A continuous flight task load can induce fatigue and lead to changes in electroencephalography (EEG). EEG microstates can reflect the activities of large-scale neural networks during mental fatigue. This exploratory experiment explored the effects of mental fatigue induced by continuous simulated flight multitasking on EEG microstate indices. Twenty-four participants performed continuous 2-hour aircraft piloting simulation while EEG were recorded. The Stanford sleepiness scale (SSS) and critical flicker fusion frequency (CFF) were measured before and after the task. Microstate analysis was applied to EEG. Four microstate classes (A-D) were identified during the pre-task, post-task, beginning, and end phases. The effects of mental fatigue were analyzed. Compared with the pre-task, the post-task had a higher global explained variance (GEV) and time parameters of class C but lower occurrence and coverage of class D. The end had a higher GEV but lower duration and coverage of class D than at the beginning. After 2 h of multitasking, the transition probability between A and D, and between B and D decreased but between A and C increased. Subjective fatigue scores were negatively correlated with occurrence and coverage of class D. Task performance was negatively correlated with duration and coverage of class C but positively correlated with duration and occurrence of class B. Time parameters and transition probability of EEG microstates can detect mental fatigue induced by continuous aircraft piloting simulation. The global brain network activation of mental fatigue can be detected by EEG microstates that can evaluate flight fatigue.

Purpose: To assess the incidence rate of myopia, refractive change, and the effects of influencing factors on a group of highly selected senior high school students in an Aviation Cadet prerecruitment class in China. Methods: A total of 800 nonmyopic, male, Grade 9 students aged 14- to 16-years old with cycloplegic refraction of −0.25 or greater diopters (D) to 1.75 D or less in both eyes were enrolled in May 2016. During their senior high school studies, students had one 20-minute physical training period a day, and they were encouraged to participate in outdoor activities during class recess without any time limits. The first follow-up was 8 months after enrollment when they were in Grade 10, and the second follow-up was 1 year after the first follow-up when they were in Grade 11. Comprehensive ocular examinations and a detailed questionnaire, which included questions about outdoor activity time, parental myopia, and near work, were completed at each follow-up. Results: The average spherical equivalent refraction (SER) of the right eyes was 0.39 ± 0.44 D at baseline, 0.16 ± 0.41 D at the first follow-up, and −0.10 ± 0.38 D at the second follow-up. The cumulative refractive change was −0.50 D (95% confidence interval [CI], −0.53 to −0.47). The cumulative incidence rate of myopia was 15.5% (124/800). Incident myopia was significantly associated with outdoor activity for more than 1 versus less than 0.5 hr/d (odds ratio [OR] = 0.272, 95% CI, 0.132–0.560), baseline refraction (OR = 0.079, 95% CI, 0.041–0.153), maternal myopia (OR = 2.251, 95% CI, 1.160–4.368), longer class time (OR =3.215, 95% CI, 1.088–9.499), frequent, continuous, and long time reading/writing (OR = 1.620, 95% CI, 1.022–2.570), and shorter reading/writing distance (OR = 1.828, 95% CI, 1.065–3.140). In multiple linear regression model, having outdoor activity for more than 1 hr/d was protective from cumulative SER decrease. A higher baseline refraction together with longer reading/writing time, frequent, continuous, and longtime reading/writing, and shorter reading/writing distance were risk factors for SER decrease. Conclusions: In this cohort of highly selected, nonmyopic students, longer outdoor activity time was a protective factor for both incident myopia and refractive change of myopic shift. The risk factors for incident myopia included lower hyperopic baseline refraction, more near work, and maternal myopia. The risk factors for refractive change of myopic shift included more hyperopic baseline refraction and more near work.

Free radicals and oxidative stress play an important role in the pathogenesis of noise-induced hearing loss (NIHL). Some ginseng monomers showed certain therapeutic effects in NIHL by scavenging free radicals. Therefore, we hypothesized that ginsenoside Rd (GSRd) may exert neuroprotective effects after noise-induced auditory system damage through a mechanism involving the SIRT1/PGC-1α signaling pathway. Forty-eight guinea pigs were randomly divided into four equal groups (normal control group, noise group, experimental group that received GSRd dissolved in glycerin through an intraperitoneal injection at a dose of 30 mg/kg body weight from 5 days before noise exposure until the end of the noise exposure period, and experimental control group). Hearing levels were examined by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). Hematoxylin–eosin and Nissl staining were used to examine neuron morphology. RT-qPCR and western blotting analysis were used to examine SIRT1/PGC-1α signaling and apoptosis-related genes, including Bax and Bcl-2, in the auditory cortex. Bax and Bcl-2 expression was assessed via immunohistochemistry analysis. Superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) levels were determined using a commercial testing kit. Noise exposure was found to up-regulate ABR threshold and down-regulate DPOAE amplitudes, with prominent morphologic changes and apoptosis of the auditory cortex neurons (p < 0.01). GSRd treatment restored hearing loss and remarkably alleviated morphological changes or apoptosis (p < 0.01), concomitantly increasing Bcl-2 expression and decreasing Bax expression (p < 0.05). Moreover, GSRd increased SOD and GSH-Px levels and decreased MDA levels, which alleviated oxidative stress damage and activated SIRT1/PGC-1α signaling pathway. Taken together, our findings suggest that GSRd ameliorates auditory cortex injury associated with military aviation NIHL by activating the SIRT1/PGC-1α signaling pathway, which can be an attractive pharmacological target for the development of novel drugs for NIHL treatment.

Lysosomal exocytosis and fusion to cellular membrane is critical in the oxidative stress formation of endothelium under apoptotic stimulus. We investigated the role therein of it in hyperglycaemia-induced endothelial dysfunction. The lysosome-membrane fusion was shown by the expression of lamp1, the lysosomal membrane marker, on cellular membrane and the transportation of lysosomal symbolic enzymes into cultural medium. We also examined the ceramide production, lipid rafts (LRs) clustering, colocalization of gp91^phox, a NADPH oxidase subunit (NOX) to LRs clusters, superoxide (O₂^.-) formation and nitric oxide (NO) content in human umbilical vein endothelial cells (HUVEC) and the endothelium-dependent NO-mediated vasodilation in isolated rat aorta. As compared to normal glucose (5.6 mmol/l, Ctrl) incubation, high glucose (22 mmol/l, HG) exposure facilitated the lysosome-membrane fusion in HUVEC shown by significantly increased quantity of lamp1 protein on cellular membrane and enhanced activity of lysosomal symbolized enzymes in cultural medium. HG incubation also elicited ceramide generation, LRs clustering and gp91^phox colocalization to LRs clusters which were proved to mediate the HG induced O₂^.- formation and NO depletion in HUVEC. Functionally, the endothelium-dependent NO-mediated vasodilation in aorta was blunted substantially after HG incubation. Moreover, the HG-induced effect including ceramide production, LRs clustering, gp91^phox colocalization to LRs clusters, O₂^.- formation and endothelial dysfunction could be blocked significantly by the inhibition of lysosome-membrane fusion. We propose that hyperglycaemia-induced endothelial impairment is closely related to the lysosome-membrane fusion and the following LRs clustering, LRs-NOX platforms formation and O₂^.- production.