Electronic Structure Regulated Nickel-Cobalt Bimetal Phosphide Nanoneedles for Efficient Overall Water Splitting.

Transition metal phosphides (TMPs) have been widely studied for water decomposition for their monocatalytic property for anodic or cathodic reactions. However, their bifunctional catalytic activity still remains a major challenge. Herein, hexagonal nickel-cobalt bimetallic phosphide nanoneedles with 1-3 µm length and 15-30 nm diameter supported on NF (NixCo2-xP NDs/NF) with adjusted electron structure have been successfully prepared. The overall alkaline water electrolyzer composed of the optimal anode (Ni0.67Co1.33P NDs/NF) and cathode (Ni1.01Co0.99P NDs/NF) provide 100 mA cm-2 at 1.62 V. Gibbs Free Energy for reaction paths proves that the active site in the hydrogen evolution reaction (HER) is Ni and the oxygen evolution reaction (OER) is Co in NixCo2-xP, respectively. In the HER process, Co-doping can result in an apparent accumulation of charge around Ni active sites in favor of promoting HER activity of Ni sites, and ΔGH* of 0.19 eV is achieved. In the OER process, the abundant electron transfer around Co-active sites results in the excellent ability to adsorb and desorb *O and *OOH intermediates and an effectively reduced ∆GRDS of 0.37 eV. This research explains the regulation of electronic structure change on the active sites of bimetallic materials and provides an effective way to design a stable and effective electrocatalytic decomposition of alkaline water.

The Upregulation of TRAF1 Induced by Helicobacter pylori Plays an Antiapoptotic Effect on the Infected Cells.

BACKGROUND: Tumor necrosis factor receptor-associated factor 1 (TRAF1) is a member of the TRAF family and is dysregulated in diseases, such as atheroma, lymphoma, and solid tumors, but the role of TRAF1 in gastric cancer remains unknown. This study was aimed to investigate the role of TRAF1 in Helicobacter pylori (H. pylori)-related cell apoptosis and gastric carcinogenesis. MATERIALS AND METHODS: The mRNA and protein expression levels of TRAF1 were measured in a panel of gastric cancer cell lines and in H. pylori -infected mice by quantitative real-time PCR (qPCR) and Western blotting. The transcription factor that mainly affects transcription of TRAF1 during H. pylori infection was identified. The roles of H. pylori virulence factors that regulate TRAF1 expression were analyzed using isogenic cagA-, vacA-, and cagE-null mutants. The effects of TRAF1 on gastric cell viability and apoptosis during H. pylori infection were detected using the standard MTS (cell viability) assay and flow cytometry, respectively. RESULTS: H. pylori infection induced TRAF1 overexpression in both gastric epithelial cells and mice. The expression of TRAF1 in response to H. pylori infection was majorly regulated by the activation of NF-κB and was strongly related to H. pylori virulence factor CagA. The upregulation of TRAF1 inhibited cell apoptosis and increased the viability of infected cells. CONCLUSIONS: H. pylori infection induces the overexpression of TRAF1 in gastric epithelial cells. The upregulation of TRAF1 plays an antiapoptotic role in H. pylori -infected gastric cells and may contribute to the gastric carcinogenesis.