Initialising ...
Initialising ...
Initialising ...
Initialising ...
Initialising ...
Initialising ...
Initialising ...
Yoshimoto, Masataka*; Tamura, Kazuhisa; Watanabe, Kenta*; Shimizu, Keisuke*; Horisawa, Yuhei*; Kobayashi, Takeshi*; Tsurita, Hanae*; Suzuki, Kota*; Kanno, Ryoji*; Hirayama, Masaaki*
Sustainable Energy & Fuels (Internet), 8(6), p.1236 - 1244, 2024/03
Times Cited Count：0Photo-rechargeable systems, which can efficiently convert and store solar energy into chemical energy within single devices, are essential to harness sunlight effectively. Photo-(de)intercalation plays a pivotal role in the functionality of photorechargeable systems. Nevertheless, the photo-(de)intercalation process has not been conclusively confirmed owing to potential interference from side reactions, such as the decomposition of liquid electrolytes and the elution of electrode materials. In this study, we successfully demonstrated photo-responsive Li
-deintercalation using an all-solid-state thin-film battery comprised of epitaxially-grown anatase TiO
doped with Nb (a-TiO:Nb) as the cathode. Under light irradiation, Li-deintercalation occurred and was subsequently reversibly intercalated into a-TiO:Nb during discharge.
Watanabe, Kenta*; Horisawa, Yuhei*; Yoshimoto, Masataka*; Tamura, Kazuhisa; Suzuki, Kota*; Kanno, Ryoji*; Hirayama, Masaaki*
Nano Letters, 24(6), p.1916 - 1922, 2024/02
Times Cited Count：1 Percentile：0.02(Chemistry, Multidisciplinary)Electrochemistry has extended from reactions at solid/liquid interfaces to those at solid/solid interfaces. In this study, we achieve the stable photoelectrochemical reaction at the semiconductor-electrode/solid-electrolyte interface in Nb-doped anatase-TiO (a-TiO:Nb)/Li
PO
(LPO)/Li all-solid-state cell. The oxidative currents of a-TiO:Nb/LPO/Li increase upon light irradiation when a-TiO:Nb is located at a potential that is more positive than its flat-band potential. The photoelectrochemical reaction at the semiconductor/solid-electrolyte interface is driven by the same principle as that at semiconductor/liquid-electrolyte interfaces. Thus, we extend photoelectrochemistry to all-solid-state systems composed of solid/solid interfaces.
Kataoka, Takahiro*; Nishiyama, Yuichi*; Toyota, Teruaki*; Yoshimoto, Masaaki*; Sakoda, Akihiro; Ishimori, Yuu; Aoyama, Yutaka*; Taguchi, Takehito*; Yamaoka, Kiyonori*
Inflammation, 34(6), p.559 - 567, 2011/12
Times Cited Count：22 Percentile：49.49(Cell Biology)We assessed whether radon inhalation provided protection from carbon tetrachloride induced hepatic and renal damage in mice. Mice were subjected to intraperitoneal injection of CCl after inhaling approximately 18 kBq/m
radon for 6 h. Radon inhalation significantly increased total glutathione content and glutathione peroxidase activity in the liver and kidney. Injection of CCl was associated with significantly higher levels of glutamic oxaloacetic transaminase and alkaline phosphatase activity and creatinine level in serum, and pretreatment with radon significantly decreased the GOT and ALP activity and creatinine level associated with CCl injection, suggesting that radon inhalation alleviates CCl-induced hepatic and renal damage. The t-GSH contents an GPx activity in the liver and kidney of animals pretreated with radon were significantly higher than those of the CCl-only group. These findings suggested that radon inhalation activated antioxidative functions and inhibited CCl-induced hepatic and renal damage in mice.
Kataoka, Takahiro*; Sakoda, Akihiro*; Yoshimoto, Masaaki*; Toyota, Teruaki*; Yamamoto, Yuki*; Ishimori, Yuu; Hanamoto, Katsumi*; Kawabe, Atsushi*; Mitsunobu, Fumihiro*; Yamaoka, Kiyonori*
Radiation Safety Management, 10(1), p.1 - 7, 2011/12
We examined the effect of continuous radon inhalation on acute alcohol-induced oxidative damage of mouse liver and brain. Assay of antioxidative functions indicated that lipid peroxide levels in both the liver and brain of the alcohol-treated mice were significantly higher than those of the saline-treated mice. However, the lipid peroxide level in the liver, but not in the brain, of alcohol-treated mice was significantly decreased by radon inhalation whereas that in the brain of saline-treated mice, but not in the liver of saline-treated mice, was significantly increased by radon inhalation. These findings suggest that radon inhalation inhibits alcohol-induced oxidative damage of liver due to activation of antioxidative functions and that radon inhalation exert only a week effect on the brains in comparing with the livers. They further suggest that alcohol administration protects against oxidative damage of the brain that is induced by radon inhalation.
Kataoka, Takahiro*; Sakoda, Akihiro*; Yoshimoto, Masaaki*; Nakagawa, Shinya*; Toyota, Teruaki*; Nishiyama, Yuichi*; Yamato, Keiko*; Ishimori, Yuu; Kawabe, Atsushi*; Hanamoto, Katsumi*; et al.
Radiation Protection Dosimetry, 146(1-3), p.360 - 363, 2011/07
Times Cited Count：6 Percentile：44.28(Environmental Sciences)Our previous studies showed the possibility that activation of the antioxidative function alleviates various oxidative damages, which are related to lifestyle diseases. Results showed that, low-dose X-ray irradiation activated superoxide dismutase and inhibits oedema following ischaemia-reperfusion. To alleviate ischaemia-reperfusion injury with transplantation, the changes of the antioxidative function in liver graft using low-dose X-ray irradiation immediately after exenteration were examined. Results showed that liver grafts activate the antioxidative function as a result of irradiation. In addition, radon inhalation enhances the antioxidative function in some organs, and alleviates alcohol-induced oxidative damage of mouse liver. Moreover, in order to determine the most effective condition of radon inhalation, mice inhaled radon before or after carbon tetrachloride (CCl) administration. Results showed that radon inhalation alleviates CCl-induced hepatopathy, especially prior inhalation. It is highly possible that adequate activation of antioxidative functions induced by low-dose irradiation can contribute to preventing or reducing oxidative damages, which are related to lifestyle diseases.
