Highlights d The lncRNA Hnscr is highly expressed in htNSCs of young mice but decreases during aging d Hnscr depletion promotes the senescence of htNSCs and aging-like phenotypes d Hnscr attenuates htNSC senescence by binding to YB-1 to prevent its degradation d Theaflavin 3-gallate mimics Hnscr and ameliorates agingrelated physiological disorders

In this work, the electrochemical properties of a MnO 2 nanocomposite electrode were investigated in 1butyl-3-methyl-imidazolium hexafluorophosphate ([Bmim]PF 6 )/N,N-dimethylformamide (DMF) electrolyte. The [Bmim]PF 6 /DMF electrolyte with different volume fractions exhibits significant influence on the electrochemical properties of the electrode. When the volume ratio of [Bmim]PF 6 and DMF was 1 : 1, the electrode showed the best electrochemical performance. The operation potential window of the MnO 2 nanocomposite electrode in ionic liquids was 2.1 V and the specific capacitance according to the mass of MnO 2 was 523.3 F g À1 at 3 A g À1 . Then, a high-voltage (3 V) MnO 2 asymmetric supercapacitor was successfully fabricated, using the MnO 2 nanocomposite electrode, activated carbon and [Bmim]PF 6 /DMF as the positive electrode, negative electrode and electrolyte, respectively. The MnO 2 asymmetric supercapacitor displayed a maximum specific energy of 67.5 W h kg À1 at a specific power of 593.8 W kg À1 and a maximum specific power of 20.4 kW kg À1 at a specific energy of 8.5 W h kg À1 . The impressive results showed that [Bmim]PF 6 /DMF could be a promising electrolyte for MnO 2 supercapacitors.

Chronic stress could induce cancer metastasis by constant activation of the sympathetic nervous system, while cellular mechanism remains obscure. The aim of this research is to explore the metastasis associated negative effect of chronic stress. The analysis of transcriptome sequencing implied that activation of STAT3 signaling pathway by downregulated miR-337-3p might be a potential mechanism to induce epithelial to mesenchymal transition (EMT) of cancer cell and promote metastasis under chronic stress. We also verified this biological process in further experiments. Downregulation of miR-337-3p could downregulate E-cadherin expression and upregulate vimentin expression in vitro and in vivo. STAT3, related signal pathways of which are involved in metastasis regulation, was directly targeted by miR-337-3p. In conclusion, the above results denoted that activation of miR-337-3p/STAT3 axis might be a potential pathway for the increasing metastasis of breast cancer under chronic stress.

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