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Notably, although the NO system is largely implicated in stomach cytoprotection and colitis lesions[2-4], the application of L-NAME (a vasoconstrictor)[11] and/or L-arginine (a vasodilator)[11] has not been investigated with respect to the immediate presentation of the blood vessels after a segment of left colic artery and vein was occluded by two ligations
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6f), suggesting that LET7-mediated CRCK3 dephosphorylation is associated with SUMM2 activation upon disruption of the MEKK1–MKK1/2–MPK4 cascade by HopAI1
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