Presentation_1.pdf

<p>Proper proliferation and differentiation of neural progenitors (NPs) in the developing cerebral cortex are critical for normal brain formation and function. Emerging evidence has shown the importance of microRNAs (miRNAs) in regulating cortical development and the etiology of neurological disorders. Here we show that miR-26 is co-expressed with its host gene Ctdsp in the mouse embryonic cortex. We demonstrate that similar to its host gene Ctdsp2, miR-26 positively regulates proliferation of NPs through controlling the cell-cycle progression, by using miR-26 overexpression and sponge approaches. On the contrary, miR-26 target gene Emx2 limits expansion of cortical NPs, and promotes transcription of miR-26 host gene Ctdsp. Our study suggests that miR-26, its target Emx2 and its host gene Ctdsp cohesively regulate proliferation of NPs during the mouse cortical development.</p

Data_Sheet_1_Counter-Balance Between Gli3 and miR-7 Is Required for Proper Morphogenesis and Size Control of the Mouse Brain.PDF

Brain morphogenesis requires precise regulation of multiple genes to control specification of distinct neural progenitors (NPs) and neuronal production. Dysregulation of these genes results in severe brain malformation such as macrocephaly and microcephaly. Despite studies of the effect of individual pathogenic genes, the counter-balance between multiple factors in controlling brain size remains unclear. Here we show that cortical deletion of Gli3 results in enlarged brain and folding structures in the cortical midline at the postnatal stage, which is mainly caused by the increased percentage of intermediate progenitors (IPs) and newborn neurons. In addition, dysregulation of neuronal migration also contributes to the folding defects in the cortical midline region. Knockdown of microRNA (miRNA) miR-7 can rescue abnormal brain morphology in Gli3 knockout mice by recovering progenitor specification, neuronal production and migration through a counter-balance of the Gli3 activity. Moreover, miR-7 likely exerts its function through silencing target gene Pax6. Our results indicate that proper brain morphogenesis is an outcome of interactive regulations of multiple molecules such as Gli3 and miR-7. Because miRNAs are easy to synthesize and deliver, miR-7 could be a potential therapeutic means to macrocephaly caused by Gli3-deficiency.</p

Additional file 1 of NMR-based metabonomics reveals the dynamic effect of electro-acupuncture on central nervous system in gastric mucosal lesions (GML) rats

Additional file 1. Additional figures and tables

Edge-by-Edge Lateral Heterostructure through Interfacial Sliding

van der Waals heterostructures (vdWHs) based on two-dimensional (2D) semiconductors have attracted considerable attention. However, the reported vdWHs are largely based on vertical device structure with large overlapping area, while the realization of lateral heterostructures contacted through 2D edges remains challenging and is majorly limited by the difficulties of manipulating the lateral distance of 2D materials at nanometer scale (during transfer process). Here, we demonstrate a simple interfacial sliding approach for realizing an edge-by-edge lateral contact. By stretching a vertical vdWH, two 2D flakes could gradually slide apart or toward each other. Therefore, by applying proper strain, the initial vertical vdWH could be converted into a lateral heterojunction with intimately contacted 2D edges. The lateral contact structure is supported by both microscope characterization and in situ electrical measurements, exhibiting carrier tunneling behavior. Finally, this approach can be extended to 3D thin films, as demonstrated by the lateral 2D/3D and 3D/3D Schottky junction