Metal oxides are a promising material for designing highly active and selective catalysts for the electrochemical reduction of carbon dioxide (CO 2 RR). Here, we designed a Cu/ceria catalyst with high selectivity of methane production at single-atomic Cu active sites. Using this, we report favorable design concepts that push the product selectivity of methane formation by combining detailed structural analysis, density functional theory (DFT), in situ Raman spectroscopy, and electrochemical measurements. We demonstrate that a higher concentration of oxygen vacancies on the catalyst surface, resulting from more available Cu + sites, enables high selectivity for methane formation during CO 2 RR and can be controlled by the calcination temperature. The DFT calculation and in situ Raman studies indicate that pH controls the surface termination; a more alkaline pH generates hydroxylated surface motifs with more active sites for the hydrogen evolution reaction. These findings provide insights into designing an efficient metal oxide electrocatalyst by controlling the atomic structure via the reaction environment and synthesis conditions.

drawing attention as a promising technology to mitigate excess anthropogenic CO 2 emissions because it can convert carbon dioxide into high-value-added chemicals and fuels in an eco-friendly and economical way. [2] Among suitable metals, Cu (and its compounds) is the only one capable of producing high value-added C 2+ products, such as C 2 H 4 and C 2 H 5 OH, with high selectivity through CO dimerization. [3] However, the C 2+ selectivity of Cu-based electrocatalysts can be further improved by tailoring the active sites of Cu through doping, [4] tuning the catalyst particle shapes and sizes, [5] and increasing the number of low coordination sites, for example, the grain boundary density. [6] In particular, the use of mixed oxidation states (i.e., Cu + and Cu 0 ) has been suggested as an effective means to achieve high C 2+ product selectivity by lowering the energy barrier for CO dimerization. [7] However, Cu + is not stable and is easily converted to metallic Cu (Cu 0 ) at the negative applied potentials used for the CO 2 RR. As a result, many strategies have been developed to sustain the mixed oxidation state of Cu during the CO 2 RR. [8] For instance, doping Cu with B atoms can induce the formation of Cu + under CO 2 RR conditions, and increase its stability. [4a,9] Nevertheless, it is still challenging to achieve controllable Cu + coverage at the catalytically active Cu top-surface.Ceria (CeO 2 ) is a reducible metal oxide and an excellent support for metal catalysts in many catalytic processes, such as the water-gas shift reaction, [10] CO oxidation, [11] and CO 2 hydrogenation reaction. [12] As a catalyst support, CeO 2 can disperse metals at various scales uniformly, from the nanometre in scale to single atoms. [13] In addition, CeO 2 forms strong metal-support interactions (SMSIs) with the active metals, which allows the formation of a partially charged metal at the metal-CeO 2 interface. [14] These unique characteristics of CeO 2 can also promote the electrocatalytic CO 2 RR activity of metals such as Au and Cu supported on CeO 2 . In particular, Cu on ceria (Cu-CeO 2 ) shows wide tunability in CO 2 RR product selectivity, and this is dependent on the sizes and compositions of Cu-CeO 2 . For example, CeO 2 can stabilize a single-atom (SA) Cu in the Cu 2+ valence state and generate CH 4 with a faradaic efficiency (FE) of Ceria (CeO 2 ) is one of the most extensively used rare earth oxides. Recently, it has been used as a support material for metal catalysts for electrochemical energy conversion. However, to date, the nature of metal/CeO 2 interfaces and their impact on electrochemical processes remains unclear. Here, a Cu-CeO 2 nanorod electrochemical CO 2 reduction catalyst is presented. Using operando analysis and computational techniques, it is found that, on the application of a reductive electrochemical potential, Cu undergoes an abrupt change in solubility in the ceria matrix converting from less stable randomly dissolved single atomic Cu 2+ ions to (Cu 0 ,Cu 1+ ) nanoclusters. Unlike single ...

