Correlation between composition, microstructure, and emission properties in Nd-doped Si-rich Si oxynitride films: investigation into the nature of the sensitizer.

Rare earth (RE) ions doped in Si-based materials, compatible with Si technology, are promising compounds with regards to optical communication and energy conversion. In this article, we show the emission properties of Nd-doped Si-rich Si oxynitride (Nd-SRSON) films, and their dependence on the dangling bond density and the nature of the sensitizer. These films were prepared by reactive magnetron sputtering and post-annealing. The film composition, microstructure, and emission properties were investigated as a function of deposition parameters and annealing temperatures. Both Fourier transform infrared (FTIR) and ellipsometry spectroscopy measurements have confirmed that the sample composition (Si/N ratio) can be carefully tuned by varying the ratio of reactive nitrogen to argon in the sputtering plasma. Moreover, FTIR and x-ray photoelectron spectroscopy measurements demonstrate the existence of both nitrogen and oxygen dangling bonds (N· and O·) in as-deposited samples. These dangling bonds were passivated during annealing. Under non-resonant excitation at 488 nm, the films exhibit a significant photoluminescence (PL) signal from Nd3+ ions demonstrating the occurrence of an effective sensitization of Nd3+ ions in the host matrix. Both PL excitation and ellipsometry results (the energy band gap from new amorphous model) exclude the sensitization by an exciton with energy over the band gap, whereas the presence of Si agglomerates, at the atomic scale, have been identified as effective sensitizers towards Nd3+ ions. This work not only provides knowledge to optimize Si-based materials for favorable emission properties, but also, presents a universal methodology to investigate the nature of sensitizers for RE emitters. This allows one to find correlations between composition, microstructure, and emission properties.

Mutational analysis of podocyte genes in children with sporadic steroid-resistant nephrotic syndrome.

Recent studies have demonstrated that mutations in 4 podocyte genes, NPHS1, NPHS2, CD2AP, and WT1, are associated with the pathogenesis of steroid-resistant nephrotic syndrome (SRNS). Systematic investigation of all 4 genes for sporadic SRNS in China has not been performed. We examined 10 Chinese children with sporadic SRNS who showed no response to immunosuppressive agents and 20 SRNS controls who exhibited a response to prolonged steroid or immunosuppressive treatment and achieved complete remission. We analyzed mutations in the 4 podocyte genes, NPHS1, NPHS2, CD2AP, and WT1. Mutational analysis was performed using polymerase chain reaction and direct sequencing. Of the 10 SRNS children who showed no response to immunosuppressive agents, the compound heterozygous NPHS1 mutations 2677A>G (T893A) and *142T>C were identified in 1 patient, while a heterozygous mutation in WT1, 1180C>T (R394W), was found in another patient. Of the 20 SRNS children showing complete remission who responded to prolonged steroid therapy or immunosuppressive agents, 4 heterozygous NPHS1 mutations, 928G>A, IVS8+30C>T, IVS21+14G>A, and IVS25-23C>T, were identified in 4 patients and a heterozygous CD2AP mutation, IVS7-135G>A, was identified in 1 patient. Our results indicate the necessity of genetic examination for mutations in podocyte genes in Chinese SRNS children who show no response to immunosuppressive agents.

Mutations in NPHS1 in a Chinese child with congenital nephrotic syndrome.

Since the identification of the NPHS1 gene, which encodes nephrin, various investigators have demonstrated that the NPHS1 mutation is a frequent cause of congenital nephrotic syndrome (CNS); it is found in 98% of Finnish children with this syndrome and in 39-80% of non-Finnish cases. In China, compound heterozygous mutations in the NPHS1 gene have been identified in two Chinese families with CNS. To our knowledge, however, whether or not NPHS1 is the causative gene in sporadic Chinese CNS cases has not been established. We identified a homozygous mutation of NPHS1, 3250insG (V1084fsX1095), in a Chinese child with sporadic CNS. This finding leads us to suggest that NPHS1 mutations are also present in sporadic Chinese CNS cases. This gives additional support for the necessity for genetic examination of mutations in the NPHS1 gene in Chinese children with sporadic CNS.