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AbstractNew anodic electrocatalysts with high performance and cost‐effectiveness at large current densities help advance the emerging anion exchange membrane water electrolyzer (AEMWE) technology. To this end, a ruthenium (Ru) single atoms and sulfur (S) anions dual‐doped NiFe layered double hydroxides (Ru‐S‐NiFe LDH) catalyst is reported with remarkably low alkaline oxygen evolution reaction (OER) overpotentials, high mass activities and prolonged stabilities at high current densities. Inspiringly, the AEMWE performance on Ru‐S‐NiFe LDH is also superior to the NiFe LDH. In‐depth mechanism investigations reveal that Ru single atoms not only act as the highly active sites, but also facilitate the conductivity of NiFe LDH. Meanwhile, S anions accelerate the electrochemical reconstruction of NiFe LDH to OER‐active NiFeOOH and alleviate the over‐oxidation issue on Ru active sites. Benefiting from these, Ru‐S‐NiFe LDH shows significantly enhanced OER activity and stability. Theoretical calculations further validate the decreased OER free energy difference brought about by the Ru single atoms and S anions dual‐doping. This study offers a proof‐of‐concept that the noble metal single atoms and anions dual‐doping is a feasible strategy to construct the promising 3d transition metal‐based electrocatalysts toward the practical alkaline water electrolyzer.- Book : ()
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Chondrosarcomas are common bone sarcomas frequently resistant to radiation and chemotherapy, with high recurrence rates, development of metastatic disease, and death. Fibrosarcomas are soft tissue sarcomas associated with poor outcomes. Translocase of outer mitochondrial membrane receptor 20 (TOMM20) is a mitochondrial receptor protein associated with cancer aggressiveness in many cancer subtypes, but the mechanisms remain poorly understood. Here, we studied the effects of TOMM20 overexpression and downregulation on the redox state, mitochondrial oxidative phosphorylation (OXPHOS), and tumor growth using fibrosarcoma and chondrosarcoma models. TOMM20 overexpression increased OXPHOS, NADH, and NADPH with reduced cellular reactive oxygen species (ROS). TOMM20 induced resistance to apoptosis, including with BCL‐2 and OXPHOS complex IV inhibitors, but with increased sensitivity to an OXPHOS complex I inhibitor. Also, TOMM20 induced cell growth and migration in vitro and promoted tumor growth in vivo. Conversely, knocking down TOMM20 using CRISPR‐Cas9 reduced cancer aggressiveness in vivo in both chondrosarcoma and fibrosarcoma mouse models. In conclusion, TOMM20 is a driver of cancer aggressiveness by OXPHOS, apoptosis resistance, and the maintenance of a reduced state.- Book : ()
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