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Rationale: Oxygen is essential for cellular energy metabolism. Neurons are particularly vulnerable to hypoxia. Increasing oxygen supply shortly after stroke onset could preserve the ischemic penumbra until revascularization occurs.

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Repetitive mild traumatic brain injuries (RmTBIs) are increasingly recognized to have long-term neurological sequelae in a significant proportion of patients. Individuals that have had RmTBIs exhibit a variety of sensory, cognitive, or behavioral consequences that can negatively impact quality of life. Brain tissue oxygen levels ([Formula: see text]) are normally maintained through exquisite regulation of blood supply to stay within the normoxic zone (18-30 mmHg in the rat hippocampus).

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Objective: In this study, it was aimed to compare various parameters during surgery and postoperative cognitive functions in patients undergoing coronary artery bypass graft (CABG) surgery using different levels of perioperative oxygen.

Methods: One hundred patients scheduled for elective CABG surgery were included in the study. The patients were divided into two groups according to arterial oxygen levels during surgery.

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Hyperoxygenation Ameliorates Stress-induced Neuronal and Behavioral Deficits.

Exp Neurobiol

December 2021

Department of Brain and Cognitive Sciences, Ewha Womans University, Seoul 03760, Korea.

Hyperoxygenation therapy remediates neuronal injury and improves cognitive function in various animal models. In the present study, the optimal conditions for hyperoxygenation treatment of stress-induced maladaptive changes were investigated. Mice exposed to chronic restraint stress (CRST) produce persistent adaptive changes in genomic responses and exhibit depressive-like behaviors.

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Recently we reported that hyperoxygenation treatment reduces amyloid-beta accumulation and rescues cognitive impairment in the Tg-APP/PS1 mouse model of Alzheimer's disease. In the present study, we continue to investigate the mechanism by which hyperoxygenation reduces amyloid-beta deposition in the brain. Hyperoxygenation treatment induces upregulation of matrix metalloproteinase-2 (MMP-2), MMP-9, and tissue plasminogen activator (tPA), the endopeptidases that can degrade amyloid-beta, in the hippocampus of Tg-APP/PS1 mice.

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