Shin Tsunekawa

Blue shift in ultraviolet absorption spectra of monodisperse CeO2−x nanoparticles

Blue shifts corresponding to the absorption edge in the UV-A (310–400 nm) range are obtained from ultraviolet (UV) absorption spectra of monodisperse CeO2−x (0<x<0.5) nanoparticles, which are produced as toluene suspensions by a successive microemulsification method. The blue shift of the nanoparticles is inversely proportional to the 2.2 power of the particle size for a direct transition, but no relation is found for an indirect transition. In contrast, the shift for thin films of 100–200 nm thickness exhibits a relation nearly inverse proportional to the square root of the thickness for the direct transition. These relations are different from that for the quantum size effect, though the difference is small for the nanoparticles. A possible explanation for the blue shift is a valence change of the Ce ions.

Structural study on monosize CeO2-x nano-particles

Electron diffraction patterns are obtained for monosize ceria nano-particles produced by a size-fractionation method with surfactants. A dependency of lattice parameters estimated by the least squares method on crystalline particle sizes strongly suggests that a C-type cerium sesquioxide, which has never been reported in the bulk crystal, exists in the particle 1.5 nm in diameter. Chemical reactions responsible for the valence change of cerium ions near the surface are proposed for the existence of the sesquioxide in a strong acid sol.

Lattice relaxation of monosize CeO2−x nanocrystalline particles

Lattice constants in monosize CeO2−x nanocrystalline particles increase with decreasing particle size. This phenomenon called lattice relaxation is well explained by the model that the number of surface oxygen is reduced to half and its nominal valence is not −2 or −0.5 but −1. This suggests that all the surface oxygen form O22− species in the nanocrystallites.

Blueshifts in the ultraviolet absorption spectra of cerium oxide nanocrystallites

Blueshifts in the ultraviolet absorption spectra have been observed in cerium oxide nanocrystallites. The mechanism of the absorption is a charge-transfer optical transition. The relationships among the blueshift, valence state of cerium ions, and the particle size are formulated. The blueshifts are well explained for diameters down to less than a few nanometers by the change in the electronic band structure.

Protection of pancreatic -cells by exendin-4 may involve the reduction of endoplasmic reticulum stress; in vivo and in vitro studies

The aim of this study was to investigate the in vivo and in vitro effectsofexendin-4,apotentglucagon-likepeptide1agonist,on theprotectionofthepancreaticb-cellsagainsttheircelldeath.In in vivo experiments, we used b-cell-specific calmodulinoverexpressing mice where massive apoptosis takes place in their b-cells, and we examined the effects of chronic treatment with exendin-4. Chronic and s.c. administration of exendin-4 reduced hyperglycemia. The treatment caused significant increases of the insulin contents of the pancreas and islets, and retained the insulin-positive area. Dispersed transgenic islet cells lived only shortly, and several endoplasmic reticulum (ER) stress-related molecules such as immunoglobulin-binding protein (Bip), inositol-requiring enzyme-1 a ,X -box-binding protein-1 (XBP-1), RNA-activated protein kinase-like endoplasmic reticulum kinase, activating transcription factor-4, and C/EBP-homologous protein (CHOP) were more expressed in the transgenic islets. We also found that the spliced form of XBP-1, a marker of ER stress, was also increased in b-cellspecific calmodulin-overexpressing transgenic islets. In the quantitative real-time PCR analyses, the expression levels of Bip and CHOP were reduced in the islets from the transgenic mice treated with exendin-4. These findings suggest that excess ofERstressoccursinthetransgenicb-cells,andthesuppression of ER stress and resultant protection against cell death may be involved in the anti-diabetic effects of exendin-4.

Growth and properties of LaNbO4 and NdNbO4 single crystals

Large single crystals of LaNbO4 and NdNbO4, up to 20 mm diameter and 120 mm long, were grown by the Czochralski method. The crystals were twinned, with twinning boundaries of (102) and (201), and were ferroelastic. The crystals, characterized by chemical and X-ray analyses, were nearly stoichiometric in their compositions and had a monoclinically distorted-scheelite structure. The transition from the monoclinic to the tetragonal phase with increasing temperature was investigated by means of a thermal dilatometer and polarizing microscope; the existence of an intermediate state in the monoclinic to tetragonal phase transition is suggested.

Surface structures of cerium oxide nanocrystalline particles from the size dependence of the lattice parameters

Cerium oxide nanocrystalline particles are synthesized and monodispersed in the size range from 2 to 8nm in diameter. The dependence of the lattice parameters on particle size is obtained by x-ray and electron diffraction analyses. The size dependence well coincides with the estimation based on the assumption that the surface is composed of one layer of Ce2O3 and the inside consists of CeO2. The effect of particle size on lattice parameters is discussed from the differences in the fabrication method and the surface structure.

