Microstructure evolution and reaction behavior of Cu–Ni alloy and B_4C powder system

Microstructure evolution and reaction behavior of Cu–Ni alloy and B_4C power system was studied by in-situ and static experimental investigations along with theoretical calculations. The reaction process was as follows. Firstly,B_4C decomposed into B and C atoms, and then B atoms diffused into Cu–Ni matrix, leading to the formation of Ni_2B particles. Subsequently, Ni atoms diffused into B_4C, forming a loose mixture of Ni_2B and amorphous C at the initial powder boundary. Finally, with the completion of reaction, Ni_2B particles at the powder boundary grew into a monolithic block, and then C substance was excluded out and accumulated at the edge of this monolithic Ni_2B block. It is believed that the formation of Ni_2B phase is caused by the most negative change of Gibbs free energy among all the potential reactions between Ni–B and Ni–B_4C systems.     

Haploinsufficiency of NSD1 causes Sotos syndrome

We isolated NSD1 from the 5q35 breakpoint in an individual with Sotos syndrome harboring a chromosomal translocation. We identified 1 nonsense, 3 frameshift and 20 submicroscopic deletion mutations of NSD1 among 42 individuals with sporadic cases of Sotos syndrome. The results indicate that haploinsufficiency of NSD1 is the major cause of Sotos syndrome.     

Tbx6-dependent Sox2 regulation determines neural or mesodermal fate in axial stem cells

The classical view of neural plate development held that it arises from the ectoderm, after its separation from the mesodermal and endodermal lineages. However, recent cell-lineage-tracing experiments indicate that the caudal neural plate and paraxial mesoderm are generated from common bipotential axial stem cells originating from the caudal lateral epiblast. Tbx6 null mutant mouse embryos which produce ectopic neural tubes at the expense of paraxial mesoderm must provide a clue to the regulatory mechanism underlying this neural versus mesodermal fate choice. Here we demonstrate that Tbx6-dependent regulation of Sox2 determines the fate of axial stem cells. In wild-type embryos, enhancer N1 of the neural primordial gene Sox2 is activated in the caudal lateral epiblast, and the cells staying in the superficial layer sustain N1 activity and activate Sox2 expression in the neural plate. In contrast, the cells destined to become mesoderm activate Tbx6 and turn off enhancer N1 before migrating into the paraxial mesoderm compartment. In Tbx6 mutant embryos, however, enhancer N1 activity persists in the paraxial mesoderm compartment, eliciting ectopic Sox2 activation and transforming the paraxial mesoderm into neural tubes. An enhancer-N1-specific deletion mutation introduced into Tbx6 mutant embryos prevented this Sox2 activation in the mesodermal compartment and subsequent development of ectopic neural tubes, indicating that Tbx6 regulates Sox2 via enhancer N1. Tbx6-dependent repression of Wnt3a in the paraxial mesodermal compartment is implicated in this regulatory process. Paraxial mesoderm-specific misexpression of a Sox2 transgene in wild-type embryos resulted in ectopic neural tube development. Thus, Tbx6 represses Sox2 by inactivating enhancer N1 to inhibit neural development, and this is an essential step for the specification of paraxial mesoderm from the axial stem cells.     

低温烧结3Y-TZP陶瓷的力学性能和耐磨性能

研究了低温烧结 3Y_TZP的烧结性能、力学性能以及耐磨性能 .经成型后的ZrO2(x(Y2 O3 ) =3% )在常压、12 5 0～ 145 0℃温度下 2h烧成 .由于该粉料有很高的烧结活性 ,在 130 0℃低温烧成下就获得了相对密度大于 99%的烧结体 ;在 140 0℃烧成温度下3Y_TZP获得最佳的力学性能和耐磨性能 ,其抗弯强度、断裂韧性和维氏硬度分别达到95 3MPa ,9.1MPa·m1/2 和 12 .7GPa .应力诱导相变是主要的增韧机理 .     

Genome-wide phenotype analysis in ES cells by regulated disruption of Bloom's syndrome gene

The chief limitation of phenotype-based genetic screening in mammalian systems is the diploid nature of the genome. Cells deficient in the Bloom's syndrome gene (Blm) show an increased rate of loss of heterozygosity. Here we have used a tetracycline-regulated Blm allele (Blm(tet)) to introduce bi-allelic mutations across the genome in mouse embryonic stem (ES) cells. Transient loss of Blm expression induces homologous recombination not only between sister chromatids but also between homologous chromosomes. We considered that the phenotype of ES cells bearing bi-allelic mutations would be maintained after withdrawal of the tetracycline analogue doxycycline. Indeed, a combination of N-ethyl-N-nitrosourea mutagenesis and transient loss of Blm expression enabled us to generate an ES cell library with genome-wide bi-allelic mutations. The library was evaluated by screening for mutants of glycosylphosphatidylinositol-anchor biosynthesis, which involves at least 23 genes distributed throughout the genome. Mutants derived from 12 different genes were obtained and two unknown mutants were simultaneously isolated. Our results indicate that phenotype-based genetic screening with Blm(tet) is very efficient and raises possibilities for identifying gene functions in ES cells.