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A number of non‐noble catalysts are developed for hydrogen production via acidic water electrolysis. Nevertheless, for the more economical alkaline hydrogen generation, the restricted kinetics of the water dissociation Volmer step along with its following proton recombination Tafel step for these non‐noble electrocatalysts generally lead to sluggish hydrogen‐production process. Here, a facile method is designed to nest nanometric Ni5P4 clusters on NiCo2O4 (achieving Ni5P4@NiCo2O4) by a phosphating process of NiO clusters on NiCo2O4. Acting as a high‐efficiency electrode for alkaline water electrolysis, the Ni5P4@NiCo2O4 can efficiently and preferentially convert H2O to H2 with a low overpotential of 27  mV at 10 mA cm−2 and the Tafel slope of 27  mV dec−1, which are comparable to the results for platinum and superior than those of the state‐of‐the‐art platinum‐free electrocatalysts. Density functional theory calculations confirm that NiCo2O4 species exhibit a higher ability to electrolyze water into H* intermediate and then Ni5P4 clusters facilitate the subsequent desorption of the H2 products. Profiting from the promoted kinetic steps, the Ni5P4@NiCo2O4 electrocatalyst is promising for scalable alkaline hydrogen production.

To determine the impact of IL-23 knockdown by RNA interference on the development and severity of ovalbumin (OVA)-induced asthmatic inflammation, and the potential mechanisms in mice, the IL-23-specific RNAi-expressing pSRZsi-IL-23p19 plasmid was constructed and inhaled into OVA-sensitized mice before each challenge, as compared with that of control mice treated with alum or budesonide. Inhalation of the pSRZsi-IL-23p19, significantly reduced the levels of OVA-challenge induced IL-23 in the lung tissues by nearly 75%, determined by RT-PCR. In addition, knockdown of IL-23 expression dramatically reduced the numbers of eosinophils and neutrophils in BALF and mitigated inflammation in the lungs of asthmatic mice. Furthermore, knockdown of IL-23 expression significantly decreased the levels of serum IgE, IL-23, IL-17, and IL-4, but not IFNγ, and its anti-inflammatory effects were similar to or better than that of treatment with budesonide in asthmatic mice. Our data support the notion that IL-23 and associated Th17 responses contribute to the pathogenic process of bronchial asthma. Knockdown of IL-23 by RNAi effectively inhibits asthmatic inflammation, which is associated with mitigating the production of IL-17 and IL-4 in asthmatic mice.

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