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Herein, we successfully synthesized C@MoSe2(1-x)S2x@MWCNT nanocomposite with heterojunctions as long-term stability anodes for sodium ion batteries (SIB). According to DFT calculations, the barrier of Na+ migration between MoSe2(1-x)S2x interlayers and that between GR@MoSe2(1-x)S2x@SWWCNT interlayers is 0.48 eV and 0.45 eV, respectively, significantly lower than that between MoSe2 interlayers (0.91 eV). Therefore, the introduction of S can enhance Na+ transport. The Se element can provide a larger interlayer spacing of MoSe2(1−x)S2x than MoS2, and MWCNT with high conductivity and thermal stability can be used as effective carriers for charge transfer. As an electrode material, PEG-200-2-C@MoSe2(1-x)S2x@MWCNT showed good performance for SIB: 300 mA h g-1 (500 cycles), 256 mA h g-1 (1000 cycles), 165 mA h g-1 (3000 cycles) and 126 mA h g-1 (6000 cycles) under the current density of 10 A g-1.

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IntroductionThe aim of this study was to investigate the effect and possible mechanisms of the blood-nerve barrier (BNB) and the coagulation-anticoagulation system in modulating the mechanical allodynia in a trigeminal neuralgia (TN) rat model induced by chronic compression of the trigeminal root entry zone (TREZ).MethodsVon Frey filaments were applied to determine the orofacial mechanical allodynia threshold. The BNB permeability was evaluated by Evans blue extravasation test. Immunohistochemical staining and laser confocal microscopy were used to measure the length of the depletion zones of the nodes of Ranvier in the TREZ, the diameter of nerve fibers and the length of the nodal gap. The transcriptional levels of prothrombin and endogenous thrombin inhibitor protease nexin-1 (PN-1) in the TREZ of TN rats were assessed by RT-qPCR. A Western blotting assay was performed to detect the expression of paranodal proteins neurofascin-155 (NF155) and neurofascin-125 (NF125) in the TREZ. The spatiotemporal expression pattern of thrombin activated receptor (i.e. protease activated receptor 1, PAR1) in TREZ were defined by immunostaining and immunoblotting assays. PAR1 receptor inhibitors SCH79797 were administrated to TN rats to analyze the effect of thrombin-PAR1 on orofacial hyperalgesia.ResultsA compression injury of a rat’s TREZ successfully induced TN-like behavior and was accompanied by the destruction of the permeability of the BNB and the promotion of prothrombin and thrombin inhibitor protease nexin-1 (PN-1) expression. The expression of the paranodal proteins neurofascin-155 (NF155) and neurofascin-125 (NF125) was increased, while the nodal gap length of the nodes of Ranvier was widened and the length of node-depleted zones was shortened. Moreover, the expression of PAR1 within the TREZ was upregulated at an early stage of TN, and administration of the PAR1 antagonist SCH79797 effectively ameliorated orofacial mechanical allodynia.ConclusionA compression injury of the TREZ increased the permeability of the BNB and induced disturbances in the local coagulation-anticoagulation system, concomitant with the structural changes in the nodes of Ranvier, thrombin-PAR1 may play a critical role in modulating orofacial mechanical hyperalgesia in a TN rat model.