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For DE, gene expression was normalised to (beta-actin) ACTB and against the starting population of pluripotent stem cells for each cell line

The increased susceptibility to cell death could exaggerate inflammation via the release of damage signals (e.g., ATP, High mobility group box 1 protein (HMGB1)) or alternatively, ferroptosis of CD16 + monocytes and/or macrophages that are reputedly more pro-inflammatory than intestinal macrophages could serve to limit inflammation

Sometimes that is through a single procedure