Results 51 to 60 of about 34,705 (216)

The Age‐Dependent Resident Myonuclear Multi‐Omic Response to an Acute Skeletal Muscle Hypertrophic Stimulus in Mice

open access: yesAdvanced Science, EarlyView.
Resident myonuclei are the molecular “control centers” for large multinuclear muscle fibers. It is presumed that, with aging, these control centers become compromised and contribute to delayed or blunted muscle adaptive potential. This study is a detailed roadmap that exposes how young versus aged myonuclei respond to a hypertrophic loading stimulus ...
Pieter J. Koopmans   +8 more
wiley   +1 more source

Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy [PDF]

open access: yes, 2009
Mammalian target of rapamycin (mTOR) is a key regulator of cell growth that associates with raptor and rictor to form the mTOR complex 1 (mTORC1) and mTORC2, respectively.
Baas, Dominique   +27 more
core   +5 more sources

Dynamic Shifts in ER–Plasma Membrane Junctions Signaling Define Pro‐Metastatic N‐Glycosylation and Predict Prostate Cancer Progression

open access: yesAdvanced Science, EarlyView.
Prostate cancer remains a leading cause of male cancer death, yet screening cannot reliably identify aggressive disease, underscoring the need for tissue biomarkers. It is shown that primary tumors increase ER–plasma membrane junction signaling via STIM1/ORP5, whereas metastasis features their loss, Golgi dispersal, and rapid conversion of high‐mannose
Amanda J. Macke   +14 more
wiley   +1 more source

Nifedipine treatment reduces resting calcium concentration, oxidative and apoptotic gene expression, and improves muscle function in dystrophic mdx mice. [PDF]

open access: yesPLoS ONE, 2013
Duchenne Muscular Dystrophy (DMD) is a recessive X-linked genetic disease, caused by mutations in the gene encoding dystrophin. DMD is characterized in humans and in mdx mice by a severe and progressive destruction of muscle fibers, inflammation ...
Francisco Altamirano   +6 more
doaj   +1 more source

Targeting a therapeutic LIF transgene to muscle via the immune system ameliorates muscular dystrophy. [PDF]

open access: yes, 2019
Many potentially therapeutic molecules have been identified for treating Duchenne muscular dystrophy. However, targeting those molecules only to sites of active pathology is an obstacle to their clinical use.
Bertoni, Carmen   +6 more
core  

Experimental investigations of synchrotron radiation at the onset of the quantum regime [PDF]

open access: yes, 2012
The classical description of synchrotron radiation fails at large Lorentz factors, $\gamma$, for relativistic electrons crossing strong transverse magnetic fields $B$.
A. Dizdar   +14 more
core   +3 more sources

A Rational Optimization Approach for the Development of a Multiplexed Lateral Flow Immunoassay: Detection of Nonepithelial Ovarian Cancer Markers in Human Serum

open access: yesAdvanced Science, EarlyView.
This study outlines the developmental pipeline of a multiplexed nanozyme‐based lateral flow immunoassay for the purpose of ovarian germ cell tumor detection. It demonstrates the application of a design of experiments optimization approach for nanozyme probe conjugate development.
Aida Abdelwahed   +10 more
wiley   +1 more source

Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice

open access: yesSkeletal Muscle, 2011
Background γ-cytoplasmic (γ-cyto) actin levels are elevated in dystrophin-deficient mdx mouse skeletal muscle. The purpose of this study was to determine whether further elevation of γ-cyto actin levels improve or exacerbate the dystrophic phenotype of ...
Baltgalvis Kristen A   +5 more
doaj   +1 more source

Altered muscle niche contributes to myogenic deficit in the D2-mdx model of severe DMD

open access: yesCell Death Discovery, 2023
Lack of dystrophin expression is the underlying genetic basis for Duchenne muscular dystrophy (DMD). However, disease severity varies between patients, based on specific genetic modifiers. D2-mdx is a model for severe DMD that exhibits exacerbated muscle
Davi A. G. Mázala   +11 more
doaj   +1 more source

Impaired respiratory function in mdx and mdx/utrn+/− mice [PDF]

open access: yesMuscle & Nerve, 2011
AbstractMuscle fibrosis is a prominent pathological feature that directly causes muscle dysfunction in Duchenne muscular dystrophy (DMD). The DMD mouse models, mdx mice and mdx mice with haploinsufficiency of the utrophin gene (mdx/utrn+/−), display progressive diaphragm fibrosis.
Ping, Huang   +5 more
openaire   +2 more sources

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