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In partial support of this, a time-dependent increase in the phosphorylation of the master inflammatory regulator NF-B p65 48 was observed in SV-HUC cells treated with these BCEV samples relative to untreated cells, although this activation was not as robust as in cells treated directly with CSE or MEL suggesting that these BCEVs do not merely deliver these toxicants to recipient urothelial cells (Fig

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