N-doped 3D carbon encapsulating nickel selenide nanoarchitecture with cation defect engineering: An ultrafast and long-life anode for sodium-ion batteries.

Transition metal chalcogenides (TMCs) hold great potential for sodium-ion batteries (SIBs) owing to their multielectron conversion reactions, yet face challenges of poor intrinsic conductivity, sluggish diffusion kinetics, severe phase transitions, and structural collapse during cycling. Herein, a self-templating strategy is proposed for the synthesis of a class of metal cobalt-doped NiSe nanoparticles confined within three-dimensional (3D) N-doped macroporous carbon matrix nanohybrids (Co-NiSe/NMC). The cation defect engineering within the developed Co-NiSe and 3D N-doped carbon plays a crucial role in enhancing intrinsic conductivity, reinforcing structural stability, and reducing the barrier to sodium ion diffusion, which are verified by a series of electrochemical kinetic analyses and density functional theory calculations. Significantly, such cation defect engineering not only reduces overpotential but also accelerates conversion reaction kinetics, ensuring both exceptional high-rate capability and extended durability. Consequently, the optimally engineered Co-NiSe/NMC demonstrates a remarkable rate performance, delivering 390 mAh g-1 at 10 A g-1. Moreover, it exhibits an unprecedented lifespan, maintaining a remarkable capacity of 403 mAh g-1 after 1400 cycles and 318 mAh g-1 after 4000 cycles, even at high rates of 1.0 and 2.0 A g-1, respectively. This work marks a substantial advancement in achieving both high performance and prolonged cycle life in sodium-ion batteries.

Glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor regulate the interaction between astrocytes and Schwann cells at the trigeminal root entry zone.

The trigeminal root entry zone is the zone at which the myelination switches from peripheral Schwann cells to central oligodendrocytes. Its special anatomical and physiological structure renders it susceptible to nerve injury. The etiology of most primary trigeminal neuralgia is closely related to microvascular compression of the trigeminal root entry zone. This study aimed to develop an efficient in vitro model mimicking the glial environment of trigeminal root entry zone as a tool to investigate the effects of glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor on the structural and functional integrity of trigeminal root entry zone and modulation of cellular interactions. Primary astrocytes and Schwann cells isolated from trigeminal root entry zone of postnatal rats were inoculated into a two-well silicon culture insert to mimic the trigeminal root entry zone microenvironment and treated with glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor. In monoculture, glial cell line-derived neurotrophic factor promoted the migration of Schwann cells, but it did not have effects on the migration of astrocytes. In the co-culture system, glial cell line-derived neurotrophic factor promoted the bidirectional migration of astrocytes and Schwann cells. Brain-derived neurotrophic factor markedly promoted the activation and migration of astrocytes. However, in the co-culture system, brain-derived neurotrophic factor inhibited the migration of astrocytes and Schwann cells to a certain degree. These findings suggest that glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor are involved in the regulation of the astrocyte-Schwann cell interaction in the co-culture system derived from the trigeminal root entry zone. This system can be used as a cell model to study the mechanism of glial dysregulation associated with trigeminal nerve injury and possible therapeutic interventions.