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The possibility that sustained folic acid intake would deplete vitamin B-12 independent of hematopoiesis suggests a plausible alternative mechanism based on the known details of the renal handling of holoTC, whereby folic acid might interfere with holoTC reuptake or cause its sequestration in the kidney, promoting the excretion of holoTC and further depleting metabolically active vitamin B-12 during vitamin B-12 deficiency

Markers The supervised lists of potential marker genes (Supplementary Table 3 and 4) were generated from the initial sequencing data (Figs

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