Spectral‐converting study of Ba9–3(m+n)/2ErmYbnY2Si6O24 (m = 0.005 – 0.2, n = 0 – 0.3) orthosilicate phosphors

Optical materials composed of Ba_9–3(m+n)/2Er_mYb_nY₂Si₆O₂₄ (m = 0.005–0.2, n = 0–0.3) were prepared using a solid‐state reaction. The X‐ray diffraction patterns of the obtained phosphors were examined to index the peak positions. The photoluminescence (PL) excitation and emission spectra of the Er³⁺‐activated phosphors and the critical emission quenching as a function of Er³⁺ content in the Ba_9–3m/2Er_mY₂Si₆O₂₄ structure were monitored. The spectral conversion properties of Er³⁺ and Er³⁺–Yb³⁺ ions doped in Ba₉Y₂Si₆O₂₄ phosphors were elucidated under diode‐laser irradiation at 980 nm. Up‐conversion emission spectra and the dependence of the emission intensity on pump power for the Ba_8.55Er_0.1Yb_0.2Y₂Si₆O₂₄ phosphor were investigated. The desired up‐conversion of the emitted light, which passed through the green, yellow, orange and red regions of the spectrum, was achieved through the use of appropriate Er³⁺ and/or Yb³⁺ concentrations in the host structure and 980 nm excitation light. The up‐conversion mechanism in the phosphors is described by an energy‐level schematic. Copyright © 2015 John Wiley & Sons, Ltd.     

“Inflammatory” Cytokines

If cytokines are constitutively expressed by and act on neurons in normal adult brain, then we may have to modify our current view that they are predominantly inflammatory mediators. We critically reviewed the literature to determine whether we could find experimental basis for such a modification. We focused on two "proinflammatory" cytokines, interleukin (IL)-1 and tumor necrosis factor-alpha (TNFalpha) because they have been most thoroughly investigated in shaping our current thinking. Evidence, although equivocal, indicates that the genes coding for these cytokines and their accessory proteins are expressed by neurons, in addition to glial cells, in normal brain. Their expression is region- and cell type-specific. Furthermore, bioactive cytokines have been extracted from various regions of normal brain. The cytokines' receptors selectively are present on all neural cell types, rendering them responsive to cytokine signaling. Blocking their action modifies multiple neural "housekeeping" functions. For example, blocking IL-1 or TNFalpha by several independent means alters regulation of sleep. This indicates that these cytokines likely modulate in the brain behavior of a normal organism. In addition, these cytokines are likely involved in synaptic plasticity, neural transmission, and Ca2+ signaling. Thus, the evidence strongly suggests that these cytokines perform neural functions in normal brain. We therefore propose that they should be thought of as neuromodulators in addition to inflammatory mediators.     

Tunable photoluminescence properties of Sr1‐yCayMoO4:Sm3+ phosphors (0 ≤ y < 1)

A series of Sr_1‐x‐yCa_yMoO₄:xSm³⁺ (0 ≤ x ≤ 7 mol% and 0 ≤ y < 1) phosphors was synthesized by a conventional solid‐state reaction method in air, and their structural and spectroscopic properties were investigated. The optimal doping concentration of Sm³⁺ in SrMoO₄:Sm³⁺ phosphor is 5 mol%. Under excitation with 275 nm, in Sr_1‐x‐yCa_yMoO₄:xSm³⁺ (0 ≤ x ≤ 7 mol% and 0 ≤ y < 1) phosphors, the emission band of the host was found to overlap with the excitation bands peaking at ~500 nm of Sm³⁺ ion, and the energy transfer from MoO₄^2? group to Sm³⁺ ion can also be observed. The International Commission on Illumination (CIE) chromaticity coordinates of Sr_0.95‐yCa_yMoO₄:0.05Sm³⁺ phosphors with excitation 275 nm varied systematically from an orange (0.4961, 0.3761) (y = 0) to a white color (0.33, 0.3442) (y = 0.95) with increasing calcium oxide (CaO) concentration. However, Sr_0.95‐yCa_yMoO₄:0.05Sm³⁺ phosphors with excitation at 404 nm only showed red emission and the energy transfer between MoO₄^2? group to Sm³⁺ ion was not observed. The complex mechanisms of luminescence and energy transfer are discussed by energy level diagrams of MoO₄^2? group and Sm³⁺ ion. Copyright © 2015 John Wiley & Sons, Ltd.