In this work, blue-emitting CexSi6−zAlz−xnormalOz+1.5xnormalN8−z−x (0.3≤z≤2.5,0.5≤x≤2.5) phosphors were synthesized by firing powder mixtures of α-Si3normalN4 , AlN, Al2normalO3 , and CeO2 at 1950°C for 2 h under 1.0 MPa normalN2 . The resultant phosphors were characterized by phase identification, diffuse reflectance spectra, photoluminescence spectra, quantum efficiency, and temperature-dependent luminescence. The samples showed high purity at the overall range of the varied x and z values. A single broad emission band centered at about 486 nm at 410 nm excitation was observed. Moreover, the CexSi6−zAlz−xnormalOz+1.5xnormalN8−z−x phosphors showed high thermal stability, which could sustain 79–88% emission intensity measured at room temperature. These results indicate that the CexSi6−zAlz−xnormalOz+1.5xnormalN8−z−x phosphors are promising wavelength-conversion materials for white light emitting diodes (LEDs) using near-UV LED chips as the primary light source.

Glucuronidation is a well-recognized phase II metabolic pathway for a variety of chemicals including drugs and endogenous substances. Although it is usually the secondary metabolic pathway for a compound preceded by phase I hydroxylation, glucuronidation alone could serve as the dominant metabolic pathway for many compounds, including some with high aqueous solubility. Glucuronidation involves the metabolism of parent compound by UDP-glucuronosyltransferases (UGTs) into hydrophilic and negatively charged glucuronides that cannot exit the cell without the aid of efflux transporters. Therefore, elimination of parent compound via glucuronidation in a metabolic active cell is controlled by two driving forces: the formation of glucuronides by UGT enzymes and the (polarized) excretion of these glucuronides by efflux transporters located on the cell surfaces in various drug disposition organs. Contrary to the common assumption that the glucuronides reaching the systemic circulation were destined for urinary excretion, recent evidences suggest that hepatocytes are capable of highly efficient biliary clearance of the gut-generated glucuronides. Furthermore, the biliary- and enteric-eliminated glucuronides participate into recycling schemes involving intestinal microbes, which often prolong their local and systemic exposure, albeit at low systemic concentrations. Taken together, these recent research advances indicate that although UGT determines the rate and extent of glucuronide generation, the efflux and uptake transporters determine the distribution of these glucuronides into blood and then to various organs for elimination. Recycling schemes impact the apparent plasma half-life of parent compounds and their glucuronides that reach intestinal lumen, in addition to prolonging their gut and colon exposure.

A series of Eu(2+)- and Mn(2+)-codoped γ-AlON (Al1.7O2.1N0.3) phosphors was synthesized at 1800 °C under 0.5 MPa N2 by using the gas-pressure sintering method (GPS). Eu(2+) and Mn(2+) ions were proved to enter into γ-AlON host lattice by means of XRD, CL, and EDS measurements. Under 365 nm excitation, two emission peaks located at 472 and 517 nm, resulting from 4f(6)5d(1) → 4f(7) and (4)T1(4G) → (6)A1 electron transitions of Eu(2+) and Mn(2+), respectively, can be observed. Energy transfer from Eu(2+) to Mn(2+) was evidenced by directly observing appreciable overlap between the excitation spectrum of Mn(2+) and the emission spectrum of Eu(2+) as well as by the decreased decay time of Eu(2+) with increasing Mn(2+) concentration. The critical energy-transfer distance between Eu(2+) and Mn(2+) and the energy-transfer efficiency were also calculated. The mechanism of energy transfer was identified as a resonant type via a dipole-dipole mechanism. The external quantum efficiency was increased 7 times (from 7% for γ-AlON:Mn(2+) to 49% for γ-AlON:Mn(2+),Eu(2+) under 365 nm excitation), and color-tunable emissions from blue-green to green-yellow were also realized with the Eu(2+) → Mn(2+) energy transfer in γ-AlON.

Thermal degradation of the Sr2Si5N8:Eu2+ phosphor reduced by the formation of a passivation surface layer around the phosphor particle, which inhibits Eu2+ oxidation.