Angela B Freie

TL;DR: It is hypothesized that the duration of ischemic tolerance could be extended from days to months by repeated intermittent hypoxia of varying magnitude and duration.

TL;DR: The early expression of CCL2 in neurons, the delayed expression in cerebral endothelial cells, and CCL1-mediated actions on circulating CCR2+ monocytes, appear to be required to establish ischemic tolerance to focal stroke in response to HPC, and thus represent a novel role for this chemokine in endogenous neurovascular protection.

TL;DR: Hypoxic preconditioning-induced attenuation of postischemic BBB disruption in wild types, evidenced by reduced extravascular immunoglobulin G intensity, suggests direct protection of BBB integrity.

TL;DR: Observations support a major contribution of residues in the β5′-loop in the function of hPTL and suggest that a third partner, bile salt micelles or the lipid interface or both, influence the binding of colipase and h PTL through interactions with the β 5′- loop.

TL;DR: These studies indicate that RHP results in a sustained upregulation of SIRT1 protein coincident with the period of LTT, and these novel signaling pathways triggered by RHP may serve as molecular targets for therapeutics designed to reduce brain injury in stroke.