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Tm(3+)-Yb(3+) codoped transparent oxyfluoride glass ceramics containing LaF(3) nanocrystals were obtained by thermal treatment on the as-made glasses. The formation of LaF(3) nanocrystals and the incorporation of Tm(3+) and Yb(3+) into LaF(3) nanocrystal lattice were confirmed by X-ray diffraction and high resolution transmission electron microscopy. Infrared quantum cutting involving Yb(3+) 950-1100 nm ((2)F(5/2)--> (2)F(7/2)) emission was achieved upon the excitation of the (1)G(4) energy level of Tm(3+) at 468 nm. We measured the photoluminescence properties of these glass ceramics. We also investigated the thermal treatment duration dependent quantum efficiency, and found that the quantum efficiency is 13% increased for the 0.5Tm(3+)-4Yb(3+) doped glass ceramic with a maximum value of 144%, and 16% increased for the 0.5Tm3+-8Yb3+ doped glass ceramic with a maximum value of 162%, respectively.

Tb 3 + – Yb 3 + codoped transparent oxyfluoride glass ceramics containing CaF2 nanocrystals were synthesized. The formation of CaF2 nanocrystals in the glass ceramics was confirmed by x-ray diffraction and high resolution transmission electron microscopy. The incorporation of Tb3+ and Yb3+ into CaF2 nanocrystal lattice was confirmed by energy dispersive spectroscopy. Infrared quantum cutting involving Yb3+ 950–1100nm (F5∕22→F7∕22) emission was achieved upon the excitation of D45 energy level of Tb3+ at 484nm. The photoluminescence properties have been studied for these glass ceramics. Yb3+ concentration dependent quantum efficiency was calculated, and the maximum efficiency approaches 155% before reaching concentration quenching threshold.

To reduce cadmium (Cd) pollution of food chains, screening and breeding of low-Cd-accumulating cultivars are the focus of much study. Two previously identified genotypes, a low-Cd-accumulating genotype (LAJK) and a high-Cd-accumulating genotype (HAJS) of pakchoi (Brassica chinesis L.), were stressed by Cd (12.5 μM) for 0 h (T0), 3 h (T3) and 24 h (T24). By comparative transcriptome analysis for root tissue, 3005 and 4343 differentially expressed genes (DEGs) were identified in LAJK at T3 (vs T0) and T24 (vs T3), respectively, whereas 8677 and 5081 DEGs were detected in HAJS. Gene expression pattern analysis suggested a delay of Cd responded transcriptional changes in LAJK compared to HAJS. DEG functional enrichments proposed genotype-specific biological processes coped with Cd stress. Cell wall biosynthesis and glutathione (GSH) metabolism were found to involve in Cd resistance in HAJS, whereas DNA repair and abscisic acid (ABA) signal transduction pathways played important roles in LAJK. Furthermore, the genes participating in Cd efflux such as PDR8 were overexpressed in LAJK, whereas those responsible for Cd transport such as YSL1 were more enhanced in HAJS, exhibiting different Cd transport processes between two genotypes. These novel findings should be useful for molecular assisted screening and breeding of low-Cd-accumulating genotypes for pakchoi.

Activity of the epithelial Na؉ channel (ENaC) is modulated by Na ؉ self-inhibition, an allosteric down-regulation of channel open probability by extracellular Na ؉ . We searched for determinants of Na ؉ self-inhibition by analyzing changes in this inhibitory response resulting from specific mutations within the extracellular domains of mouse ENaC subunits. Mutations at ␥Met 438 altered the Na ؉ self-inhibition response in a substitution-specific manner. Fourteen substitutions (Ala, Arg, Asp, Cys, Gln, Glu, His, Ile, Phe, Pro, Ser, Thr, Tyr, and Val) significantly suppressed Na ؉ self-inhibition, whereas three mutations (Asn, Gly, and Leu) moderately enhanced the inhibition. Met to Lys mutation did not alter Na ؉ self-inhibition. Mutations at the homologous site in the ␣ subunit (G481A, G481C, and G481M) dramatically increased the magnitude and speed of Na ؉ self-inhibition. Mutations at the homologous ␤Ala 422 resulted in minimal or no change in Na ؉ self-inhibition. Low, high, and intermediate open probabilities were observed in oocytes expressing ␣G481M␤␥, ␣␤␥M438V, and ␣G481M/ ␤␥M438V, respectively. This pair of residues map to the ␣5 helix in the extracellular thumb domain in the chicken acid sensing ion channel 1 structure. Both residues likely reside near the channel surface because both ␣G481C␤␥ and ␣␤␥M438C channels were inhibited by an externally applied and membrane-impermeant sulfhydryl reagent. Our results demonstrate that ␣Gly 481 and ␥Met 438 are functional determinants of Na ؉ self-inhibition and of ENaC gating and suggest that the thumb domain contributes to the channel gating machinery.Maintenance of body fluid volume homeostasis requires a collaborative interaction of many Na ϩ transport mechanisms. Na ϩ transport in epithelia that line the late distal convoluted tubule, connecting tubule, and collecting tubule relies on apical Na ϩ entry through epithelial Na ϩ channels (ENaC self-inhibition (4, 6 -8). However, detailed elements regarding its mechanism have not been revealed.A logical place to search for structural elements associated with Na ϩ self-inhibition is the large extracellular domain (ECD) that connects the two transmembrane domains (M1 and M2) within each ENaC subunit. The ECD likely exists as well structured subdomains with 16 conserved Cys residues. We recently reported that point mutations at multiple ␣ and ␥ ECD Cys residues blunted Na ϩ self-inhibition, and certain double or triple mutations rendered ENaC insensitive to high concentration of extracellular Na ϩ . These results suggest that multiple Cys residues are required to establish the proper tertiary structure permitting this allosteric regulation (9). In addition, the N-terminal portion of ECD contains ␥His 239 , a previously identified residue critical for Na ϩ self-inhibition, as well as defined protease cleavage sites (4, 10 -12). Various proteases have been shown to regulate ENaC activity, in part, by interfering with Na ϩ self-inhibition (6, 7, 13). The resolved high resolution structure of the chicken acidsensing i...