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An accelerator is an organic additive used in Cu electrodeposition, crucial for achieving superfilling during the fabrication of Cu interconnects in microelectronics. 3- N,N -dimethylaminodithiocarbamoyl-1-propanesulfonic acid (DPS) has been proposed and investigated as a substitute for SPS. However, its acceleration mechanism associated with its interaction with Cu ions has not been intensively investigated. In this study, the interaction between DPS and Cu+ was investigated using various spectroscopic analyses, including ultraviolet–visible–near-infrared absorption (UV–VIS–NIR), electron paramagnetic resonance (EPR), and nuclear magnetic resonance (NMR) spectroscopy. UV–VIS–NIR and EPR spectroscopy revealed that DPS forms a complex with Cu+, namely Cu(I)(DPS) 2. The kinetic study on the complexation of DPS with Cu+ indicated second-order reaction characteristics. The structure of the complex was suggested using 1H and 13C NMR spectroscopy. Furthermore, electrochemical analyses, including cyclic voltammetry (CV) and linear sweep voltammetry (LSV), were conducted to investigate the electrochemical behaviors of the Cu(I)(DPS) 2 complex, demonstrating its acceleration effect on Cu electrodeposition. These results will provide valuable insights for understanding the acceleration mechanism of DPS in Cu electrodeposition. [Display omitted] [ABSTRACT FROM AUTHOR]

Imbalances between excitation and inhibition in synaptic transmission and neural circuits have been implicated in autism spectrum disorders. Excitation and inhibition imbalances are frequently observed in animal models of autism spectrum disorders, and their correction normalizes key autistic-like phenotypes in these animals. These results suggest that excitation and inhibition imbalances may contribute to the development and maintenance of autism spectrum disorders and represent an important therapeutic target. [ABSTRACT FROM AUTHOR]

Abstract Background Autism spectrum disorder involves neurodevelopmental dysregulations that lead to visible symptoms at early stages of life. Many autism spectrum disorder–related mechanisms suggested by animal studies are supported by demonstrated improvement in autistic-like phenotypes in adult animals following experimental reversal of dysregulated mechanisms. However, whether such mechanisms also act at earlier stages to cause autistic-like phenotypes is unclear. Methods We used Shank2 −/− mice carrying a mutation identified in human autism spectrum disorder (exons 6 and 7 deletion) and combined electrophysiological and behavioral analyses to see whether early pathophysiology at pup stages is different from late pathophysiology at juvenile and adult stages and whether correcting early pathophysiology can normalize late pathophysiology and abnormal behaviors in juvenile and adult mice. Results Early correction of a dysregulated mechanism in young mice prevents manifestation of autistic-like social behaviors in adult mice. Shank2 −/− mice, known to display N -methyl-D-aspartate receptor (NMDAR) hypofunction and autistic-like behaviors at postweaning stages after postnatal day 21 (P21), show the opposite synaptic phenotype—NMDAR hyperfunction—at an earlier preweaning stage (∼P14). Moreover, this NMDAR hyperfunction at P14 rapidly shifts to NMDAR hypofunction after weaning (∼P24). Chronic suppression of the early NMDAR hyperfunction by the NMDAR antagonist memantine (P7–P21) prevents NMDAR hypofunction and autistic-like social behaviors from manifesting at later stages (∼P28 and P56). Conclusions Early NMDAR hyperfunction leads to late NMDAR hypofunction and autistic-like social behaviors in Shank2 −/− mice, and early correction of NMDAR dysfunction has the long-lasting effect of preventing autistic-like social behaviors from developing at later stages. [ABSTRACT FROM AUTHOR]

Abstract Closed Li O 2 batteries consisting of electrolytes derived from molten salt have emerged as attractive energy-storage cells because of their unique oxygen-supply mechanism to form a stable Li 2 O discharge product without requiring an oxygen-gas-reservoir. However, the formation of stable Li 2 O discharge product increases the overpotential during the charging process, which compromises the cell performance because of the resulting parasitic reaction. In this study, we demonstrate a potent approach to reversibly operate an oxygen-gas-reservoir-free Li O 2 battery by using chemically impregnated nickel oxide (NiO) nanoparticles as a catalyst on the carbon electrode. The efficient bottom-up process for decorating NiO on a carbon material in binary molten electrolyte enables not only to significantly reduce the loading level of the catalyst but also to enhance the electrochemical performance with preventing the detrimental parasitic reaction in the oxygen-gas-reservoir-free Li O 2 cell. In particular, using the in situ gas analysis with electrochemical measurements, the 20 wt% NiO added to the carbon cathode is sufficient to reduce the charging potential without generation of parasitic gas evolution. Highlights • Oxygen gas tank free Li O 2 battery is demonstrated by using nitrate molten salt. • Chemically impregnated nickel oxide cathode enables to reduce the over potential. • Gas analysis results suggest the reliable electrochemical reaction. [ABSTRACT FROM AUTHOR]