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If the signal for DSBs is uniquely associated with the cell cycle phase, we would expect cells under proliferation to carry a higher signal for DSB

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Preventing this decrease, with the administration of a SIRT-1 activator, reversed ROS bursts, increased downstream nuclear PGC-1a and Nrf2 expression, and attenuated increases in mitochondrial membrane potential and neuronal apoptosis induced by ischemia/reperfusion injury [78]

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