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The authors proposed that L-carnitine could prevent the accumulation of acyl-CoAs in mitochondria, which they hypothesized is a key early event involved in the pathophysiology of hypoxic-ischemic injury [19]

Feasible solutions include engineered probiotic vectors (e.g., Flavonifractor plautii overexpressing flavonoid-degrading enzymes) to achieve 150200 M intratumoral DAT with serum levels 250 mg/kg induce liver/kidney damage and dysbiosis) (119)

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