Results 101 to 110 of about 1,104,554 (244)
Adeno‐associated viral vector was used to elevate the expression of muscle specific kinase (MuSK) and rapsyn (a cytoplasmic MuSK effector protein) in the tibialis anterior muscle of wild‐type and dystrophic (mdx) mice. In mdx mice, enhanced expression of
S. Trajanovska +6 more
semanticscholar +1 more source
Propylene glycol modulated lipid metabolism in gluteal fat tissue. Expression of FABP4 at Day 60 and 120, and PPARγ and C/EBPα at Day 120 were upregulated, while SREBP1c was downregulated at both the mRNA (Day 120) and protein levels (Day 60 and 120).
Akın Yakan +14 more
wiley +1 more source
A nitric oxide synthase transgene ameliorates muscular dystrophy in mdx mice. [PDF]
Dystrophin-deficient muscles experience large reductions in expression of nitric oxide synthase (NOS), which suggests that NO deficiency may influence the dystrophic pathology.
Spencer, MJ, Tidball, JG, Wehling, M
core
ABSTRACT Background Skeletal muscle plays a vital role in voluntary movement and locomotion. Fast‐twitch muscle fibres are characterized by their rapid contraction kinetics, high‐force generation and a distinct gene expression profile compared to slow‐twitch fibres.
Akhil Baby +4 more
wiley +1 more source
Prmt5 is a regulator of muscle stem cell expansion in adult mice. [PDF]
Skeletal muscle stem cells (MuSC), also called satellite cells, are indispensable for maintenance and regeneration of adult skeletal muscles. Yet, a comprehensive picture of the regulatory events controlling the fate of MuSC is missing.
Braun, Thomas +7 more
core
Exploring Desmin as a Potential Modifier in Duchenne Muscular Dystrophy–Associated Cardiomyopathy
ABSTRACT Aim Duchenne muscular dystrophy (DMD), a rare X‐linked genetic disorder, is affecting skeletal and cardiac muscles due to the loss of the dystrophin protein. Modifier proteins, whose expression is altered in DMD patients, may influence disease progression.
Brice‐Emmanuel Guennec +12 more
wiley +1 more source
Restoration of pharyngeal dilator muscle force in dystrophin-deficient (mdx) mice following co-treatment with neutralizing interleukin-6 receptor antibodies and urocortin-2 [PDF]
New Findings: What is the central question of this study? We previously reported impaired upper airway dilator muscle function in the mdx mouse model of Duchenne muscular dystrophy (DMD).
Brannock, Molly +7 more
core +1 more source
BackgroundThe treatments currently approved for Duchenne muscular dystrophy (DMD), a progressive skeletal muscle wasting disease, address the needs of only a small proportion of patients resulting in an urgent need for therapies that benefit all patients
Michael St. Andre +9 more
semanticscholar +1 more source
ABSTRACT There is a need to improve the translation of gastric cancer molecular classification schemes, such as those proposed by the Cancer Genome Atlas (TCGA) and Tumour Microenvironment score (TME), to clinical specimens and three‐dimensional organoid culture models.
D. Skubleny +12 more
wiley +1 more source
Background Duchenne muscular dystrophy (DMD) is caused by the absence of the cytoskeletal protein, dystrophin. In DMD patients, dilated cardiomyopathy leading to heart failure may occur during adolescence. However, early cardiac dysfunction is frequently
Zhong Jia, Liu Wei, Li Wei, Yu Xin
doaj +1 more source

