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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]

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]

Histamine H1 receptor (H1R) levels vary under various pathological conditions, and these changes may be responsible for some pathogenesis such as in allergic rhinitis. Several stimulants, including histamine, muscarinic agonists and platelet-activating factor, have now been shown to regulate H1R levels and may have roles in regulating the H1R level in physiological and pathological conditions. Results for beta2-adrenoceptor (beta2AR) stimulation are conflicting, however.beta2AR up-regulated H1R in bovine tracheal smooth muscle, but down-regulated human H1R expressed in Chinese hamster ovary (CHO) cells. It is possible that this discrepancy comes from the differences in the preparations used for each study: the former cell expressed bovine H1R and the latter cell expressed human H1R. Moreover, CHO cells have been shown to be inadequate for studying the effects on H1R gene expression, because the cells express non-endogenous stably transfected H1R under the control of the SV40 promoter. Therefore, in this study, we have investigated the role of beta2AR stimulation in H1R gene regulation using human U373 astrocytoma cells that express endogenous H1R and transfected beta2AR. Stimulation of beta2AR significantly reduced H1R promoter activity and H1R mRNA levels. H1R mRNA stability was slightly reduced by beta2AR stimulation, although this was not significant. The decrease of H1R mRNA by beta2AR stimulation was blocked by the protein kinase A (PKA) inhibitor KT5720, suggesting the involvement of PKA. These results indicate that the beta2AR is involved in the down-regulation of human H1R by inhibiting H1R gene transcription through a PKA-dependent process.

To clarify heterologous regulation of a receptor is important in considering medication. Histamine constricts the airway smooth muscle through the action to the H(1) receptor (H1R), which contributes to asthma. beta(2)-Adrenergic receptor (beta2R) agonists are widely used in asthmatic therapy for their bronchodilating effects. In this study, we investigated the effect of beta2R activation on the H1R function using Chinese hamster ovary cells stably co-expressing human histamine H1R and beta2R (CHO-H1/beta2 cell). The stimulation of beta2R resulted in the decrease of H1R in the membrane. Heterologous H1R down-regulation was significantly reversed in the presence of the cyclic AMP-dependent protein kinase (PKA) inhibitor KT5720. Since phosphorylation of G protein-coupled receptor (GPCR) by second messenger-dependent kinases, is proposed to be a key step initiating heterologous receptor desensitization, we examined whether heterologous H1R down-regulation was accompanied by H1R phosphorylation. H1R was phosphorylated by beta2R stimulation; however, a PKA inhibitor did not inhibit heterologous H1R phosphorylation. Our results suggest that H1R was heterologously regulated by beta2R. Not only a direct action of beta2R agonist to beta2R causing bronchodilation but also indirect action that reduces the number of H1R responsible for bronchoconstriction might contribute to a decrease in the bronchial resistance, which proposes another possible advantage of beta2R agonists for asthmatic medication.