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Thus, it seems that the succinylcholine effects were attenuated, directly and/or indirectly (i.e., single action potential in adjacent membrane after binding, while succinylcholine remains bound there, keeping the end plate potential depolarized)

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These findings provide compelling evidence for the role of epigenetic regulation of CCL11 and suggest that supplemental B12 has potential as an epidrug to treat neurodegenerative conditions associated with aberrant CCL11 expression