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Carbon dioxide (CO2) adsorption and electron transport play an important role in CO2 reduction reaction (CO2RR). Herein, we have demonstrated a new class of diverse hollow ZnSnOx (ZSO) through the amorphization of hydroxides to enhance CO2 adsorption and accelerate electron transport. The amorphization is occurred by calcination process, as indicated by Fourier transform infrared spectroscopy and Raman spectra. In particular, the ZnSnOx hollow spheres (ZSO HSs) achieve a high Faradaic efficiency (FE) of HCOOH up to 92.7 % at best, outperforming the commercial ZSO (Comm. ZSO, 85.7 %). ZSO HSs also exhibit durable stability with negligible activity decay after 10 h of successive electrolysis. In‐situ attenuated total reflectance infrared absorption spectroscopy further reveals strong adsorption of CO2 and rapid intermediate configuration transformation in amorphous ZSO HSs. This work demonstrates the practical application of ZSO for CO2RR and provides a new insight to create efficient CO2RR electrocatalysts. [ABSTRACT FROM AUTHOR]

Lattice strain engineering optimizes the interaction between the catalytic surface and adsorbed molecules. This is done by adjusting the electron and geometric structure of the metal site to achieve high electrochemical performance, but, to date, it has been rarely reported on anti‐poisoned oxygen reduction reaction (ORR). Herein, lattice‐strained Pd@PdBiCo quasi core‐shell metallic aerogels (MAs) were designed by "one‐pot and two‐step" method for anti‐poisoned ORR. Pd@PdBiCo MAs/C maintain their original activity (1.034 A mgPd−1) in electrolytes with CH3OH and CO at 0.85 V vs. reversible hydrogen electrode (RHE), outperforming the commercial Pd/C (0.156 A mgPd−1), Pd MAs/C (0.351 A mgPd−1), and PdBiCo MAs/C (0.227 A mgPd−1). Moreover, Pd@PdBiCo MAs/C also show high stability and anti‐poisoning with negligible activity decay after 8000 cycles in 0.1 m KOH+0.3 m CH3OH. These results of X‐ray photoelectron spectroscopy, CO stripping, and diffuses reflectance FTIR spectroscopy reveal that the tensile strain and strong interaction between different elements of Pd@PdBiCo MAs/C effectively optimize the electronic structure to promote O2 adsorption and activation, while suppressing CH3OH oxidation and CO adsorption, leading to high ORR activity and anti‐poisoning property. This work inspires the rational design of MAs in fuel cells and beyond. [ABSTRACT FROM AUTHOR]

Mutations in the type III receptor tyrosine kinase FLT3 are frequent in patients with acute myeloid leukemia (AML) and are associated with a poor prognosis. AML is characterized by the overproduction of reactive oxygen species (ROS), which can induce cysteine oxidation in redox-sensitive signaling proteins. Here, we sought to characterize the specific pathways affected by ROS in AML by assessing oncogenic signaling in primary AML samples. The oxidation or phosphorylation of signaling proteins that mediate growth and proliferation was increased in samples from patient subtypes with FLT3 mutations. These samples also showed increases in the oxidation of proteins in the ROS-producing Rac/NADPH oxidase-2 (NOX2) complex. Inhibition of NOX2 increased the apoptosis of FLT3-mutant AML cells in response to FLT3 inhibitors. NOX2 inhibition also reduced the phosphorylation and cysteine oxidation of FLT3 in patient-derived xenograft mouse models, suggesting that decreased oxidative stress reduces the oncogenic signaling of FLT3. In mice grafted with FLT3 mutant AML cells, treatment with a NOX2 inhibitor reduced the number of circulating cancer cells, and combining FLT3 and NOX2 inhibitors increased survival to a greater extent than either treatment alone. Together, these data raise the possibility that combining NOX2 and FLT3 inhibitors could improve the treatment of FLT3 mutant AML. Blocking NOX2 bolsters AML precision therapy: Internal tandem duplication of Fms-like tyrosine kinase 3 (FLT3-ITD) is a common activating mutation in acute myeloid leukemia (AML) and leads to the increased production of reactive oxygen species (ROS). AML patients on FLT3-targeting therapies have a high rate of relapse. By performing a proteome-wide analysis of cysteine oxidation and phosphorylation of AML blast cells from patients harboring FLT3 mutations, Germon et al. identified the Rac-NOX2 complex as a driver of ROS production in AML cells. Inhibition of NOX2 promoted apoptosis of AML cells carrying the FLT3-ITD mutation and increased the survival of mice grafted with FLT3-ITD AML cells and treated with FLT3 inhibitors. Thus, targeting NOX2 may increase the effectiveness of precision therapy targeting AML. —AB [ABSTRACT FROM AUTHOR]