Ionic Conduction at Interfaces of Solid Electrolytes and Electrodes

ナノダイナミクス国際シンポジウム 平成22年1月21日(木) 於長崎大学Nagasaki Symposium on Nano-Dynamics 2010 (NSND2010), January 21, 2010, Nagasaki University, Nagasaki, Japan, Invited Lectur

Lithium Depletion in the Solid Electrolyte Adjacent to Cathode Materials

Nanocomposites of lithium ion conductors (Li2SiO3 and Li1.3Al0.3Ti1.7(PO4)3) and electrode materials (TiO2, Li0.01TiO2 and FePO4) were prepared to investigate interfacial structure and ionic conductivity at the interface between solid electrolytes and electrode materials. It was revealed that lithium ions in the solid electrolytes were attracted to the cathode materials with increasing electrode potential, which increases lithium vacancies in solid electrolytes. For the FePO4 containing composites, due to the high electrode potential, lithium transfer across the interface and ionic conduction through the cathode materials was remarkable. The results suggest that severe lithium depletion occurs and interfacial resistance is large at the interface of high ionic conductors and cathode materials.Interfaces and Interphases in Battery Systems - PRiME 2012; Honolulu, HI; United States; 7 October 2012 ～ 12 October 201

Local Structure and Ionic Conduction at Interfaces of Electrode and Solid Electrolytes

All solid state batteries are attracting interests as next generation energy storage devices. However, little is known on interfaces between active materials and solid electrolytes, which may affect performance of the devices. In this study, interfacial phenomena between electrodes and solid electrolytes of all solid state batteries were investigated by using nano-composites of Li 2SiO 3-TiO 2, Li 2SiO 3-LiTiO 2, and Li 2SiO 3-FePO 4. Studies on ionic conductivity of these composites revealed lithium ion transfer across the interfaces without electric field, which depended on electrode potentials. For Li 2SiO 3-TiO 2, conductivity of the composites was enhanced by addition of TiO 2 and well explained by space charge layer model. With LiTiO 2 which shows lower electrode potential, the conductivity was deteriorated due to decrease in vacancies in Li 2SiO 3. At the interface of Li 2SiO 3-FePO 4, a lot of Li ions in Li 2SiO 3 are trapped at the interface or maybe are inserted into FePO 4, resulting in many vacancies in Li 2SiO 3 and lattice distortion. The results show the ionic conduction at the interface is strongly affected by the electrode potential and the importance of design of interfaces of all solid state batteries is pointed out

Mutated G-protein-coupled receptor GPR10 is responsible for the hyperphagia/dyslipidaemia/obesity locus of Dmo1 in the OLETF rat.

1. We have confirmed the Diabetes Mellitus OLETF type I (Dmo1) effect on hyperphagia, dyslipidaemia and obesity in the Otsuka Long-Evans Tokushima Fatty (OLETF) strain. The critical interval was narrowed down to 570 kb between D1Got258 to p162CA1 by segregation analyses using congenic lines. 2. Within the critical 570 kb region of the Dmo1 locus, we identified the G-protein-coupled receptor gene GPR10 as the causative gene mutated in the OLETF strain. The ATG translation initiation codon of GPR10 is changed into ATA in this strain and, so, is unavailable for the initiation of translation. 3. The GPR10 protein has a cognate ligand, namely prolactin-releasing peptide (PrRP). Centrally administered PrRP suppressed the food intake of congenic rats that have a Brown Norway derived Dmo1 region (i.e. with wild-type GPR10), but did not suppress that of the OLETF strain, indicating that GPR10 is without function and could explain hyperphagia in the OLETF strain. 4. Moreover, when restricted in food volume to the same level consumed by the congenic strain, OLETF rats showed few differences in the parameters of dyslipidaemia and obesity compared with congenic strains. 5. Taken together, these results demonstrate that the mutated GPR10 receptor is responsible for the hyperphagia leading to obesity and dyslipidaemia in the obese diabetic strain rat

TRPA1 underlies a sensing mechanism for O(2).

新たな生体内酸素センサー機構の発見. 京都大学プレスリリース. 2011-08-29.Oxygen (O(2)) is a prerequisite for cellular respiration in aerobic organisms but also elicits toxicity. To understand how animals cope with the ambivalent physiological nature of O(2), it is critical to elucidate the molecular mechanisms responsible for O(2) sensing. Here our systematic evaluation of transient receptor potential (TRP) cation channels using reactive disulfides with different redox potentials reveals the capability of TRPA1 to sense O(2). O(2) sensing is based upon disparate processes: whereas prolyl hydroxylases (PHDs) exert O(2)-dependent inhibition on TRPA1 activity in normoxia, direct O(2) action overrides the inhibition via the prominent sensitivity of TRPA1 to cysteine-mediated oxidation in hyperoxia. Unexpectedly, TRPA1 is activated through relief from the same PHD-mediated inhibition in hypoxia. In mice, disruption of the Trpa1 gene abolishes hyperoxia- and hypoxia-induced cationic currents in vagal and sensory neurons and thereby impedes enhancement of in vivo vagal discharges induced by hyperoxia and hypoxia. The results suggest a new O(2)-sensing mechanism mediated by TRPA1

A radiation hybrid map of the rat genome containing 5,255 markers

A whole-genome radiation hybrid (RH) panel was used to construct a high-resolution map of the rat genome based on microsatellite and gene markers. These include 3,019 new microsatellite markers described here for the first time and 1,714 microsatellite markers with known genetic locations, allowing comparison and integration of maps from different sources. A robust RH framework map containing 1,030 positions ordered with odds of at least 1,000:1 has been defined as a tool for mapping these markers, and for future RH mapping in the rat. More than 500 genes which have been mapped in mouse and/or human were localized with respect to the rat RH framework, allowing the construction of detailed rat-mouse and rat-human comparative maps and illustrating the power of the RH approach for comparative mapping