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At this point, the injured brain tissue rapidly produces pro-inflammatory cytokines, causing leukocyte infiltration and eventually inducing ferroptosis and exaggerating brain edema, neuron death and progress of IS (Jin et al., 2013) (Figure 2)

Based on overall FISH and Hi-C results, our model is that domain-based chromosomal compaction is diminished in the cnd1-K658E mutant, whereas domain compaction is partially compromised in Pmc4-depleted cells, coinciding with impaired boundary formation (Fig