Objective To investigate status about the heart rate variability and executive function in patients with insomnia.Methods The study involves 165 cases of patients with insomnia and 92 cases normal.The Pittsburgh Sleep Quality Index (PSQI) screening for insomnia,Wisconsin Card Sorting Test (WCST) for the assessment of executive function and Self-generate Physiological Coherence System (SPCS) were used to collect the data of heart rate variability (HRV).Results The SDNN,RMSSD,TP,LF,HF of HRV of the insomnia group were significantly higher than these factors of control group (t=2.712,2.726,2.427,2.542,2.338,P＜0.05 or P＜ 0.01).In the WCST,number of completed categories,conceptualization percentage of the group of patients with insomnia were significantly lower than the control group (t=-2.368,-2.165,all P＜0.05),persistent errors,persistent error percentages,continuous number of responses of patients' group were significantly higher than the control group (t=2.712,2.991,2.690,all P＜0.01).TP,LF,HF,LF/HF of HRV and the number of error responses,persistent errors,persistent error percentages,continuous number of responses of WCST had significant negative correlations (r=-0.171--0.245,P＜0.05 or P＜0.01),while the conceptualization percentage were significantly positively correlated (r=0.198-0.227,P＜0.05 or P＜0.01).Conclusion The results show that insomnia not only cause individual autonomic disorders,but damage the executive function of prefrontal.HRV and executive function in patients with insomnia have close relationships.

Central nervous system (CNS) injuries, including stroke, traumatic brain injury, and spinal cord injury, are essential causes of death and long-term disability and are difficult to cure, mainly due to the limited neuron regeneration and the glial scar formation. Herein, we apply extracellular vesicles (EVs) secreted by M2 microglia to improve the differentiation of neural stem cells (NSCs) at the injured site, and simultaneously modify them with the injured vascular targeting peptide (DA7R) and the stem cell recruiting factor (SDF-1) on their surface via copper-free click chemistry to recruit NSCs, inducing their neuronal differentiation, and serving as the nanocarriers at the injured site (Dual-EV). Results prove that the Dual-EV could target human umbilical vascular endothelial cells (HUVECs), recruit NSCs, and promote the neuronal differentiation of NSCs in vitro. Furthermore, 10 miRNAs are found to be upregulated in Dual-M2-EVs compared to Dual-M0-EVs via bioinformatic analysis, and further NSC differentiation experiment by flow cytometry reveals that among these miRNAs, miR30b-3p, miR-222-3p, miR-129-5p, and miR-155-5p may exert effect of inducing NSC to differentiate into neurons. In vivo experiments show that Dual-EV nanocarriers achieve improved accumulation in the ischemic area of stroke model mice, potentiate NSCs recruitment, and increase neurogenesis. This work provides new insights for the treatment of neuronal regeneration after CNS injuries as well as endogenous stem cells, and the click chemistry EV/peptide/chemokine and related nanocarriers for improving human health.