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It is possible that dehydroascorbylation could act as a specific regulatory post-translational protein modification responding to increased ascorbate oxidation rather than as generic damage, but so far there is no evidence for this role

A phase 2 randomized trial of ELND005, scyllo-inositol, in mild to moderate Alzheimer disease

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OCTN2 has a K m of 26 M for carnitine and is expressed in a variety of tissues including muscle, heart, kidney, and fibroblasts [12,13]
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