Discussion on the lapping and polishing process of 4H-SiC wafer

Conference Name:8th Annual IEEE International Conference on Nano/Micro Engineered and Molecular Systems, IEEE NEMS 2013. Conference Address: Suzhou, China. Time:April 7, 2013 - April 10, 2013.Institute of Electrical and Electronics Engineers (IEEE); IEEE Nanotechnology Council (NTC); Peking University; Soochow University; Chinese Academy of SciencesIn order to achieve a high quality silicon carbide (SiC) film, the lapping and polishing process scheme was introduced in this paper. The ductile iron was utilized as lapping disc material, which can quickly thin the SiC wafer to the film of uniform thickness. After three-step lapping process, the thickness of the SiC wafer was reduced to 35 ± 4μm. In the process of polishing, a rough polishing and a fine polishing were studied by selecting suitable polishing liquid, polishing pad and parameters. The results show that the lapping and polishing procedure can realize large area and high quality SiC films: the film thickness, 30 ± 2μm and the surface roughness RMS, 0.69nm. ? 2013 IEEE

Fabrication of mesoporous silica-coated CNTs and application in size-selective protein separation

In this study, we report a simple method to coat mesoporous silica onto carbon nanotubes (CNTs) via a two-step procedure. Mesoporous CNTs@SiO(2) composites have been obtained by extracting cetyltrimethylammonium bromide (CTAB) via an ion-exchange procedure after silica-coated carbon nanotubes were synthesized with the aid of the cationic surfactant CTAB. The coating process was explicitly investigated, and a possible formation mechanism of the mesoporous CNTs@SiO(2) was proposed, which reveals that the ratio of CTAB/CNTs plays a critical role in the coating process. Furthermore, the pore size of the as-prepared mesoporous silica could be exactly controlled by using different amounts of the bromide surfactant CTAB. The obtained mesoporous CNTs@SiO(2) composite nanomaterial was evaluated with three typical proteins, cytochrome c (Cyt c), bovine serum albumin (BSA) and lysozyme (Lyz), with different molecular sizes. The adsorption and desorption of binary mixtures of Cyt c and BSA, Cyt c and Lyz, and a ternary mixture of Cyt c, BSA and Lyz showed that the mesoporous CNTs@SiO(2) are effective and highly selective adsorbents for Cyt c. The as-prepared mesoporous CNTs@SiO(2) composites have shown effective performance in size-selective adsorption of biomacromolecules, demonstrating great potential in biomacromolecular separation

MiR‐223‐3p alleviates trigeminal neuropathic pain in the male mouse by targeting MKNK2 and MAPK/ERK signaling

Abstract Background Trigeminal neuralgia (TN) is a neuropathic pain that occurs in branches of the trigeminal nerve. MicroRNAs (miRNAs) have been considered key mediators of neuropathic pain. This study was aimed to elucidate the pathophysiological function and mechanisms of miR‐223‐3p in mouse models of TN. Methods Infraorbital nerve chronic constriction injury (CCI‐ION) was applied in male C57BL/6J mice to establish mouse models of TN. Pain responses were assessed utilizing Von Frey method. The expression of miR‐223‐3p, MKNK2, and MAPK/ERK pathway protein in trigeminal ganglions (TGs) of CCI‐ION mice was measured using RT‐qPCR and Western blotting. The concentrations of inflammatory cytokines were evaluated using Western blotting. The relationship between miR‐223‐3p and MKNK2 was tested by a luciferase reporter assay. Results We found that miR‐223‐3p was downregulated, while MKNK2 was upregulated in TGs of CCI‐ION mice. MiR‐223‐3p overexpression by an intracerebroventricular injection of Lv‐miR‐223‐3p attenuated trigeminal neuropathic pain in CCI‐ION mice, as well as reduced the protein levels of pro‐inflammatory cytokines in TGs of CCI‐ION mice. MKNK2 was verified to be targeted by miR‐223‐3p. Additionally, miR‐223‐3p overexpression decreased the phosphorylation levels of ERK1/2, JNK, and p38 protein in TGs of CCI‐ION mice to inhibit MAPK/ERK signaling. Conclusions Overall, miR‐223‐3p attenuates the development of TN by targeting MKNK2 to suppress MAPK/ERK signaling