Sulfur vacancy regulation and multipolarization of NixCo1S nanowires-decorated biotemplated structures to promote microwave absorption.

It is a novel and practical method to use natural porous biomaterials as microwave absorber. In this study, NixCo1S nanowires (NWs)@diatomite (De) composites with one-dimensional (1D)-NWs and three-dimensional(3D)-De composites were prepared by a two-step hydrothermal method using De as template. The effective absorption bandwidth (EAB) of the composite reaches 6.16 GHz at 1.6 mm and 7.04 GHz at 4.1 mm, covering the entire Ku band, and the minimum reflection loss (RLmin) is less than -30 dB. The excellent absorption performance is mainly due to the bulk charge modulation provided by the 1D NWs and the extended microwave transmission path within the absorber, coupled with the high dielectric loss and magnetic loss of the metal-NWS after vulcanization. We present a high-value method that combines vulcanized 1D materials with abundant De to achieve the lightweight broadband efficient microwave absorption at the first time.

Diatomite-like KFeS2 for Use in High-Performance Electrodes for Energy Storage and Oxygen Evolution.

Bifunctional materials possess remarkable properties that allow them to store and convert electrical energy easily. In this paper, diatomite-like potassium iron disulfide (KFeS2) was synthesized by a multistep sacrificial template method, and its morphological, electrochemical, and oxygen evolution reaction (OER) properties were investigated. KFeS2 was found to be porous, hollow, and cake-like, which suggests a high specific surface area (SSA) and abundant electrochemically active sites. A very high specific capacitance of 651 F g-1 at 1.0 A g-1 was also obtained due to the substance's unique structure and high porosity. Additionally, the diatomite-like KFeS2 possessed a very low overpotential ƞ10 of 254 mV at a current density of 10 mA cm-2 and a small Tafel slope of about 48.4 mV dec-1. Thus, the diatomite-like KFeS2 demonstrates broad application prospects for both energy storage and conversion.

Melatonin promotes Schwann cell proliferation and migration via the shh signalling pathway after peripheral nerve injury.

Peripheral nerve injury (PNI) is a common and incurable disease in the clinic, but the effects of available treatments are still not satisfactory. Therefore, it is necessary to explore new treatment methods. To explore the effect and mechanism of melatonin in peripheral nerve regeneration, we administered melatonin to mice with PNI by intraperitoneal injection. We applied microarray analysis to detect differentially expressed genes of mice with sciatic nerve injury after melatonin application. Then, we conducted gene ontology and protein-protein interactions to screen out the key genes related to peripheral nerve regeneration. Cell biology and molecular biology experiments were performed in Schwann cells in vitro to verify the key genes identified by microarray analysis. Our results showed that a total of 598 differentially expressed genes were detected after melatonin subcutaneously injecting into mice with sciatic nerve injury. Bioinformatics analysis showed that Shh may be the key gene for the promotion of peripheral nerve regeneration by melatonin. In vitro, the proliferation and migration abilities of schwann cells in the melatonin group were significantly higher than those of Schwann cells in the control group; while after treating with both melatonin and luzindole (a Shh signalling pathway inhibitor), the proliferation and migration abilities of Schwann cells decreased compared with the melatonin group. Our study suggests that melatonin might improve the proliferation and migration of Schwann cells via the Shh signalling pathway after PNI, thus promoting peripheral nerve regeneration. Our study provides a new approach and target for the clinical treatment of PNI.

Exendin-4 Promotes Schwann Cell Proliferation and Migration via Activating the Jak-STAT Pathway after Peripheral Nerve Injury.

Peripheral nerve injury (PNI) is a common clinical disease that causes the partial loss of segmental exercise and sensory and autonomic nervous function, placing a heavy burden on patients and their families. A previous study confirmed that exendin-4 can effectively improve nerve regeneration and functional recovery after PNI. However, the specific mechanisms by which exendin-4-mediates this repair have not been clarified. To explore the mechanism of exendin-4 in the treatment of PNI, we used microarray analysis to detect gene expression in the distal segment of the sciatic nerve after sciatic injury. Bioinformatics analyses were used to predict the roles of differentially expressed genes (DEGs) in nerve damage repair. Schwann cells (SCs) were cultured, and we verified the molecular mechanism of exendin-4 in SCs and the effect of exendin-4 on peripheral nerve regeneration through in vitro molecular biology and cell biology experiments. In vivo, exendin-4 could significantly promote peripheral nerve regeneration. A total of 180 DEGs between the exendin-4 group and the control group were detected. Bioinformatics analysis indicated that these DEGs were mainly enriched in the Jak-STAT signaling pathway. In vitro, exendin-4 could significantly promote the proliferation and migration of SCs by activating the Jak-STAT pathway, which promoted peripheral nerve regeneration. Our results indicate that exendin-4 promotes SC proliferation, migration and nerve regeneration after PNI by activating the Jak-STAT pathway. Our findings provide a basis and direction for further elucidation of the mechanisms of exendin-4 in the repair of PNI and provide a new way to treat PNI.