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Total amplitude of systolic annular excursion was measured from the nadir of M-mode profile corresponding to the point furthest from LV apex to the point of maximal excursion towards LV apex [25]

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Thus, accumulation of -ketoglutarate upon CSE treatment might lead to enhanced PHD activation resulting in increased HIF-degradation at least under hypoxia, where hydroxylated HIF-1 was increased by CSE