Porous carbons represent a typical class of electrode materials for electric double-layer capacitors. However, less attention has been focused on the study of the capacitive mechanism of electrochemically active surface oxygen groups rooted in porous carbons. Herein, the degree and variety of oxygen surface groups of HNO3-modified samples (N-CS) are finely tailored by a mild hydrothermal oxidation (0.0–3.0 mol L–1), while the micro–meso–macroporous structures are efficiently preserved from the original sample. Thus, N-CS is a suitable carrier for separately discussing the contribution of oxygen functional groups to the electrochemical property. The optimized N-CS shows a high capacitance of 279.4 F g–1 at 1 A g–1, exceeding 52.8% of pristine carbon sphere (CS) (182.8 F g–1 at 1 A g–1) in KOH electrolyte. On further deconvoluting the redox peaks of cyclic voltammetry curves, we find that the pseudocapacitance not only associates with the surface-controlled faradic reaction at high scan rate but also dramatically stems from the diffusion-controlled capacitance through potassium and hydroxyl ion insertion/deinsertion into the underutilized micropores at low scan rate. The assembled supercapacitor based on N-CS presents a stable energy density of 5 Wh kg–1 over a wide range of power density of 250–5000 W kg–1, which is higher than 0.0N-CS in KOH electrolyte. In TEABF4 electrolyte, the N-CS supercapacitor has an energy density of 26.9 Wh kg–1 at the power density of 1350 W kg–1 and exhibits excellent cycling stability with a capacitance retention of 93.2% at 2 A g–1 after 10 000 cycles. These results demonstrate that surface oxygen groups alter the capacitive mechanism and contribution of porous carbons.

Brain-derived neurotrophic factor (BDNF) plays an important role in promoting the growth, differentiation, survival and synaptic stability of neurons. Presently, the transplantation of neural stem cells (NSCs) is known to induce neural repair to some extent after injury or disease. In this study, to investigate whether NSCs genetically modified to encode the BDNF gene (BDNF/NSCs) would further enhance synaptogenesis, BDNF/NSCs or naive NSCs were directly engrafted into lesions in a rat model of traumatic brain injury (TBI). Immunohistochemistry, western blotting and RT-PCR were performed to detect synaptic proteins, BDNF-TrkB and its downstream signaling pathways, at 1, 2, 3 or 4 weeks after transplantation. Our results showed that BDNF significantly increased the expression levels of the TrkB receptor gene and the phosphorylation of the TrkB protein in the lesions. The expression levels of Ras, phosphorylated Erk1/2 and postsynaptic density protein-95 were elevated in the BDNF/NSCs-transplanted groups compared with those in the NSCs-transplanted groups throughout the experimental period. Moreover, the nuclear factor (erythroid-derived 2)-like 2/Thioredoxin (Nrf2/Trx) axis, which is a specific therapeutic target for the treatment of injury or cell death, was upregulated by BDNF overexpression. Therefore, we determined that the increased synaptic proteins level implicated in synaptogenesis might be associated with the activation of the MAPK/Erk1/2 signaling pathway and the upregulation of the antioxidant agent Trx modified by BDNF-TrkB following the BDNF/NSCs transplantation after TBI.

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