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Non‐oxide materials such as oxynitrides are good candidates as photoanodes for visible‐light‐driven water oxidation, but most of them suffer from oxidative degradation by photogenerated holes, resulting in low stability. Herein we developed a photoanode using a visible‐light‐responsive TiO2 powder doped with tantalum and nitrogen (TiO2:Ta/N) for water oxidation. The Ta/N codoping enabled a stable anodic photocurrent response attributable to water oxidation under visible‐light irradiation. Surface modification of the TiO2:Ta/N anode with RuOx species further facilitated water oxidation catalysis, achieving stable O2 evolution over 5 h of operation with no sign of deactivation. Operando XAFS measurements revealed an important function of the RuOx species as a collector of photogenerated holes in TiO2:Ta/N, facilitating the photoelectrochemical water oxidation. Visible‐light‐driven H2 evolution and solar‐driven CO2 reduction into CO were both achieved by using water as an electron donor in photoelectrochemical cells with the TiO2:Ta/N photoanode coupled to a Pt cathode and a Ru(II)–Re(I) binuclear complex photocathode, respectively. Jack of all trades: A photoanode composed of TiO2 doped with tantalum and nitrogen worked for stable photoelectrochemical water oxidation coupled to hydrogen evolution and carbon dioxide reduction under visible and solar light. Operando XAFS measurements revealed a key function of RuOx species as a collector of photogenerated holes in TiO2:Ta/N, facilitating the photoelectrochemical water oxidation. [ABSTRACT FROM AUTHOR]

Objective Developmental disorders including cognitive deficit, hyperkinetic disorder, and autistic behaviors are frequently comorbid in epileptic patients with SCN1 A mutations. However, the mechanisms underlying these developmental disorders are poorly understood and treatments are currently unavailable. Using a rodent model with an Scn1a mutation, we aimed to elucidate the pathophysiologic basis and potential therapeutic treatments for developmental disorders stemming from Scn1a mutations. Methods We conducted behavioral analyses on rats with the N1417 H- Scn1a mutation. With high-performance liquid chromatography, we measured dopamine and its metabolites in the frontal cortex, striatum, nucleus accumbens, and midbrain. Methylphenidate was administered intraperitoneally to examine its effects on developmental disorder-like behaviors and hyperthermia-induced seizures. Results Behavioral studies revealed that Scn1a-mutant rats had repetitive behavior, hyperactivity, anxiety-like behavior, spatial learning impairments, and motor imbalance. Dopamine levels in the striatum and nucleus accumbens in Scn1a-mutant rats were significantly lower than those in wild-type rats. In Scn1a-mutant rats, methylphenidate, by increasing dopamine levels in the synaptic cleft, improved hyperactivity, anxiety-like behavior, and spatial learning impairments. Surprisingly, methylphenidate also strongly suppressed hyperthermia-induced seizures. Significance Dysfunction of the mesolimbic dopamine reward pathway may contribute to the hyperactivity and learning impairments in Scn1a-mutant rats. Methylphenidate was effective for treating hyperactivity, learning impairments, and hyperthermia-induced seizures. We propose that methylphenidate treatment may ameliorate not only developmental disorders but also epileptic seizures in patients with SCN1 A mutations. [ABSTRACT FROM AUTHOR]

The Front Cover shows CO2 reduction and H2 production coupled to water oxidation by a photoelectrochemical system based on a Ta/N codoped rutile TiO2 anode under irradiation with sunlight. More information can be found in the Article by A. Nakada et al on page 37 in Issue 1, 2019 (DOI: 10.1002/cptc.201800157). [ABSTRACT FROM AUTHOR]