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GH, and circulating IGF1) seen during aging causes the cognitive impairment often found in senescence. Accordingly, there has been no description of cases of dementia in the almost 30 years of follow-up of this cohort, nor a mention of dementia as a
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-dependent and adiponectin-independent mechanisms ( 26 ). Yan et al . ( 8 ) found that FGF21 protects the cells from premature aging induced by H 2 O 2 by delaying the replicative senescence of the endothelial cells. This study found that FGF21 was positively
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had no effect in DU145. (6) 0.1 nM–1 µM for 6 days LNCaP Induces senescence (β-galactosidase assay) in a dose-dependent manner. (45) T4 100 nM for 7 days PC-3 Increases cell migration (transwell assay) and reduces
Tulane University School of Medicine, Department of Psychiatry, Division of Child and Adolescent Psychiatry, Tulane University, New Orleans, Louisiana, USA
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Tulane University School of Medicine, Department of Psychiatry, Division of Child and Adolescent Psychiatry, Tulane University, New Orleans, Louisiana, USA
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biological aging. Telomeres are the protective caps at the ends of chromosomes that shorten with every cell division and serve as a molecular clock, with shorter TL reflecting older cellular age. TL is critical for cellular senescence and apoptosis and may
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T2DM, CVD and vascular ageing processes (17) . These observations suggest that T2DM plays an important role in the processes of replicative senescence. However, despite obvious scientific achievements in the field of vascular ageing, there are many
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accelerated metabolic senescence of bone marrow stromal stem cells ( 21 ). Despite these possibilities, further studies are needed to explore the molecular mechanism towards the association of WC with BMD. Moreover, our results revealed that men and
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Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität München, Munich, Germany
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.09.070 ) 19889414 10.1016/j.atherosclerosis.2009.09.070 10 Harte AL da Silva NF Miller MA Cappuccio FP Kelly A O’Hare JP Barnett AH Al-Daghri NM Al-Attas O Alokail M , et al . Telomere length attrition, a marker of biological senescence, is inversely correlated
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embryonic fibroblasts (MEFs) (9) , associated with poor cell growth and senescence. Overexpression of CUL7 in an immortalised cancer cell line leads to decreased p53-mediated apoptosis (10, 11, 12) . In contrast to the data in MEFs, AKT signalling was
Endocrine Unit, Royal Victoria Infirmary, Newcastle upon Tyne, UK
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reached senescence after 3rd passage ( Fig. 1D (i)). The colony-forming unit fibroblast-like cells (CFU-F) were seen in the primary culture in either medium but cells seeded in MGPM exhibited a higher number of CFUs ( Fig. 1B (i) and (ii)). On average, 4
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mixture, as signs of early reproductive senescence were seen at the lowest TotalMix dose, though these findings were not as consistent across groups as the sperm count effect ( 46 ). At the next dose levels (the TotalMix-200 and -450 and the AAMix-200 and