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rENP induced a statistically significant (p < 0.
In this case, rENP noticeably blocked the secretion of IL-6 stimulated by P[M.
10] strongly induced the secretion of TNF-[alpha] and IL-6 (Figures 3 and 5), and this was due at least in part to endotoxin, because the rENP reduced cytokine release in response to these particles.
10] from the southeastern region could explain the proinflammatory potential of these particles because the cytokine stimulatory effects of these particles on confluent cell cultures were blocked by rENP.