Results 41 to 50 of about 73,071 (237)

Targeting PKCθ promotes satellite cell self-renewal [PDF]

open access: yes, 2020
Skeletal muscle regeneration following injury depends on the ability of satellite cells (SCs) to proliferate, self-renew, and eventually differentiate. The factors that regulate the process of self-renewal are poorly understood. In this study we examined
Benedetti, Anna   +4 more
core   +1 more source

Development of the accredited duchenne centers program, a global program to achieve uniform and up-to-date care for all people living with duchenne muscular dystrophy

open access: yesOrphanet Journal of Rare Diseases
The Accredited Duchenne Centers (ADC) Program is a global program initiated by the World Duchenne Organization (WDO). The aim of the ADC Program is to achieve global, uniform and up-to-date care for all people living with Duchenne Muscular Dystrophy (DMD)
Imelda J. M. de Groot   +6 more
doaj   +1 more source

Proximity Begins with a Smile, But Which One? Associating Non-duchenne Smiles with Higher Psychological Distance

open access: yesFrontiers in Psychology, 2017
This study reveals that Duchenne (genuine) and non-Duchenne (non-genuine, polite) smiles are implicitly associated with psychological proximity and distance, respectively.
Yevgen Bogodistov, Florian Dost
doaj   +1 more source

Osteopontin ablation ameliorates muscular dystrophy by shifting macrophages to a pro-regenerative phenotype. [PDF]

open access: yes, 2016
In the degenerative disease Duchenne muscular dystrophy, inflammatory cells enter muscles in response to repetitive muscle damage. Immune factors are required for muscle regeneration, but chronic inflammation creates a profibrotic milieu that exacerbates
Barton, Elisabeth R   +7 more
core   +2 more sources

Whole‐Body Pattern of Muscle Degeneration and Progression in Sarcoglycanopathies

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective To characterize whole‐body intramuscular fat distribution pattern in patients with sarcoglycanopathies and explore correlations with disease severity, duration and age at onset. Methods Retrospective, cross‐sectional, multicentric study enrolling patients with variants in one of the four sarcoglycan genes who underwent whole‐body ...
Laura Costa‐Comellas   +39 more
wiley   +1 more source

Genetic diagnosis as a tool for personalized treatment of Duchenne muscular dystrophy [PDF]

open access: yes, 2016
Accurate definition of genetic mutations causing Duchenne muscular dystrophy (DMD) has always been relevant in order to provide genetic counseling to patients and families, and helps to establish the prognosis in the case where the distinction between ...
Bello, Luca, Pegoraro, Elena
core  

The quality of life in boys with Duchenne muscular dystrophy [PDF]

open access: yes, 2016
We conducted a study to evaluate the quality of life in boys with Duchenne muscular dystrophy aged 8–18 years, compared with that in matched healthy controls. A total of 85 boys with Duchenne muscular dystrophy aged 8–18 years and 136 age, sex and living
Ashrafi, M.R.   +10 more
core   +1 more source

Patient‐Derived 3D Bioprinted Cardiac Organoid Constructs Reveal Key Pathological Features of Duchenne Muscular Dystrophy

open access: yesAdvanced Healthcare Materials, EarlyView.
Patient‐derived cardiac organoids reveal key features of Duchenne muscular dystrophy cardiomyopathy, including apoptosis, oxidative stress, calcium handling defects, and mechanical remodeling. By integrating organoids into alginate–gelatin bioprinted constructs, disease phenotypes are organized into scalable 3D cardiac tissues displaying extracellular ...
Vittoria Marini   +15 more
wiley   +1 more source

Increased circulating levels of interleukin-6 induce perturbation in redox-regulated signaling cascades in muscle of dystrophic mice [PDF]

open access: yes, 2017
Duchenne muscular dystrophy (DMD) is an X-linked genetic disease in which dystrophin gene is mutated, resulting in dysfunctional or absent dystrophin protein.
Forcina, Laura   +4 more
core   +3 more sources

Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism

open access: yesAdvanced Science, EarlyView.
The study demonstrated that connexin43 (Cx43) knockout caused arrhythmic phenotype and decreased proline content in vitro and in vivo. Mechanistically, Cx43 interacts with the amino acid transporter SNAT2 (sodium‐dependent neutral amino acid transporter), and its deficiency disrupts proline transport and metabolism.
Hangying Ying   +8 more
wiley   +1 more source

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