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These data suggest that PI-mediated induction of endogenous ChaC1 functionally mimics genetic overexpression of ChaC1 to potentiate AUR cytotoxicity

and were subsequently subjected to a 10-week observation period (Pimentel et al., 2011)

The aim of the present study was to identify clinical and plasma metabolite markers associated with freedom from vascular complications in people with very long duration of type 1 diabetes (T1D)