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The pathogenic mechanism of homocysteine -induced endothelial nitric oxide synthase dysfunction and the antagonistic effects by folic acid
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NEK1 mutations in familial amyotrophic lateral sclerosis
Its selective GHS-R1a mechanism creates non-redundant synergy with both GHRH analogs and healing-focused peptides
Sir-mediated repression can occur independently of chromosomal and subnuclear contexts