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Activation of microglia, which is the primary immune cell of the central nervous system, plays an important role in neuroinflammation associated with several neuronal diseases. Aminoacyl tRNA synthetase (ARS) complex-interacting multifunctional protein 1 (AIMP1), a structural component of the multienzyme ARS complex, is secreted to trigger a pro-inflammatory function and has been associated with several inflammatory diseases. However, the effect of AIMP1 on microglial activation remains unknown. AIMP1 elevated the expression levels of activation-related cell surface markers and pro-inflammatory cytokines in primary and BV-2 microglial cells. In addition to the AIMP1-mediated increase in the expression levels of M1 markers [interleukin (IL)-6, tumor necrosis factor-α, and IL-1β], the expression levels of CD68, an M1 cell surface molecule, were also increased in AIMP-1-treated microglial cells, while those of CD206, an M2 cell surface molecule, were not, indicating that AIMP1 triggers the polarization of microglial cells into the M1 state but not the M2 state. AIMP1 treatment induced the phosphorylation of mitogen-activated protein kinases (MAPKs), while MAPK inhibitors suppressed the AIMP1-induced microglial cell activation. AIMP1 also induced the phosphorylation of the nuclear factor-kappa B (NF-κB) components and nuclear translocation of the NF-κB p65 subunit in microglial cells. Furthermore, c-Jun N-terminal kinase (JNK) and p38 inhibitors markedly suppressed the AIMP1-induced phosphorylation of NF-κB components as well as the nuclear translocation of NF-κB p65 subunit, suggesting the involvement of JNK and p38 as upstream regulators of NF-κB in AIMP1-induced microglial cell activation. The NF-κB inhibitor suppressed the AIMP1-induced M1 polarization of the microglial cells. Taken together, AIMP1 effectively induces M1 microglial activation via the JNK and p38/NF-κB-dependent pathways. These results suggest that AIMP1 released under stress conditions may be a pathological factor that induces neuroinflammation.

BackgroundActivation of microglia, which are the primary immune cell of the central nervous system, plays an important role in neuroinflammation associated with several neuronal diseases. Aminoacyl tRNA synthetase (ARS) complex-interacting multifunctional protein 1 (AIMP1), a structural component of the multienzyme ARS complex, is secreted to trigger a pro-inflammatory function and has been associated with several inflammatory diseases. However, the effect of AIMP1 on microglial activation remains unknown.MethodsPrimary microglial cells were obtained from mixed glial cultures prepared from the cerebral cortexes of postnatal 3-5-day mice. Cultured primary microglia and BV-2 microglial cells were treated with various concentrations of AIMP1, after which the activation-related factors were determined by flow cytometric analysis and ELISA. Immunoblot analysis of major components of MAPKs and NF-κB was proceeded to investigate the underlying mechanism of microglial activation. Immunofluorescent assay of the cell-surface markers indicated the polarization of microglia.ResultsAIMP1 elevated the expression levels of activation-related cell surface markers and pro-inflammatory cytokines in primary and BV-2 microglial cells. In addition to the AIMP1-mediated increase in the expression levels of M1 markers (interleukin (IL)-6, tumor necrosis factor-α, and IL-1β), the expression levels of CD68, an M1 cell surface molecule, were also increased in AIMP-1-treated microglial cells, while those of CD206, an M2 cell surface molecule, were decreased, indicating that AIMP1 triggers the polarization of microglial cells into the M1 state but not the M2 state. AIMP1 treatment induced the phosphorylation of mitogen-activated protein kinases (MAPKs), while MAPK inhibitors suppressed the AIMP1-induced microglial cell activation. AIMP1 also induced the phosphorylation of the nuclear factor-kappa B (NF-κB) components and nuclear translocation of the NF-κB p65 subunit in microglial cells. Furthermore, c-Jun N-terminal kinase (JNK) and p38 inhibitors markedly suppressed the AIMP1-induced phosphorylation of NF-κB components as well as the nuclear translocation of NF-κB p65 subunit, suggesting the involvement of JNK and p38 as upstream regulators of NF-κB in AIMP1-induced microglial cell activation.ConclusionAIMP1 effectively induces M1 microglial activation via the JNK and p38/NF-κB-dependent pathways. These results suggest that AIMP1 secreted under stress conditions may be a pathological factor that induces neuroinflammation.