Results 71 to 80 of about 1,087,549 (254)

An herbal medicine, Go-sha-jinki-gan (GJG), increases muscle weight in severe muscle dystrophy model mice

Clinical Nutrition Experimental, 2017
Go-sha-jinki-gan (GJG), a traditional Japanese herbal medicine has a clinical implication to alleviate age-related symptoms, especially in some motor disorders. However, the scientific evidence is limited, and there is a possibility to expand the medical
Yusei Takemoto, Shoya Inaba, Lidan Zhang, Kousuke Baba, Keisuke Hagihara, So-ichiro Fukada   +5 more
doaj   +1 more source

In vivo cerebellar circuit function is disrupted in an mdx mouse model of Duchenne muscular dystrophy

Disease Models & Mechanisms, 2019
Duchenne muscular dystrophy (DMD) is a debilitating and ultimately lethal disease involving progressive muscle degeneration and neurological dysfunction.
Trace L. Stay, Lauren N. Miterko, M. Arancillo, Tao Lin, R. Sillitoe   +4 more
semanticscholar   +1 more source

Lipid Nanoparticles for Delivery of CRISPR Gene Editing Components

Small Methods, EarlyView.
The review presents a comprehensive overview of each component of lipid nanoparticles（LNPs）and their effects on editing efficiency. It specifically highlights strategies for achieving non‐liver delivery, aiming for broader applications in gene editing. Furthermore, this review summarizes the applications of LNPs in gene editing and offers insights for ...
Fan Wu, Nei Li, Yudian Xiao, Rohan Palanki, Hannah Yamagata, Michael J. Mitchell, Xuexiang Han   +6 more
wiley   +1 more source

Chronic Dosing with Membrane Sealant Poloxamer 188 NF Improves Respiratory Dysfunction in Dystrophic Mdx and Mdx/Utrophin-/- Mice. [PDF]

PLoS ONE, 2015
Poloxamer 188 NF (national formulary (NF) grade of P-188) improves cardiac muscle function in the mdx mouse and golden retriever muscular dystrophy models. However in vivo effects on skeletal muscle have not been reported.
Bruce E Markham, Stace Kernodle, Jean Nemzek, John E Wilkinson, Robert Sigler   +4 more
doaj   +1 more source

Cardiac Protection after Systemic Transplant of Dystrophin Expressing Chimeric (DEC) Cells to the mdx Mouse Model of Duchenne Muscular Dystrophy

Stem Cell Reviews and Reports, 2019
Duchenne Muscular Dystrophy (DMD) is a progressive lethal disease caused by X-linked mutations of the dystrophin gene. Dystrophin deficiency clinically manifests as skeletal and cardiac muscle weakness, leading to muscle wasting and premature death due ...
M. Siemionow, M. Siemionow, M. Malik, Paulina Langa, J. Cwykiel, S. Brodowska, A. Heydemann   +6 more
semanticscholar   +1 more source

The Female mdx Mouse: An Unexpected Vascular Story [PDF]

Journal of Neurology and Neuromedicine, 2016
Duchenne muscular dystrophy (DMD) is a progressive neuromuscular disease, caused by absence of functional dystrophin and inevitably leading to death. A variable proportion of women carriers (2.5 to 19%) can also manifest symptoms ranging from myalgia to cardiomyopathy, and pathophysiological mechanisms are still not completely understood.
Lorna Guéniot, Cédric Thépenier, Laurent Chatre, Fabrice Chrétien, Daniel Fiole, Claire Latroche, Aurélien Mazeraud, Pierre L. Goossens, Grégory Jouvion   +8 more
openaire   +2 more sources

CRISPR Technology in Disease Management: An Updated Review of Clinical Translation and Therapeutic Potential

Cell Proliferation, EarlyView.
CRISPR‐Cas systems offer transformative genome editing capabilities for precise manipulation of cellular genes. This enables two main therapeutic avenues: ex vivo modification of patient cells for re‐transplantation or direct in vivo gene targeting via advanced delivery methods.
Bahareh Farasati Far, Marziyeh Akbari, Mohammad Amin Habibi, Morteza Katavand, Sherko Nasseri   +4 more
wiley   +1 more source

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

Journal 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, Cristi L. Galindo, Kyungsoo Kim, John Jonghyun Shin, James B. Atkinson, Ines Macias‐Perez, Leo Pavliv, Bjorn C. Knollmann, Jonathan H. Soslow, Larry W. Markham, Erica J. Carrier   +10 more
doaj   +1 more source

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

The 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, Raz Ben‐David, Shenhav Shemer   +2 more
wiley   +1 more source

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

PLoS 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, Dounia Hamoudi, Laetitia Marcadet, Frédérique Kyomi Labelle, Rares Ovidiu David, Sabrina Bossé, Anteneh Argaw, Jérôme Frenette   +7 more
doaj   +1 more source