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Upon ischemic injury in stroke, neuronal HMGB1 is abundantly released into the extracellular space, both by active secretion and passive release, to accumulate in the ischemic core of the acute phase and to activate resident brain immune cells, leading to the recruitment of mononuclear cells that further amplify inflammation (Singh et al., 2016)

Am J Pathol 2003

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Q1) and lipid cluster levels LC3, LC4, LC5, LC6, and LC7, their strength of association based on LR models was comparatively weaker (Fig