Oxide dispersion strengthened (ODS) steels exhibit exceptional radiation resistance and hightemperature creep strength when compared to traditional ferritic and ferritic/martensitic (F/M) steels. Their excellent mechanical properties result from very fine nanoparticles dispersed within the matrix. In this work, we applied a high-energy synchrotron radiation X-ray to study the deformation process of a 9Cr ODS steel. The load partitioning between the ferrite/martensite and the nanoparticles was observed during sample yielding. During plastic deformation, the nanoparticles experienced a dramatic loading process, and the internal stress on the nanoparticles increased to a maximum value of 3.5 GPa, which was much higher than the maximum applied stress (~986 MPa). After necking, the loading capacity of the nanoparticles was significantly decreased due to a debonding of the particles from the matrix, as indicated by a decline in lattice strain/internal stress. Due to the load partitioning, the ferrite/martensite slightly relaxed during early yielding, and slowly strained until failure. This study develops a better understanding of loading behavior for various phases in the ODS F/M steel.

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The dentate gyrus (DG) of the hippocampal formation plays essential roles in learning and memory. Defective DG development is associated with neurological disorders. Here, we show that transcription factor 4 (Tcf4) is essential for DG development. Tcf4 expression is elevated in neural progenitors of the dentate neuroepithelium in the developing mouse brain. We demonstrate that conditional disruption of Tcf4 in the dentate neuroepithelium leads to abnormal neural progenitor migration guided by disorganized radial glial fibers, which further leads to hypoplasia in the DG. Moreover, we reveal that Wnt7b is a key downstream effector of Tcf4 in regulating neural progenitor migration. Behavioral analysis shows that disruption of integrity of the DG impairs the social memory highlighting the importance of proper development of the DG. These results reveal a critical role for Tcf4 in regulating DG development. As mutations in TCF4 cause Pitt–Hopkins syndrome (PTHS) characterized by severe intellectual disability, our data also potentially provide insights into the basis of neurological defects linked to TCF4 mutations.

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