Specific Glucose-Induced Control of Insulin Receptor Substrate-2 Expression Is Mediated via Ca2+-Dependent Calcineurin/NFAT Signaling in Primary Pancreatic Islet β-Cells

OBJECTIVE Insulin receptor substrate-2 (IRS-2) plays an essential role in pancreatic islet β-cells by promoting growth and survival. IRS-2 turnover is rapid in primary β-cells, but its expression is highly regulated at the transcriptional level, especially by glucose. The aim was to investigate the molecular mechanism on how glucose regulates IRS-2 gene expression in β-cells. RESEARCH DESIGN AND METHODS Rat islets were exposed to inhibitors or subjected to adenoviral vector–mediated gene manipulations and then to glucose-induced IRS-2 expression analyzed by real-time PCR and immunoblotting. Transcription factor nuclear factor of activated T cells (NFAT) interaction with IRS-2 promoter was analyzed by chromatin immunoprecipitation assay and glucose-induced NFAT translocation by immunohistochemistry. RESULTS Glucose-induced IRS-2 expression occurred in pancreatic islet β-cells in vivo but not in liver. Modulating rat islet β-cell Ca2+ influx with nifedipine or depolarization demonstrated that glucose-induced IRS-2 gene expression was dependent on a rise in intracellular calcium concentration derived from extracellular sources. Calcineurin inhibitors (FK506, cyclosporin A, and a peptide calcineurin inhibitor [CAIN]) abolished glucose-induced IRS-2 mRNA and protein levels, whereas expression of a constitutively active calcineurin increased them. Specific inhibition of NFAT with the peptide inhibitor VIVIT prevented a glucose-induced IRS-2 transcription. NFATc1 translocation to the nucleus in response to glucose and association of NFATc1 to conserved NFAT binding sites in the IRS-2 promoter were demonstrated. CONCLUSIONS The mechanism behind glucose-induced transcriptional control of IRS-2 gene expression specific to the islet β-cell is mediated by the Ca2+/calcineurin/NFAT pathway. This insight into the IRS-2 regulation could provide novel therapeutic means in type 2 diabetes to maintain an adequate functional mass.

Domain Switching Behaviour of Ferroelastic LaNbO4 and NdNbO4

Ferroelastic domain switching behaviour is observed in large and high quality LaNbO 4 and NdNbO 4 single crystals grown by the Czochralski method. The domain walls which are (10\bar2) and (201) twin planes move when a small stress is applied, and return to the initial positions when the stress is removed. This back - switching behaviour is much influenced by a strain rate: the perfect back-switching is not expected by decreasing the strain rate. This behaviour may be explained by assuming a restoring force due to the restricted rotation of NbO 4 tetrahedra in the distorted Scheelite-structure.

FoxO Feedback Control of Basal IRS-2 Expression in Pancreatic β-Cells Is Distinct From That in Hepatocytes

OBJECTIVE Appropriate regulation of insulin receptor substrate 2 (IRS-2) expression in pancreatic β-cells is essential to adequately compensate for insulin resistance. In liver, basal IRS-2 expression is controlled via a temporal negative feedback of sterol regulatory element–binding protein 1 (SREBP-1) to antagonize transcription factors forkhead box class O (FoxO)1/FoxO3a at an insulin response element (IRE) on the IRS-2 promoter. The purpose of the study was to examine if a similar mechanism controlled IRS-2 expression in β-cells. RESEARCH DESIGN AND METHODS IRS-2 mRNA and protein expression, as well as IRS-2 gene promoter activity, were examined in isolated rat islets. Specific transcription factor association with the IRE on the IRS-2 promoter was examined by chromatin immunoprecipitation (ChIP) assay, and their nuclear translocation was examined by immunofluorescence. A direct in vivo effect of insulin on control of IRS-2 expression in liver and pancreatic islets was also investigated. RESULTS In IRS-2 promoter-reporter assays conducted in isolated islets, removal of the IRE decreased basal IRS-2 promoter activity in β-cells up to 80%. Activation of IRS signaling in isolated rat islets by insulin/IGF-I (used as an experimental in vitro tool) or downstream constitutive activation of protein kinase B (PKB) significantly decreased IRS-2 expression. In contrast, inhibition of phosphatidylinositol 3-kinase (PI3K) or PKB significantly increased IRS-2 levels in β-cells. ChIP assays indicated that transcription factors FoxO1 and FoxO3a associated with the IRE on the IRS-2 promoter in β-cells in a PI3K/PKB–dependent manner, whereas others, such as SREBP-1, the transcription factor binding to immunoglobulin heavy chain enhancer 3′, and the aryl hydrocarbon receptor nuclear translocator (ARNT), did not. However, only FoxO3a, not FoxO1, was capable of driving IRS-2 promoter activity via the IRE in β-cells. In vivo studies showed insulin was able to suppress IRS-2 expression via activation of SREBP-1 in the liver, but this mechanism was not apparent in pancreatic islets from the same animal. CONCLUSIONS The molecular mechanism for feedback control of IRS signaling to decrease IRS-2 expression in liver and β-cells is quite distinct, with a predominant role played by FoxO3a in β-cells.