Visualization of TiO2 Reduction Behavior in Molten Salt Electrolysis

An in situ observation technique of the TiO2 interfacial behavior in molten LiCl-KCl electrolysis was developed. The variation of the thin TiO2 electrode surface were tracked through the high-speed digital microscopy synchronized with the electrochemical measurement. Two characteristic interfacial behaviors were discovered: physical breakage of the titanium oxide and Li(l) spreading on electrode surface. These electrochemically induced interfacial behaviors affect the current-time curves due to the heterogeneity of the titanium oxide film shape

Pharmacological nNOS inhibition modified small-conductance Ca2+-activated K plus channel without altering Ca2+dynamics

Atrial fibrillation (AF) is associated with electrical remodeling processes that promote a substrate for the maintenance of AF. Although the small-conductance Ca2+-activated K+ (SK) channel is a key factor in atrial electrical remodeling, the mechanism of its activation remains unclear. Regional nitric oxide (NO) production by neuronal nitric oxide synthase (nNOS) is involved in atrial electrical remodel-ing. In this study, atrial tachyarrhythmia (ATA) induction and optical mapping were performed on perfused rat hearts. nNOS is pharma-cologically inhibited by S-methylthiocitrulline (SMTC). The influence of the SK channel was examined using a specific channel inhibitor, apamin (APA). Parameters such as action potential duration (APD), conduction velocity, and calcium transient (CaT) were evaluated using voltage and calcium optical mapping. The dominant frequency was examined in the analysis of AF dynamics. SMTC (100 nM) increased the inducibility of ATA and apamin (100 nM) mitigated nNOS inhibition-induced arrhythmogenicity. SMTC caused abbrevia-tions and enhanced the spatial dispersion of APD, which was reversed by apamin. By contrast, conduction velocity and other parame-ters associated with CaT were not affected by SMTC or apamin administration. Apamin reduced the frequency of SMTC-induced ATA. In summary, nNOS inhibition abbreviates APD by modifying the SK channels. A specific SK channel blocker, apamin, mitigated APD abbreviation without alteration of CaT, implying an underlying mechanism of posttranslational modification of SK channels. NEW & NOTEWORTHY We demonstrated that pharmacological nNOS inhibition increased the atrial arrhythmia inducibility and a specific small-conductance Ca2 +-activated K+ channel blocker, apamin, reversed the enhanced atrial arrhythmia inducibility. Apamin mitigated APD abbreviation without alteration of Ca2+ transient, implying an underlying mechanism of posttranslational modification of SK channels

Solubility of gaseous carbon dioxide in molten LiCl-Li2O

Carbonate ions in LiCl-Li2O salt are a source of carbon contamination in the electrolytic refining of metal oxides, and their concentration is also an essential information for understanding the CO2 decomposition process. In this study, the solubility of gaseous CO2 in molten LiCl-Li2O was studied with the goal of developing processes to decompose the oxides effectively. Ar-CO2 gas mixtures were dissolved in molten salts containing various amounts of Li2O, and the solubility of the CO2 gas was calculated by measuring the mass difference between the molten salts before and after the CO2 dissolution. The molar amount of dissolved CO2 gas was almost as large as the molar quantity of Li2O when the partial pressure of CO2 was 1.0 or 0.5 atm for Li2O concentrations in the range of 0-60 mol%. This confirms that a large quantity of the oxide ions reacted with the CO2 gas, resulting in the generation of carbonate ions

Pharmacological nNOS inhibition modified small-conductance Ca2+-activated K plus channel without altering Ca2+dynamics

Atrial fibrillation (AF) is associated with electrical remodeling processes that promote a substrate for the maintenance of AF. Although the small-conductance Ca2+-activated K+ (SK) channel is a key factor in atrial electrical remodeling, the mechanism of its activation remains unclear. Regional nitric oxide (NO) production by neuronal nitric oxide synthase (nNOS) is involved in atrial electrical remodel-ing. In this study, atrial tachyarrhythmia (ATA) induction and optical mapping were performed on perfused rat hearts. nNOS is pharma-cologically inhibited by S-methylthiocitrulline (SMTC). The influence of the SK channel was examined using a specific channel inhibitor, apamin (APA). Parameters such as action potential duration (APD), conduction velocity, and calcium transient (CaT) were evaluated using voltage and calcium optical mapping. The dominant frequency was examined in the analysis of AF dynamics. SMTC (100 nM) increased the inducibility of ATA and apamin (100 nM) mitigated nNOS inhibition-induced arrhythmogenicity. SMTC caused abbrevia-tions and enhanced the spatial dispersion of APD, which was reversed by apamin. By contrast, conduction velocity and other parame-ters associated with CaT were not affected by SMTC or apamin administration. Apamin reduced the frequency of SMTC-induced ATA. In summary, nNOS inhibition abbreviates APD by modifying the SK channels. A specific SK channel blocker, apamin, mitigated APD abbreviation without alteration of CaT, implying an underlying mechanism of posttranslational modification of SK channels. NEW & NOTEWORTHY We demonstrated that pharmacological nNOS inhibition increased the atrial arrhythmia inducibility and a specific small-conductance Ca2 +-activated K+ channel blocker, apamin, reversed the enhanced atrial arrhythmia inducibility. Apamin mitigated APD abbreviation without alteration of Ca2+ transient, implying an underlying mechanism of posttranslational modification of SK channels

Optogenetic termination of atrial tachyarrhythmias by brief pulsed light stimulation

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