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Abstract In situ exploration of the dynamic structure evolution of catalysts plays a key role in revealing reaction mechanisms and designing efficient catalysts. In this work, PtCu/MgO catalysts, synthesized via the co-impregnation method, outperforms monometallic Pt/MgO and Cu/MgO. Utilizing quasi/in-situ characterization techniques, it is discovered that there is an obvious structural evolution over PtCu/MgO from Pt x Cu y O z oxide cluster to PtCu alloy with surface CuO x species under different redox and CO oxidation reaction conditions. The synergistic effect between PtCu alloy and CuO x species enables good CO oxidation activity through the regulation of CO adsorption and O2 dissociation. At low temperatures, CO oxidation is predominantly catalyzed by surface CuO x species via the Mars-van Krevelen mechanism, in which CuO x can provide abundant active oxygen species. As the reaction temperature increases, both surface CuO x species and PtCu alloy collaborate to activate gaseous oxygen, facilitating CO oxidation mainly through the Langmuir-Hinshelwood mechanism.

The effects of SAP97 mutations associated with schizophrenia on synaptic function are unclear. Here, the authors show that schizophrenia-related SAP97 mutations enhance glutamatergic synapse strength in the dentate gyrus, impairing contextual episodic memory in rats.

SFTSV is a novel phlebovirus associated with high fatality, but understanding of pathogenesis is lacking. Here the authors show defective cellular immunity, deficient antibody production and defunct humoral immunity is associated with fatal infection in human cases of infection.

Trio is a RhoGEF protein that promotes actin polymerization and is implicated in the regulation of glutamatergic synapses in autism spectrum disorder (ASD). Here the authors identify a large cluster of de novo mutations in the GEF1 domain of Trio in whole-exome sequencing data from individuals with ASD, and confirm that some of these mutations lead to glutamatergic dysregulation in vitro.

Although molecular vibronic spectra generation is pivotal for chemical analysis, tackling such exponentially complex tasks on classical computers remains inefficient. Quantum simulation, though theoretically promising, faces technological challenges in experimentally extracting vibronic spectra for molecules with multiple modes. Here, we propose a nontrivial algorithm to generate the vibronic spectra using states with zero displacements (squeezed vacuum states) coupled to a linear optical network, offering ease of experimental implementation. We also fabricate an integrated quantum photonic microprocessor chip as a versatile simulation platform containing 16 modes of single-mode squeezed vacuum states and a fully programmable interferometer network. Molecular vibronic spectra of formic acid and thymine under the Condon approximation are simulated using the quantum microprocessor chip with high reconstructed fidelity (> 92%). Furthermore, vibronic spectra of naphthalene, phenanthrene, and benzene under the non-Condon approximation are also experimentally simulated. Such demonstrations could pave the way for solving complicated quantum chemistry problems involving vibronic spectra and computational tasks beyond the reach of classical computers. Proof-of-principle photonic quantum simulations of molecular vibronic spectra have been realised, but scalability to more complex systems is hindered by the difficulties in generating squeezed coherent states with multiple modes. Here, the authors demonstrate an alternative approach relying on vacuum-squeezed state. [ABSTRACT FROM AUTHOR]

The Rho guanine nucleotide exchange factor (RhoGEF) Trio promotes actin polymerization by directly activating the small GTPase Rac1. Recent studies suggest that autism spectrum disorder (ASD)-related behavioral phenotypes in animal models of ASD can be produced by dysregulation of Rac1's control of actin polymerization at glutamatergic synapses. Here, in humans, we discover a large cluster of ASD-related de novo mutations in Trio's Rac1 activating domain, GEF1. Our study reveals that these mutations produce either hypofunctional or hyperfunctional forms of Trio in rodent neurons in vitro. In accordance with pathological increases or decreases in glutamatergic neurotransmission observed in animal models of ASD, we find that these mutations result in either reduced synaptic AMPA receptor expression or enhanced glutamatergic synaptogenesis. Together, our findings implicate both excessive and reduced Trio activity and the resulting synaptic dysfunction in ASD-related pathogenesis, and point to the Trio-Rac1 pathway at glutamatergic synapses as a possible key point of convergence of many ASD-related genes. [ABSTRACT FROM AUTHOR]

This corrects the article DOI: 10.1038/ncomms15544 [ABSTRACT FROM AUTHOR]