Sabatier principle of metal-support interaction for design of ultrastable metal nanocatalysts.

The stability of supported nanocatalysts is crucial to meeting environmental and energy challenges and necessitates fundamental theory to relieve trial-and-error experimentation and accelerate lab-to-fab translation. Here, we report a Sabatier principle of metal-support interaction for stabilizing metal nanocatalysts against sintering based on the kinetic simulations of 323 metal-support pairs using scaling relations from 1252 energetics data. Too strong of an interaction is shown to trigger Ostwald ripening, whereas too weak of an interaction stimulates particle migration and coalescence. High-throughput screening of supports enables the sintering resistance of nanocatalysts to reach the Tammann temperature on homogeneous supports and far beyond it on heteroenergetic supports. This theory, which is substantiated by first-principles neural network molecular dynamics simulations and experiments, paves the way for the design of ultrastable nanocatalysts.

Quantification of critical particle distance for mitigating catalyst sintering.

Supported metal nanoparticles are of universal importance in many industrial catalytic processes. Unfortunately, deactivation of supported metal catalysts via thermally induced sintering is a major concern especially for high-temperature reactions. Here, we demonstrate that the particle distance as an inherent parameter plays a pivotal role in catalyst sintering. We employ carbon black supported platinum for the model study, in which the particle distance is well controlled by changing platinum loading and carbon black supports with varied surface areas. Accordingly, we quantify a critical particle distance of platinum nanoparticles on carbon supports, over which the sintering can be mitigated greatly up to 900 °C. Based on in-situ aberration-corrected high-angle annular dark-field scanning transmission electron and theoretical studies, we find that enlarging particle distance to over the critical distance suppress the particle coalescence, and the critical particle distance itself depends sensitively on the strength of metal-support interactions.

ZIF-L membrane with a membrane-interlocked-support composite architecture for H2/CO2 separation.

Metal-organic framework (MOF) membranes hold great promise in energy-efficient chemical separations. The outstanding challenges of the microstructural design stem from (1) thinning of membranes to immensely reduce the mass-transfer resistance (for high permeances); (2) tuning of orientation to optimize the selective transport of gas molecules, and (3) reinforcement of intercrystalline structure to subside leakage through defective gaps (for high selectivity). Here, we propose the ZIF-L membrane that is completely confined into the voids of the alumina support through an interfacial assembly process, producing an appealing membrane-interlocked-support (MIS) composite architecture that meets the requirements of the microstructural design of MOF membranes. Consequently, the membranes show average H2 permeances of above 4000 GPU and H2/CO2 separation factor (SF) of above 200, representing record-high separation performances of ZIF-L membranes and falling into the industrial target zone (H2 permeance > 1000 GPU and H2/CO2 SF > 60). Furthermore, the ZIF-L membrane possessing the MIS composite architecture that is established with alumina particles as scaffolds shows mechanical stability, scraped repeatedly by a piece of silicon rubber causing no selectivity loss.

First-principles investigation of electrochemical dissolution of Pt nanoparticles and kinetic simulation.

Dissolution is the primary route of Pt nanoparticle degradation in electrochemical devices, e.g., fuel cells. Investigation of potential-dependent dissolution kinetics of Pt nanoparticles is crucial to optimize the nanoparticle size and operating conditions for better performance. A mean-field kinetic theory under the steady-state approximation, combined with atomistic thermodynamics and Wulff construction, was developed to study the interplay between oxygen chemisorption, electrode potential, and particle size on the dissolution of Pt nanoparticles. We found that although oxygen chemisorption from electrode potential-induced water splitting can stabilize Pt nanoparticles through decreasing the surface energy and increasing the redox potential, the electrode potential plays a more decisive role in facilitating the dissolution of Pt nanoparticles. In comparison with the minor effect of oxygen chemisorption, an increase in the particle size, though reducing the dispersion, has a more significant effect on the suppression of the dissolution. These theoretical understandings on the effects of electrode potential and particle size on the dissolution are crucial for optimizing the nanoparticle size under oxidative operating conditions.

Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax.

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro-survival and anti-apoptotic roles through molecule phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p-ERK1/2 and pro-apoptotic molecule Bax. In this study, the rat-derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the cardiomyocytes. Then, contrary experiments were conducted using C3G overexpression. The cell proliferation and apoptosis were analyzed in the cardiomyocytes which were treated with or without hypoxia/reoxygenation (H/R). Silencing of C3G leaded to significant increase in cell survival inhibition and apoptosis, combined with aggravated the injuries induced by H/R. Overexpression of C3G reduced the injuries induced by the silencing of C3G in the cardiomyocytes via regulation of p-ERK1/2 and Bax. In conclusion, our results provide new experimental evidence that silencing of C3G can increase cell survival inhibition and apoptosis in cardiomyocytes via regulation of p-ERK1/2 and Bax.