van der Waals solid solution crystals for highly efficient in-air photon upconversion under subsolar irradiance.

Triplet-sensitized photon upconversion (UC) has been proposed for broad applications. However, the quest for superior solid materials has been challenged by the poor exciton transport often caused by low crystallinity, a small crystal domain, and aggregation of triplet sensitizers. Here, we demonstrate substantial advantages of the van der Waals solid solution concept to yield molecular crystals with extraordinary performance. A 0.001%-order porphyrin sensitizer is dissolved during recrystallization into the molecular crystals of a blue-fluorescent hydrocarbon annihilator, 9-(2-naphthyl)-10-[4-(1-naphthyl)phenyl]anthracene (ANNP), which contains bulky side groups. This attempt yields millimeter-sized, uniformly colored, transparent solid solution crystals, which resolves the long-standing problem of sensitizer aggregation. After annealing, the crystals exhibit unprecedented UC performance (UC quantum yield reaching 16% out of a maximum of 50% by definition; excitation intensity threshold of 0.175 sun; and high photostability of over 150 000 s) in air, which proves that this concept is highly effective in the quest for superior UC solid materials.

Class-IA phosphoinositide 3-kinase p110ß Triggers GPCR-induced superoxide production in p110γ-deficient murine neutrophils.

Studies with knockout mice have indicated that the only isoform of phosphoinositide 3-kinase (PI3K) functioning in the oxidative burst of mouse neutrophils in response to heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR) agonists is a class-IB PI3K, p110γ. In the present study, we observed that the cells from p110γ(-/-) mice gain a response to N-formyl-Met-Leu-Phe (fMLP) after priming with cytochalasin E. Even the unprimed cells, which show no response to fMLP, produce a significant amount of superoxide, when an effective agonist of the mouse-type fMLP receptors, Trp-Lys-Tyr-Met-Val-D-Met, is used to stimulate the cells. These results suggested that the class-IA isoforms (p110α, p110ß, and p110δ) of PI3K are sufficient to trigger and maintain superoxide production. Examination of the effects of isoform-specific inhibitors suggested that the p110ß isoform is the primary PI3K triggering the response to GPCR agonists when p110γ is absent.

Critical roles of the p110 beta subtype of phosphoinositide 3-kinase in lipopolysaccharide-induced Akt activation and negative regulation of nitrite production in RAW 264.7 cells.

It has been suggested that PI3K participates in TLR signaling. However, identifying specific roles for individual PI3K subtypes in signaling has remained elusive. In macrophages from the p110gamma(-/-) mouse, LPS-induced phosphorylation of Akt occurred normally despite the fact that the action of anaphylatoxin C5a was impaired markedly. In RAW 264.7 cells expressing short hairpin RNA that targets p110beta, LPS-induced phosphorylation of Akt was significantly attenuated. In contrast, the LPS action was not impaired, but was rather augmented in the p110alpha-deficient cells. Previous pharmacologic studies have suggested that a PI3K-Akt pathway negatively regulates TLR-induced inducible NO synthase expression and cytokine production. In the p110beta-deficient cells, inducible NO synthase expression and IL-12 production upon stimulation by LPS were increased, whereas LPS-induced expression of COX-2 and activation of MAPKs were unaffected. Together, the results suggest a specific function of p110beta in the negative feedback regulation of TLR signaling.