154 research outputs found
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
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