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Red Blood Cell Distribution Width, Vascular Aging Biomarkers, and Endothelial Progenitor Cells for Predicting Vascular Aging and Diagnosing/Prognosing Age-Related Degenerative Arterial Diseases.

I normally wouldn't have included this paper in my reporting because it was not clear in the abstract exactly how good of a predictor of cardiovascular disease RDW was observed in this study. But since it was published in Rejuvenation Research , I retained it in this report for readers to investigate further.
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Cell cycle-dependent and -independent telomere shortening accompanies murine brain aging.

This group reports on some telomere and telomerase dynamics in the brains of aging mice. They observe that telomeres were shortened in old mice according to both proliferating and non-proliferating cell types. But this seems to be old news; I thought Oki told me years ago that during his PhD or post-doc work, he learned that the majority of telomere shortening was due to oxidative stress and other non-cell-cycle-related phenomena.
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Distributed hepatocytes expressing telomerase repopulate the liver in homeostasis and injury.

This looks like a sufficiently interesting biology lesson that I thought I should include it in this report. This group reports that a small subset of hepatocytes apparently express high levels of telomerase, and these are the cells that may be involved in rejuvenation in response to liver injury. This might have implications for WILT, especially if these high-TERT-expressing hepatocytes are not stem cells that can simply be replenished periodically.
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miR-380-5p-mediated repression of TEP1 and TSPYL5 interferes with telomerase activity and favours the emergence of an “ALT-like” phenotype in diffuse malignant peritoneal mesothelioma cells.

I retained this report because if I'm understanding it correctly, repeated exposure to miR-380-5p seems to have induced an ALT-like phenotype in these mesothelioma cells. miR-380-5p is apparently very effective at inhibiting telomerase activity, so I wonder if that's part of what may be required to activate ALT in some circumstances: inhibition of telomerase (or the consequent telomere shortening).
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Extensive Proliferation of Human Cancer Cells with Ever-Shorter Telomeres.

These researchers report that there are some cancer types that apparently don't need to maintain their telomeres; they can continue dividing with ever-shortening telomeres. This might have some relevance in ALT research (particularly their mention of sarcomas, which I understood were largely found to utilize ALT). Are they missing something with the assays they used here, or is there something useful we can learn from this report?
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