Photoluminescence and thermoluminescence characteristics of Sr3B2O6:Eu2+ yellow phosphor

Sr₃B₂O₆:Eu²⁺ yellow phosphor was prepared by the combustion method. The crystalline structure, photoluminescence and thermoluminescence properties of Sr₃B₂O₆:Eu²⁺ were investigated extensively. The X‐ray diffraction result indicates that the Sr₃B₂O₆:Eu²⁺ phosphor exhibited a rhombohedral crystal structure. The emission spectra under a 435 nm excited wavelength showed an intense broad band peaking at 574 nm, which corresponds to the 4f⁶5d¹ → 4f⁷ transition of Eu²⁺ ion. There were two different sites of Sr replaced by Eu in host lattice. The concentration quenching process between Eu²⁺ ions is determined and the corresponding concentration quenching mechanism was verified as dipole‐quadrupole interaction. The glow curve under 3 Gy β‐ ray irradiation had the glow peak at 160°C and the average activation energy was defined as about 0.98 eV. Copyright © 2015 John Wiley & Sons, Ltd.     

Kruppel-like factor 5 is an important mediator for lipopolysaccharide-induced proinflammatory response in intestinal epithelial cells

Lipopolysaccharide (LPS) is a bacterially-derived endotoxin that elicits a strong proinflammatory response in intestinal epithelial cells. It is well established that LPS activates this response through NF-κB. In addition, LPS signals through the mitogen-activated protein kinase (MAPK) pathway. We previously demonstrated that the Krüppel-like factor 5 [KLF5; also known as intestine-enriched Krüppel-like factor (IKLF)] is activated by the MAPK. In the current study, we examined whether KLF5 mediates the signaling cascade elicited by LPS. Treatment of the intestinal epithelial cell line, IEC6, with LPS resulted in a dose- and time-dependent increase in KLF5 messenger RNA (mRNA) and protein levels. Concurrently, mRNA levels of the p50 and p65 subunits of NF-κB were increased by LPS treatment. Pretreatment with the MAPK inhibitor, U0126, or the LPS antagonist, polymyxin B, resulted in an attenuation of KLF5, p50 and p65 NF-κB subunit mRNA levels from LPS treatment. Importantly, suppression of KLF5 by small interfering RNA (siRNA) resulted in a reduction in p50 and p65 subunit mRNA levels and NF-κB DNA binding activity in response to LPS. LPS treatment also led to an increase in secretion of TNF-α and IL-6 from IEC6, both of which were reduced by siRNA inhibition of KLF5. In addition, intercellular adhesion molecule-1 (ICAM-1) levels were increased in LPS-treated IEC6 cells and this increase was associated with increased adhesion of Jurkat lymphocytes to IEC6. The induction of ICAM-1 expression and T cell adhesion to IEC6 by LPS were both abrogated by siRNA inhibition of KLF5. These results indicate that KLF5 is an important mediator for the proinflammatory response elicited by LPS in intestinal epithelial cells.