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, NiCoS 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.

Diatomite-like KFeS 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 (KFeS) was synthesized by a multistep sacrificial template method, and its morphological, electrochemical, and oxygen evolution reaction (OER) properties were investigated. KFeS was found to be porous, hollow, and cake-like, which suggests a high specific surface area (SSA) and abundant electrochemically active sites.

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.

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.