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Loss of VSMCs within the medial layer of the arterial wall represents a key pathophysiological hallmark of AA, which can result in the weakening of the vessel wall and subsequent dilatation [53, 54]

And so I did some in-silico work as well, looking at vitamin D response elements in, uh, genes that were regulated by vitamin D

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Host cell oxidative stress induces dormant Staphylococcus aureus persisters