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OBJECTIVES: Traumatic brain injury (TBI) triggers multiple cell death pathways, possibly including ferroptosis -a recently described cell death pathway that results from accumulation of 15-lipoxygenase (15-LOX)-mediated lipid oxidation products, specifically oxidized phosphatidylethanolamine (PE) containing arachidonic (AA) or adrenic (AdA) acid. This study aimed to investigate whether ferroptosis contributed to the pathogenesis of in vitro and in vivo TBI, and whether inhibition of 15-LOX provided neuroprotection. DESIGN:Cell culture study and randomized, controlled animal study.

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Anterior cruciate ligament (ACL) injuries commonly occur during jump-landing tasks when individuals' attention is simultaneously allocated to other objects and tasks. The purpose of the current study was to investigate the effect of allocation of attention imposed by a secondary cognitive task on landing mechanics and jump performance. Thirty-eight recreational athletes performed a jump-landing task in three conditions: no counting, counting backward by 1 s from a randomly given number, and counting backward by 7 s from a randomly given number. Three-dimensional kinematics and ground reaction forces were collected and analysed. Participants demonstrated decreased knee flexion angles at initial contact (p = 0.001) for the counting by 1 s condition compared with the no counting condition. Participants also showed increased peak posterior and vertical ground reaction forces during the first 100 ms of landing (p ≤ 0.023) and decreased jump height (p < 0.001) for the counting by 1 s and counting by 7 s conditions compared with the no counting condition. Imposition of a simultaneous cognitive challenge resulted in landing mechanics associated with increased ACL loading and decreased jump performance. ACL injury risk screening protocols and injury prevention programmes may incorporate cognitive tasks into jump-landing tasks to better simulate sports environments.