Results 11 to 20 of about 18,188 (219)

Increased caveolin‐3 levels in mdx mouse muscles [PDF]

FEBS Letters, 1998
The density of skeletal muscle caveolae is increased in Duchenne muscular dystrophy and its genetic homologue, the mdx mouse. This structural change is significant as it may indicate muscle regeneration. We identified in mdx mouse tibialis anterior muscles significantly increased levels of caveolin‐3, the chief protein in muscle caveolae, and reduced ...
Vaghy, Pal L., Fang, Jin, Wu, Wenrong, P. Vaghy, Laszlo   +3 more
openaire   +4 more sources

X chromosome-linked muscular dystrophy (mdx) in the mouse. [PDF]

Proceedings of the National Academy of Sciences, 1984
An X chromosome-linked mouse mutant (gene symbol, mdx) has been found that has elevated plasma levels of muscle creatine kinase and pyruvate kinase and exhibits histological lesions characteristic of muscular dystrophy. The mutants show mild clinical symptoms and are viable and fertile.
Bulfield, G, Siller, W G, Wight, P A, Moore, K J   +3 more
openaire   +4 more sources

Towards developing standard operating procedures for pre-clinical testing in the mdx mouse model of Duchenne muscular dystrophy

Neurobiology of Disease, 2008
This review discusses various issues to consider when developing standard operating procedures for pre-clinical studies in the mdx mouse model of Duchenne muscular dystrophy (DMD).
Miranda D. Grounds, Hannah G. Radley, Gordon S. Lynch, Kanneboyina Nagaraju, Annamaria De Luca   +4 more
doaj   +3 more sources

Cognitive impairment appears progressive in the mdx mouse. [PDF]

Neuromuscul Disord, 2020
Duchenne muscular dystrophy (DMD) is an X-linked recessive muscle wasting disease caused by mutations in the DMD gene, which encodes the large cytoskeletal protein dystrophin. Approximately one-third of DMD patient's exhibit cognitive problems yet it is unknown if cognitive impairments worsen with age.
Bagdatlioglu E, Porcari P, Greally E, Blamire AM, Straub VW.   +4 more
europepmc   +4 more sources

Plantarflexion Contracture in the mdx Mouse [PDF]

American Journal of Physical Medicine & Rehabilitation, 2010
Contractures are a major clinical issue for patients with muscular dystrophies. However, it is unknown whether contractures are present in the widely used mdx mouse model of Duchenne muscular dystrophy. Therefore, the objectives of this study were to develop methods to measure muscle contractures in mice, to determine whether plantarflexion ...
Michael W, Garlich, Kristen A, Baltgalvis, Jarrod A, Call, Lisa L, Dorsey, Dawn A, Lowe   +4 more
openaire   +2 more sources

Hematopoietic Prostaglandin D Synthase Inhibitor PK007 Decreases Muscle Necrosis in DMD mdx Model Mice

Life, 2021
Duchenne muscular dystrophy (DMD) is characterized by progressive muscle weakness and wasting due to the lack of dystrophin protein. The acute phase of DMD is characterized by muscle necrosis and increased levels of the pro-inflammatory mediator ...
Sai Yarlagadda, Christina Kulis, Peter G. Noakes, Mark L. Smythe   +3 more
doaj   +1 more source

"Of Mice and Measures": A Project to Improve How We Advance Duchenne Muscular Dystrophy Therapies to the Clinic [PDF]

, 2018
A new line of dystrophic mdx mice on the DBA/2J (D2) background has emerged as a candidate to study the efficacy of therapeutic approaches for Duchenne muscular dystrophy (DMD). These mice harbor genetic polymorphisms that appear to increase the severity
Aartsma-Rus, A., Bogdanik, L, Davies, K, De Luca, A, Demonbruen, Ar, Duan, D, Elsey, D, Fukada, Si, Girgenrath, M, Gonzalez, Jp, Gordish-Dressman, H, Grounds, Md, Heydemann, A, Kreibich, A, Lutz, C, Nagaraju, K, Nichols, A, Partridge, T, Passini, M, Pazze, Ld, Sanarica, F, Schnell, Fj, Spencer, M, Spurney, C, van Putten, M, Wells, Dj, Willmann, R, Yokota, T, Young, Cs, Zhong, Z   +29 more
core   +3 more sources

Wild-type mouse models to screen antisense oligonucleotides for exon-skipping efficacy in Duchenne muscular dystrophy. [PDF]

PLoS ONE, 2014
A readily available animal model is essential for rapidly identifying effective treatments for Duchenne muscular dystrophy (DMD), a devastating neuromuscular disorder caused by the lack of dystrophin protein, which results from frame-disrupting mutations
Limin Cao, Gang Han, Ben Gu, HaiFang Yin
doaj   +1 more source

GsMTx4-D provides protection to the D2.mdx mouse. [PDF]

Neuromuscul Disord, 2018
Duchenne muscular dystrophy is a life-limiting muscle disease that has no current effective therapy. Despite mounting evidence that dysregulation of mechanosensitive ion channels is a significant contributor to dystrophy pathogenesis, effective pharmacologic strategies targeting these channels are lacking.
Ward CW, Sachs F, Bush ED, Suchyna TM.
europepmc   +4 more sources

How much dystrophin is enough: the physiological consequences of different levels of dystrophin in the mdx mouse [PDF]

, 2015
Splice modulation therapy has shown great clinical promise in Duchenne muscular dystrophy, resulting in the production of dystrophin protein. Despite this, the relationship between restoring dystrophin to established dystrophic muscle and its ability to ...
Betts, C, Coursindel, T, El Andaloussi, S, Gait, M J, Godfrey, C, Hammond, S, Hildyard, J C W, McClorey, G, Muses, S, O'Donovan, L, Terry, R L, Wells, D J, Wells, K E, Wood, M J   +13 more
core   +2 more sources