Results 81 to 90 of about 1,104,554 (244)

Visual Discrimination, Serial Reversal, and Extinction Learning in the mdx Mouse

open access: yesFrontiers in Behavioral Neuroscience, 2019
Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy and the most common neuromuscular disorder. In addition to neuromuscular consequences, some individuals with DMD experience global intellectual dysfunction and executive ...
Price E. Dickson, Guy Mittleman
doaj   +1 more source

Angiotensin II type 1 receptor antagonists alleviate muscle pathology in the mouse model for laminin-alpha2-deficient congenital muscular dystrophy (MDC1A) [PDF]

open access: yes, 2012
BACKGROUND: Laminin-alpha2-deficient congenital muscular dystrophy (MDC1A) is a severe muscle-wasting disease for which no curative treatment is available.
Lin, Shuo   +2 more
core   +1 more source

Combating muscle atrophy: emerging therapeutic targets that are fiber‐type‐specific

open access: yesThe FEBS Journal, EarlyView.
Inflammation, denervation or decreased insulin signaling activate proteolysis and cause muscle wasting. Pathological conditions like obesity and DMD can also exacerbate atrophy via PGD2–RhoA–ROCK2 signaling. In contrast, exercise, dietary interventions, and pharmacological agents can activate Ca2+/calcineurin–NFAT and AMPK–PGC‐1α–MEF pathways ...
Samrat Chakraborty   +2 more
wiley   +1 more source

Oxidative stress in Duchenne muscular dystrophy: focus on the NRF2 redox pathway [PDF]

open access: yes, 2015
Oxidative stress is involved in the pathogenesis of Duchenne muscular dystrophy (DMD), an X-linked genetic disorder caused by mutations in the dystrophin gene and characterized by progressive, lethal muscle degeneration and chronic inflammation.
Petrillo, Sara   +10 more
core   +5 more sources

Utrophin haploinsufficiency does not worsen the functional performance, resistance to eccentric contractions and force production of dystrophic mice. [PDF]

open access: yesPLoS ONE, 2018
The lack of dystrophin in Duchenne muscular dystrophy (DMD) compromises the integrity and function of muscle fibers. Skeletal muscles, except the diaphragm, do not undergo progressive degeneration in adult mdx mice due to compensatory mechanisms ...
Antoine Boulanger Piette   +7 more
doaj   +1 more source

Diaphragm degeneration and cardiac structure in mdx mouse: potential clinical implications for Duchenne muscular dystrophy [PDF]

open access: bronzeJournal of Anatomy, 2016
Isabel Cristina Chagas Barbin   +5 more
semanticscholar   +2 more sources

Clinical application of additive manufacturing in maxillofacial prosthetics: A scoping review

open access: yesJournal of Prosthodontics, EarlyView.
Abstract Purpose Digital workflows provide significant advances in prosthodontics, especially in terms of accuracy, reduced treatment duration, and quality of life. Moreover, additive manufacturing (AM) is particularly adapted for the fabrication of personalized complex prototypes required for the prosthetic rehabilitation of maxillofacial defects ...
Hélène Magro   +2 more
wiley   +1 more source

Utrophin Compensates dystrophin Loss during Mouse Spermatogenesis

open access: yesScientific Reports, 2017
Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder resulting from mutations in the dystrophin gene. The mdx/utrn −/− mouse, lacking in both dystrophin and its autosomal homologue utrophin, is commonly used to model the clinical symptoms of
Hung-Chih Chen   +6 more
doaj   +1 more source

Antagonism of the Thromboxane‐Prostanoid Receptor as a Potential Therapy for Cardiomyopathy of Muscular Dystrophy

open access: yesJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 2019
Background Muscular dystrophy (MD) causes a progressive cardiomyopathy characterized by diffuse fibrosis, arrhythmia, heart failure, and early death. Activation of the thromboxane‐prostanoid receptor (TPr) increases calcium transients in cardiomyocytes ...
James D. West   +10 more
doaj   +1 more source

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