The desirability of being able to search for specific persons in surveillance videos captured by different cameras has increasingly motivated interest in the problem of person re-identification, which is a critical yet under-addressed challenge in multi-camera tracking systems. The main difficulty of person re-identification arises from the variations in human appearances from different camera views. In this paper, to bridge the human appearance variations across cameras, two coupled dictionaries that relate to the gallery and probe cameras are jointly learned in the training phase from both labeled and unlabeled images. The labeled training images carry the relationship between features from different cameras, and the abundant unlabeled training images are introduced to exploit the geometry of the marginal distribution for obtaining robust sparse representation. In the testing phase, the feature of each target image from the probe camera is first encoded by the sparse representation and then recovered in the feature space spanned by the images from the gallery camera. The features of the same person from different cameras are similar following the above transformation. Experimental results on publicly available datasets demonstrate the superiority of our method.

A one-step procedure has been developed to grow β-SiC nanorods from a solid carbon and silicon source on a Si substrate by hot filament chemical vapor deposition. This process is catalyzed by metallic particles which come from impurities in the solid source which is a plate made by pressing a mixture graphite and silicon powders at 150 °C. Hydrogen was introduced into the reaction chamber to react with the solid plate to produce hydrocarbon and hydrosilicon radicals which presumably reacted to form SiC nanorods. The nanorods consisted of a crystalline β-SiC core with an amorphous silicon oxide shell layer and grew along the [100] direction. The nanorods were 10–30 nm in diameter and less than 1 μm in length.

Background Glioma initiating cells (GICs), also known as glioma stem cells (GSCs), play an important role in the progression and recurrence of glioblastoma multiforme (GBM) due to their potential for self-renewal, multiple differentiation and tumor initiation. In the recent years, Notch1 has been found to be overexpressed in GICs. However, the regulatory mechanism of Notch1 in the self-renewal and invasion ability of GICs remains unclear. This study aims to explore the effect of Notch pathway on self-renewal and invasion of GICs and the underlying mechanisms. Methods Bioinformatic analysis and immunohistochemistry (IHC) were performed to evaluate the expression of Notch1 and Hes1 in GBM samples. Immunofluorescent (IF) staining was performed to observe the distribution of Notch1 and CXCR4 in GBM and GICs. Both pharmacological intervention and RNA interference were employed to investigate the role of Notch1 in GICs self-renewal, invasion and tumor growth in vitro or in vivo. The crosstalk effect of Notch1 and CXCL12/CXCR4 system on GIC self-renewal and invasion was explored by sphere formation assay, limiting dilution assay and Transwell assay. Western blots were used to verify the activation of Notch1/CXCR4/AKT pathway in self-renewal, invasion and tumor growth of GICs. Luciferase reporter assay was used to testify the potential binding site of Notch1 signaling and CXCR4. The orthotopic GICs implantations were established to analyze the role and the mechanism of Notch1 in glioma progression in vivo. Results Notch1 signaling activity was elevated in GBM tissues. Notch1 and CXCR4 were both upregulated in GICs, compared to Notch1 positive glioma cells comprised a large proportion in the CD133+ glioma cell spheres, CXCR4 positive glioma cells which usually expressed Notch1 both and dispersed in the periphery of the sphere, only represent a small subset of CD133+ glioma cell spheres. Furthermore, downregulation of the Notch1 pathway by shRNA and MK0752 significantly inhibited the PI3K/AKT/mTOR signaling pathway via the decreased expression of CXCR4 in GICs, and weakened the self-renewal, invasion and tumor growth ability of GICs. Conclusions These findings suggest that the cross-talk between Notch1 signaling and CXCL12/CXCR4 system could contribute to the self-renewal and invasion of GICs, and this discovery could help drive the design of more effective therapies in Notch1-targeted treatment of GBMs. Electronic supplementary material The online version of this article (10.1186/s13046-019-1319-4) contains supplementary material, which is available to authorized users.

Silicon carbide (SiC) nanowires on a silicon substrate were prepared using hot-filament-assisted chemical-vapor deposition with a solid silicon and carbon source. The SiC nanowires show good field-emitting properties as revealed by the current–voltage characteristics. Together with its ease of preparation, these SiC nanowires are shown to have great potential in the area of electron field-emitting devices.

Epidermal growth factor receptor (EGFR) overexpression and activation result in increased proliferation and migration of solid tumors including ovarian cancer. In recent years, mounting evidence indicates that EGFR is a direct and functional target of miR-7. In this study, we found that miR-7 expression was significantly downregulated in highly metastatic epithelial ovarian cancer (EOC) cell lines and metastatic tissues, whereas the expression of, EGFR correlated positively with metastasis in both EOC patients and cell lines. Overexpression of miR-7 markedly suppressed the capacities of cell invasion and migration and resulted in morphological changes from a mesenchymal phenotype to an epithelial-like phenotype in EOC. In addition, overexpression of miR-7 upregulated CK-18 and β-catenin expression and downregulated Vimentin expression, accompanied with EGFR inhibition and AKT/ERK1/2 inactivation. Similar to miR-7 transfection, silencing of EGFR with this siRNA in EOC cells also upregulated CK-18 and β-catenin expression and downregulated Vimentin expression, and decreased phosphorylation of both Akt and ERK1/2, confirming that EGFR is a target of miR-7 in reversing EMT. The pharmacological inhibition of PI3K-AKT and ERK1/2 both significantly enhanced CK-18 and β-catenin expression and suppressed vimentin expression, indicating that AKT and ERK1/2 pathways are required for miR-7 mediating EMT. Finally, the expression of miR-7 and EGFR in primary EOC with matched metastasis tissues was explored. It was showed that miR-7 is inversely correlated with EGFR. Taken together, our results suggested that miR-7 inhibited tumor metastasis and reversed EMT through AKT and ERK1/2 pathway inactivation by reducing EGFR expression in EOC cell lines. Thus, miR-7 might be a potential prognostic marker and therapeutic target for ovarian cancer metastasis intervention.