Publications by authors named "E Mosca"

This study explores the application of Universal Design (UD) principles to university environments, aiming to improve the experiences of students and staff by fostering inclusivity in educational and social spaces. The research began with a literature review and employed the 'Design for All A.U.

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Nintedanib (NIN), a multi-tyrosine kinase inhibitor clinically approved for idiopathic pulmonary fibrosis and lung cancer, is characterized by protonation-dependent lysosomotropic behavior and appearance of lysosome-specific fluorescence emission properties. Here we investigate whether spontaneous formation of a so far unknown NIN matter within the acidic cell compartment is underlying these unexpected emissive properties and investigate the consequences on lysosome functionality. Lysosomes of cells treated with NIN, but not non-protonatable NIN derivatives, exhibited lysosome-associated birefringence signals co-localizing with the NIN-derived fluorescence emission.

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Glial cells provide physical and chemical support and protection for neurons and for the extracellular compartments of neural tissue through secretion of soluble factors, insoluble scaffolds, and vesicles. Additionally, glial cells have regenerative capacity by remodeling their physical microenvironment and changing physiological properties of diverse cell types in their proximity. Various types of aberrant glial and macrophage cells are associated with human diseases, disorders, and malignancy.

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Article Synopsis
  • Multiple sclerosis (MS) is a diverse condition with varying symptoms and treatment responses, prompting a study on its genetic causes related to disease activity over time.
  • Researchers analyzed genetic data from two groups of relapsing-remitting MS patients, examining their genomes and specific gene interactions in brain and lymphocyte tissues to identify key genetic variants and pathways involved in MS.
  • The study found 23 genetic variants and 223 associated genes, with significant genes such as PON2 and ILRUN linked to oxidative stress and immune modulation, revealing shared and tissue-specific mechanisms driving MS disease activity.
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