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Amelioration of premature aging in Werner syndrome stem cells by targeting SHIP/AKT pathway.
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School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.
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School of Medicine, Qom University of Medical Sciences, Qom, Iran.
Introduction: Intrinsic Capacity in integrated geriatric care emphasizes the importance of a thorough functional assessment. Monitoring the intrinsic capacity of older individuals provides standardized and reliable information to prevent early disability. This study assessed the relationship between intrinsic capacity and functional ability in older adults.
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Optical techniques, such as functional near-infrared spectroscopy (fNIRS), contain high potential for the development of non-invasive wearable systems for evaluating cerebral vascular condition in aging, due to their portability and ability to monitor real-time changes in cerebral hemodynamics. In this study, thirty-six healthy adults were measured by single channel fNIRS to explore differences between two age groups using machine learning (ML). The subjects, measured during functional magnetic resonance imaging (fMRI) at Oulu University Hospital, were divided into young (age ≤ 32) and elderly (age ≥ 57) groups.
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Division of Urology, Department of Surgery, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
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Laboratory of Human Physiology and Pathology, Faculty of Pharmaceutical Sciences, Teikyo University, Tokyo, Japan.
In most patients with type 1 xanthinuria caused by mutations in the xanthine dehydrogenase gene (XDH), no clinical complications, except for urinary stones, are observed. In contrast, all Xdh(- / -) mice die due to renal failure before reaching adulthood at 8 weeks of age. Hypoxanthine or xanthine levels become excessive and thus toxic in Xdh(- / -) mice because enhancing the activity of hypoxanthine phosphoribosyl transferase (HPRT), which is an enzyme that uses hypoxanthine as a substrate, slightly increases the life span of these mice.
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