Sarbesh R., Janice A. Nagy, Daniela Riveros, Carson Semple, Rebecca S. Taylor, Benjamin Sanchez y Seward B. Rutkove. "Relationships between in vivo surface and ex vivo electrical impedance myography measurements in three different neuromuscular disorder mouse models". PLOS ONE 16, n.º 10 (29 de octubre de 2021): e0259071. http://dx.doi.org/10.1371/journal.pone.0259071.
Texto completoEnglish, Katherine G., Andrea L. Reid, Adrienne Samani, Gerald J. F. Coulis, S. Armando Villalta, Christopher J. Walker, Sharon Tamir y Matthew S. Alexander. "Next-Generation SINE Compound KPT−8602 Ameliorates Dystrophic Pathology in Zebrafish and Mouse Models of DMD". Biomedicines 10, n.º 10 (26 de septiembre de 2022): 2400. http://dx.doi.org/10.3390/biomedicines10102400.
Texto completoTesis sobre el tema "D2-mdx"
Monceau, Alexandra. "Effet de l'exercice physique, combiné ou non à une thérapie génique, sur la fonction musculaire de modèles murins de dystrophie musculaire de Duchenne". Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS172.pdf.
Texto completoDuchenne muscular dystrophy (DMD) is a neuromuscular disease caused by mutations in the DMD gene encoding dystrophin, a protein essential for the integrity of the skeletal muscle fiber. Its absence causes increased muscle fragility, and extreme muscle weakness. Currently, there is no curative treatment, but the use of several combined therapeutic approaches seems promising. We tested the idea that regular physical activity could be a way to decrease dystrophic symptoms of skeletal muscle, especially those related to muscle function, in mice models of DMD. First, we evaluated the effect of chronic endurance exercise when combined with overexpression of Prox1, a transcription factor known to promote slower fibers in healthy muscle, which are less affected in DMD. We demonstrated that this combination allowed to decrease muscle fragility in mdx mice, the classical mouse model of DMD, and thus had the potential to stop the progression of the disease. Subsequently, we were interested in the effect of chronic endurance exercise when combined with gene therapy, which restores dystrophin expression, in D2-mdx mouse, a severe model of DMD. We showed that chronic endurance exercise decreased the efficiency of the gene therapy, by decreasing the restoration of dystrophin. Finally, we characterized the effects of chronic resistance exercise in D2-mdx mice. Our results indicate an incredibly significant improvement in muscle function in response to mechanical overload, without obvious muscle damage in this severe model
(11191884), Bohyun Ro. "IMPACT OF HEAT THERAPY ON SKELETAL MUSCLE FUNCTION IN A MODEL OF DUCHENNE MUSCULAR DYSTROPHY". Thesis, 2021.
Buscar texto completoCapítulos de libros sobre el tema "D2-mdx"
Kennedy, Tahnee L. y Hannah F. Dugdale. "Cardiac and Skeletal Muscle Pathology in the D2/mdx Mouse Model and Caveats Associated with the Quantification of Utrophin". En Methods in Molecular Biology, 55–66. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2772-3_4.
Texto completoKennedy, Tahnee L. y Hannah F. Dugdale. "Correction to: Cardiac and Skeletal Muscle Pathology in the D2/mdx Mouse Model and Caveats Associated with the Quantification of Utrophin". En Methods in Molecular Biology, C1. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2772-3_31.
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