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Abstract The electrocatalytic hydrogen evolution reaction (HER) is one of the most studied and promising processes for hydrogen fuel generation. Single-atom catalysts have been shown to exhibit ultra-high HER catalytic activity, but the harsh preparation conditions and the low single-atom loading hinder their practical applications. Furthermore, promoting hydrogen evolution reaction kinetics, especially in alkaline electrolytes, remains as an important challenge. Herein, Pt/C₆₀catalysts with high-loading, high-dispersion single-atomic platinum anchored on C₆₀are achieved through a room-temperature synthetic strategy. Pt/C₆₀-2 exhibits high HER catalytic performance with a low overpotential (η₁₀) of 25 mV at 10 mA cm⁻². Density functional theory calculations reveal that the Pt-C₆₀polymeric structures in Pt/C₆₀-2 favors water adsorption, and the shell-like charge redistribution around the Pt-bonding region induced by the curved surfaces of two adjacent C₆₀facilitates the desorption of hydrogen, thus favoring fast reaction kinetics for hydrogen evolution. 

Abstract Neuronal cell death and subsequent brain dysfunction are hallmarks of aging and neurodegeneration, but how the nearby healthy neurons (bystanders) respond to the death of their neighbors is not fully understood. In theDrosophilalarval neuromuscular system, bystander motor neurons can structurally and functionally compensate for the loss of their neighbors by increasing their terminal bouton number and activity. We term this compensation as cross-neuron plasticity, and in this study, we demonstrate that theDrosophilaengulfment receptor, Draper, and the associated kinase, Shark, are required for cross-neuron plasticity. Overexpression of the Draper-I isoform boosts cross-neuron plasticity, implying that the strength of plasticity correlates with Draper signaling. In addition, we find that functional cross-neuron plasticity can be induced at different developmental stages. Our work uncovers a role for Draper signaling in cross-neuron plasticity and provides insights into how healthy bystander neurons respond to the loss of their neighboring neurons.