Incorporation of Y2O3 Particles into 410L Stainless Steel by a Powder Metallurgy Route

Addition of yttria to steels has been proposed for the fabrication of oxide-dispersion-strengthened materials for nuclear power applications. We have investigated materials prepared from 12 Cr martensitic stainless steel, AISI 410L, produced by powder metallurgy. Materials were produced with and without yttria addition, and two different sizes of yttria were used, 0.9 µm and 50 nm. Tensile and mini-creep tests were performed to determine mechanical properties. Optical microscopy, SEM, TEM, and EDX analysis were used to investigate the microstructures and deformation mechanisms and to obtain information about non-metallic inclusion particles. SiO2, MnS, and Y2Si2O7 inclusion particles were observed. An SiO2 and Y2O3 interaction was seen to have occurred during the ball milling, which impaired the final mechanical properties. Small-angle neutron scattering experiments showed that the matrix chemistry prevented effective dissolution of the yttria. © The Author(s) 201

Gitelman's Syndrome: characterization of a novel c.1181G>A point mutation and functional classification of the known mutations.

We have investigated the mechanisms by which a novel missense point mutation (c.1181G>A) found in two sisters causes Gitelman’s syndrome by impairing the sodium chloride co-transporter (NCC, encoded by SLC12A3 gene) function. The cDNA and in vitro transcribed mRNA of either wild-type or mutated SLC12A3 were transfected into HEK293 cells and injected into Xenopus laevis oocytes, respectively. The expression, maturation, trafficking, and function of the mutated and wild-type NCC were assessed by Western blotting, immunohistochemistry and 22Na+ uptake studies. By immunoblotting of lysates from HEK293 cells and oocytes expressing wild-type NCC, two NCC-related bands of approximately 130 kDa and 115 kDa, corresponding to fully and core-glycosylated NCC, respectively, were identified. In contrast, the mutant NCC only showed a single band of approximately 115 kDa, indicating impaired maturation of the protein. Moreover, oocytes injected with wild-type NCC showed thiazide-sensitive 22Na+ uptake, which was absent in those injected with the mutant NCC. The novel mutation was discussed in the context of the functionally characterized NCC mutations causing Gitelman’s syndrome, which fit into five classes. In conclusion, the functional characterization of this novel Gly394Asp NCC and its localization on the NCC structure, alongside that of previously known mutations causing Gitelman’s syndrome, may provide novel information on the function of the different domains of the human NCC