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| http://dx.doi.org/10.4103/aian.aian_552_23 | DOI Listing |
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Systemic calcinosis in horses: Pathological and genetic aspects.
Equine Vet J
January 2025
Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.
Background: In horses, systemic calcinosis is a rare syndrome characterised by muscle lesion associated with the mineralisation of large muscle groups or other organs, in the absence of an alternative cause for the calcification, such as toxic, enzootic or metabolic. Molecular and histopathological aspects of the disease are still poorly elucidated.
Objectives: To describe the epidemiological, pathological and molecular aspects of systemic calcinosis in a convenience sample of six horses submitted to necropsy in the Southern and Midwestern regions of Brazil.
Hibernating brown bears, due to a drastic reduction in metabolic rate, show only moderate muscle wasting. Here, we evaluate if ATPase activity of resting skeletal muscle myosin can contribute to this energy sparing. By analyzing single muscle fibers taken from the same bears, either during hibernation or in summer, we find that fibers from hibernating bears have a mild decline in force production and a significant reduction in ATPase activity.
View Article and Find Full Text PDFIn Vivo-Like Scaffold-Free 3D In Vitro Models of Muscular Dystrophies: The Case for Anchored Cell Sheet Engineering in Personalized Medicine.
Adv Healthc Mater
December 2024
Evolved.Bio, 280 Joseph Street, Kitchener, Ontario, N2G4Z5, Canada.
Progress in understanding the underlying mechanisms of muscular dystrophies is hindered by the lack of pathophysiologically relevant in vitro models. Here, an entirely scaffold-free anchored cell sheet engineering platform is used to create patient-specific three-dimensional (3D) skeletal muscle in vitro models. This approach effectively replicates mature muscle phenotypes and tissue- and disease-specific extracellular matric (ECM).
View Article and Find Full Text PDFQuantum dot-based thermometry uncovers decreased myosin efficiency in an experimental intensive care unit model.
Front Physiol
November 2024
Department of Clinical Neurophysiology, Karolinska Hospital, Stockholm, Sweden.
Article Synopsis
- Critical illness myopathy (CIM) leads to severe muscle function decline in ICU patients, characterized by muscle mass loss where the reduction in specific force outpaces the muscle mass decrease.
- The hallmark of CIM is marked by a significant reduction in the molecular motor protein myosin, which severely impacts the muscle's ability to generate force.
- An innovative study using cadmium telluride quantum dots revealed that muscle efficiency declines before myosin loss occurs, highlighting early changes in myosin function as potential targets for future CIM treatments.
A Novel MYH14 Variant Presenting as a New Phenotype of MYH14-Associated Neuromuscular Disorders-Clinicohistologic Findings and Review of the Literature.
J Clin Neuromuscul Dis
December 2024
Department of Neurology, Martin Luther University Halle-Wittenberg and University Hospital Halle, Halle (Saale), Germany.
Background: Pathogenic variants in the nonmuscle myosin, MYH14, have been associated with several pathologic conditions including a complex phenotype with peripheral neuropathy, myopathy, hoarseness, and hearing loss. Since its first description in a large Korean kindred, this rare neuromuscular disorder has further been characterized in 1 American and 1 Canadian pedigree.
Case Presentation: Here, we describe a German patient with atypical MYH14-related neuromuscular disorder.
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