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| http://dx.doi.org/10.1186/s12954-023-00848-0 | DOI Listing |
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Inactivation of the SLC25A1 gene during embryogenesis induces a unique senescence program controlled by p53.
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Germline inactivating mutations of the SLC25A1 gene contribute to various human disorders, including Velocardiofacial (VCFS), DiGeorge (DGS) syndromes and combined D/L-2-hydroxyglutaric aciduria (D/L-2HGA), a severe systemic disease characterized by the accumulation of 2-hydroxyglutaric acid (2HG). The mechanisms by which SLC25A1 loss leads to these syndromes remain largely unclear. Here, we describe a mouse model of SLC25A1 deficiency that mimics human VCFS/DGS and D/L-2HGA.
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Health and Sports Medicine Department, Faculty of Sports Sciences and Health, University of Tehran, North Karegar St, P.O.B: 1439813117, Tehran, Iran.
Although the connection between muscular strength and flatfoot condition is well-established, the impact of corrective exercises on these muscles remains inadequately explored. This study aimed to assess the impact of intrinsic- versus extrinsic-first corrective exercise programs on muscle morphometry and navicular drop in boys with flexible flatfoot. Twenty-five boys aged 10-12 with flexible flatfoot participated, undergoing a 12-week corrective exercise program, with a shift in focus at six weeks.
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