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42 Further analysis of DNA damage signalling demonstrates the causal role of P53 in low-dose CSC-induced endothelial cell death by showing an upregulation in P53 protein expression and the cell death protective activity of the P53 knock down

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We found that relative to Non-M-CS exposure, M-CS exposure induced greater increases in the above-mentioned lung inflammatory indices, as well as in the epithelial and lung expression of TRPM8, p-ERK, and p-JNK (Figures 16)

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