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An early-senescence state in aged mesenchymal stromal cells contributes to hematopoietic stem and progenitor cell clonogenic impairment through the activation of a pro-inflammatory program.

This group characterized mesenchymal stem cells (MSC) from the bone marrow of humans of different ages and found older MSC to have many concerning characteristics, including senescent-like (enlarged) morphology, reduced proliferation ability, increased SA-beta-galactosidase, increased lipofuscin, and increased DNA damage and DNA damage response. Exposure of young hematopoetic stem cells to factors secreted by aged MSC impaired some aspects of their function.
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Topical applications of an emollient reduce circulating pro-inflammatory cytokine levels in chronically aged humans: a pilot clinical study.

I found this study interesting: topical application of an emollient to the skin (i.e. applying lotion) "normalized" several * systemic* inflammatory factors such as IL-6 in older humans. This makes me wonder: how much of the increase in circulating inflammatory factors during aging could be caused by dysfunctional, damaged, or senescent skin? I wonder how long this reduction of inflammation persisted after the application of emollient.
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Excessive Cell Growth Causes Cytoplasm Dilution And Contributes to Senescence.

These authors suggest that cell size can affect whether a cell becomes senescent; larger cells have a diluted cytoplasm, and this causes cellular dysfunction (including possibly senescence). This idea seemed extra interesting to me because of the association between mTOR inhibition and longevity (I would think mTOR inhibition would tend to restrict cell growth and prevent cytoplasmic dilution), while mTOR activation may tend to increase cell growth, and without cell division to dilute this growth, cells may tend to swell to the point that their cytoplasm is diluted and the cells become senescent.
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Cells exhibiting strong p16 INK4a promoter activation in vivo display features of senescence.

This group reports on a "knock-in fluorochrome", tandem dimer Tomato, for assessing the prevalence of senescent cells in the whole, live organism (in mice). This fluorochrome was apparently better at assessing p16INK4a promoter activation than mRNA abundance. I wonder what method they used to visualize the increase in p16INK4a promoter activation with aging (e.g. biopsy and fluorescence microscopy? Something else?) If it was not particularly invasive or toxic, perhaps it would be useful for the evaluation of promising medical interventions in aging humans.
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