Numerical calculation of thermoreflectance coefficient of c-Si for wavelengths of 200-800 nm and temperatures of 300-500 K

In this paper, the thermoreflectance (TR) coefficient of c-Si is numerically calculated over the wavelength range of 200–800 nm and the temperature range of 300–500 K using a complex permittivity model that considers interband transitions and free carriers. The calculated results are in good agreement with literature values, and it is found that the temperature dependence of the TR coefficient is almost negligible at wavelengths above 500 nm. On the other hand, in the wavelength range of 200–500 nm, the TR coefficient depends strongly on the wavelength, and the temperature stability also changes significantly depending on the wavelength. This suggests that the wavelength of the probe light for TR measurement should be appropriately selected to realize high sensitivity and temperature stability, considering the constraints of the optical system and the temperature range of the sample

Novel Charge Ordering in the Trimer Iridium Oxide BaIrO3

We have prepared polycrystalline samples of the trimer Ir oxide BaIrO3 with face-shared Ir3O12 trimers, and have investigated the origin of the phase transition at 182 K by measuring resistivity, thermopower, magnetization and synchrotron x-ray diffraction. We propose a possible electronic model and transition mechanism, starting from a localized electron picture on the basis of the Rietveld refinement. Within this model, BaIrO3 can be basically regarded as a Mott insulator, when the Ir3O12 trimer is identified to one pseudo-atom or one lattice site. The transition can be viewed as a transition from the Mott insulator phase to a kind of charge ordered insulator phase.Comment: 8 pages 5 figures, Crystals (in press

Flash Controls of Proliferation and Senescence through p21

Dysregulation of the cell proliferation has been implicated in the pathophysiology of a number of diseases. Cellular senescence limits proliferation of cancer cells, preventing tumorigenesis and restricting tissue damage. However, the role of cellular senescence in proliferative nephritis has not been determined. The proliferative peak in experimental rat nephritis coincided with a peak in E2A expression in the glomeruli. Meanwhile, E12 (an E2A-encoded transcription factor) did not promote proliferation of Mesangial cells (MCs) by itself. We identified caspase-8-binding protein FLICE-associated huge protein (FLASH) as a novel E2A-binding partner by using a yeast two-hybrid screening. Knockdown of FLASH suppressed proliferation of MCs. This inhibitory effect was partially reversed by the knockdown of E2A. In addition, the knockdown of FLASH induced cyclin-dependent kinase inhibitor p21WAF1/CIP1 (p21) expression, but did not affect p53 expression. Furthermore, overexpression of E12 and E47 induced p21, but not p53 in MCs, in the absence of FLASH. We also demonstrated that E2A and p21 expression at the peak of proliferation was followed by significant induction of FLASH in mesangial areas in rat proliferative glomerulonephritis. Moreover, we revealed that FLASH negatively regulates cellular senescence via the interaction with E12. We also demonstrated that FLASH is involved in the TNF-α-induced p21 expressions. These results suggest that the functional interaction of E2A and FLASH play an important role in cell proliferation and cellular senescence via regulation of p21 expression in experimental glomerulonephritis