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Jastreboff AM, Kaplan LM, Frias JP, Wu Q, Du Y, Gurbuz S, et al

However, with the emergence of a body of data documenting differences in autistic brains that were most likely of physiological originparticularly neuropathological identification of neural and glial inflammation associated with enlargement of the areas of the brain, including cerebrum, that continue to grow and mature postnatallythe assumption of congenital origin came under question, since the processes of generating such changes are often associated with environmental etiologies including oxidative stress and neuroinflammation generated by noxious environmental exposures, including activation of glial cells [46, 271, 315, 377, 411, 522, 548]

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Not so with grxA and trxC (Table 1)

For example, the multienzyme complex pyruvate dehydrogenase [7] at the junction of glycolysis and the citric acid cycle requires five organic cofactors and one metal ion: loosely bound thiamine pyrophosphate (TPP), covalently bound lipoamide and flavin adenine dinucleotide (FAD), cosubstrates nicotinamide adenine dinucleotide (NAD + ) and coenzyme A (CoA), and a metal ion (Mg 2+ )