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Circulating nucleic acids damage DNA of healthy cells by integrating into their genomes.

Wow, this is fascinating; exogenous DNA and chromatin fragments are taken up by cells and end up in nuclei, associating with resident DNA, ultimately being integrated into organs? I'm fascinated by the implications of this: could it be that a significant amount of aging dysfunction is caused by this process happening over and over throughout one's life? That is, cells can be killed or destroyed by viruses, bacteria, trauma, etc., presumably releasing some DNA into circulation. Moreover, cellular senescence is characterized by DNA damage response (DDR)-like reactions; perhaps some age-related cellular senescence is caused in this way? Is there some way to test for whether these "fragments" accumulate in long-lived cells' DNA? Perhaps one way is to sequence the DNA of short-lived cells, and compare it to long-lived cells.
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Misfolding of Apoprotein B 100, LDL Aggregation and 17-Beta-Estradiol In Atherogenesis.

I retained this because of the possibility that this "apoprotein misfolding" and "LDL aggregation" strikes me as potential Damage. I haven't read about this possibility before, and have spent considerable time in this literature (although perhaps someone else has heard of this hypothesis and its supporting evidence). I *have* heard of *glycated* LDL, and maybe that's related to what they present here.
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Immunolocalization of Smurf1 in Hirano bodies.

I left the intro part of the abstract to acquaint readers with this somewhat-arcane aspect of aging (Hirano bodies). From the abstract alone, this doesn't implicate Hirano bodies as "Damage", but I tagged it with "Damage-Identification" as something that needs to be considered further for that category. Abstract portions (underlined) self-explanatory - no further comment by me.
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Immune-mediated pore-forming pathways induce cellular hypercitrullination and generate citrullinated autoantigens in rheumatoid arthritis.

Here they report on some causes of hypercitrullination in RA. This is not an area I'm well-read in, but I'm curious whether hypercitrullination could be classified as SENSible damage. I suspect that messing with this peptidylarginine deiminase activity would be MWM (Messing With Metabolism), but would cleanup of hypercitrullination help reverse RA? Of course, this would heavily depend on whether these proteins accumulate, vs. simply achieving a higher steady-state concentration for some reason related to metabolism.
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Material properties of aged human mitral valve leaflets.

This looks like damage-identification in mitral valves in aged individuals. Note that I underlined the parts of the abstract I found to be particularly interesting and relevant. I will make a habit to continue to do this. It likely will not show up in the database once these are entered there, but I suspect it may be useful for readers of this report to quickly pick out the portions of the abstract that are highly representative of the reason(s) why I chose it for inclusion. Thus, the reader can decide more quickly whether they want to read further.
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Free report on high blood pressure

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Free diabetes report

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