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Aims: To verify the hypothesis that an enriched environment (EE) alleviates sleep deprivation‐induced fear memory impairment by modulating the basal forebrain (BF) PIEZO1/calpain/autophagy pathway. Methods: Eight‐week‐old male mice were housed in a closed, isolated environment (CE) or an EE, before 6‐h total sleep deprivation. Changes in fear memory after sleep deprivation were observed using an inhibitory avoidance test. Alterations in BF PIEZO1/calpain/autophagy signaling were detected. The PIEZO1 agonist Yoda1 or inhibitor GsMTx4, the calpain inhibitor PD151746, and the autophagy inducer rapamycin or inhibitor 3‐MA were injected into the bilateral BF to investigate the pathways involved in the memory‐maintaining role of EE in sleep‐deprived mice. Results: Mice housed in EE performed better than CE mice in short‐ and long‐term fear memory tests after sleep deprivation. Sleep deprivation resulted in increased PIEZO1 expression, full‐length tropomyosin receptor kinase B (TrkB‐FL) degradation, and autophagy, as reflected by increased LC3 II/I ratio, enhanced p62 degradation, increased TFEB expression and nuclear translocation, and decreased TFEB phosphorylation. These molecular changes were partially reversed by EE treatment. Microinjection of Yoda1 or rapamycin into the bilateral basal forebrain induced excessive autophagy and eliminated the cognition‐protective effects of EE. Bilateral basal forebrain microinjection of GsMTx4, PD151746, or 3‐MA mimicked the cognitive protective and autophagy inhibitory effects of EE in sleep‐deprived mice. Conclusions: EE combats sleep deprivation‐induced fear memory impairments by inhibiting the BF PIEZO1/calpain/autophagy pathway. [ABSTRACT FROM AUTHOR]

Background: Polymorphonuclear neutrophil (PMN), one of the most important inflammatory cells, functions throughout the initiation, progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma., Methods: PMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis, necrosis, survival and respiratory burst were detected by flow cytometry. Meanwhile, lactate dehydrogenase and (LDH) [Ca2+]i were measured., Results: The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma, and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile, lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control (P < 0.05) from 4 hours to 24 hours, and intracellular free Ca2+ in PMN was increased temporarily., Conclusions: Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury. The temporary increase of intracellular free Ca2+ may be responsible for the delayed apoptosis of PMN.