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In conclusion, the data reported here provide new insights into the mechanisms underlying the deleterious effects of high glucose on endothelial cells by illustrating the likely central pathophysiologic role for decreased G6PD activity and increased PKA in endothelial cells

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Identifying similarities between metabolite alterations in GWS and ME/CFS is an important step toward uncovering potential therapeutic targets and enhancing our understanding of the underlying pathophysiology that contributes to shared symptoms, such as fatigue

Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings

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