A non-rare-earth doped Mn4+:Y3Al5O12red phosphor and the related glass–ceramics were fabricated to explore their application in white light-emitting diodes.

In the past few decades, efficient photon upconversion (anti-Stokes) luminescence has been extensively studied and is almost exclusively restricted to lanthanide (Ln3+) doped fluorophores.

In this paper, we present the synthesis of S- and N-heterocyclic annelated di(perylene bisimide) with extraordinary doubly bowl-shaped structures. The structures of fused PBI bowls confirmed by single-crystal X-ray structure analysis and temperature-dependent (1)H NMR are realized by the introduction of the steric congestion in nonbay regions and by the concurrent formation of the five-membered heterorings strain in bay regions. On the basis of the geometry obtained from the X-ray analysis, the maximum POAV1 pyramidalization angle is found in N-heterocyclic annelated diPBI 7, as large as 4.7 degrees , indicating the formation of two PBI bowls with significant curvatures. Furthermore, to assist the electrochemical and spectroscopic characterization of the two bowl-shaped derivatives and to assess the influence of heteroatoms on the bowl curvature, quantum-chemically optimized atomic structures, electronic properties, and optical signatures were computed with density functional theory.

Enterococcus faecalis is a leading causative agent of catheter-associated urinary tract infection (CAUTI), the most common hospital-acquired infection. Its ability to grow and form catheter biofilm is dependent upon host fibrinogen (Fg). Examined here are how bacterial and host proteases interact with Fg and contribute to virulence. Analysis of mutants affecting the two major secreted proteases of E. faecalis OG1RF (GelE, SprE) revealed that while the loss of either had no effect on virulence in a murine CAUTI model or for formation of Fg-dependent biofilm in urine, the loss of both resulted in CAUTI attenuation and defective biofilm formation. GelE−, but not SprE− mutants, lost the ability to degrade Fg in medium, while paradoxically, both could degrade Fg in urine. The finding that SprE was activated independently of GelE in urine by a host trypsin-like protease resolved this paradox. Treatment of catheter-implanted mice with inhibitors of both host-derived and bacterial-derived proteases dramatically reduced catheter-induced inflammation, significantly inhibited dissemination from bladder to kidney and revealed an essential role for a host cysteine protease in promoting pathogenesis. These data show that both bacterial and host proteases contribute to CAUTI, that host proteases promote dissemination and suggest new strategies for therapeutic intervention.