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Vitamin B12 deficiency results in megaloblastic anemia, GI lesions, and neurologic damage (which begins with an inability to produce myelin and is followed by gradual degeneration of the axon and nerve head)

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In isolated rat aorta preparations, the peptide produced concentration-dependent vasodilation that was endothelium-dependent and abolished by L-NAME, and co-immunoprecipitation work traced the response to phosphorylation of Src, caveolin-1, and endothelial nitric oxide synthase, with reduced binding between caveolin-1 and eNOS [1]