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        Low-temperature insertion bonding using electroless Cu-Co-P micro-cones array with controllable morphology

        Yaqian Sun,Jing Wang,Xundi Zhang,Chenlin Yang,Anmin Hu,Tao Hang,Yunwen Wu,Huiqin Ling,Ming Li 대한금속·재료학회 2021 ELECTRONIC MATERIALS LETTERS Vol.17 No.6

        At present, thermal compression bonding based on Cu and lead-free Sn based solder is often limited by high bonding temperature,which is higher than the melting point of solder (218 ℃). In this paper, we reported a low-temperature solid stateinsertion bonding method based on electroless Cu-Co-P micro-cones array. By adjusting the mass ratio of CuSO 4 ·5H 2 O andCoSO 4 ·7H 2 O, a series of Cu-Co-P micro-cones with diff erent morphologies were prepared. The Cu-Co-P micro-cones withhigher proportion of copper were sharper and denser and (111) orientation was also more. It was found that reducing theheight and density of micro-cones was conducive to achieve seamless bonding at lower temperature and force such as 170℃ and 750 gf. By optimizing the morphology of micro-cones, such as height, bottom diameter, vertex angle and density, theseamless and reliable bonding with high shear strength (39.9 MPa) could be achieved at 170 ℃ bonding temperature and1000 gf bonding force. The transmission electron microscopy results showed that intermetallic compounds including Cu 6 Sn 5and Cu 3 Sn existed at bonding interface, which indicated that signifi cant atomic diff usion had occurred between Cu-Co-Pmicro-cones and Sn based solder. Probable mechanisms for low-temperature insertion bonding were discussed.

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        Centromere protein N promotes lung adenocarcinoma progression by activating PI3K/AKT signaling pathway

        Zheng Yi,You Hui,Duan Jingzhu,Chen Biyu,Wu Chenlin,Chen Peipei,Wang Meifang 한국유전학회 2022 Genes & Genomics Vol.44 No.9

        Background: As an important member of centromere family, centromere associated protein N (CENPN) was abnormally expressed in varied malignant tumors. Objective: This paper aimed to analyze the expression and related mechanism of CENPN in lung adenocarcinoma (LUAD). Methods: The expression of CENPN in LUAD was analyzed by Gene Expression Profiling Interactive Analysis (GEPIA) database. The mRNA expression, protein expression, cell viability, cell invasion, cell apoptosis, cell stem like characteristics were detected by RT-PCR, western blot, CCK8 assay, transwell assay, flow cytometry and spheroidization assay, respectively. Finally, the pathological changes of xenograft were estimated by H&E staining, and the expression of proteins was detected by immunohistochemistry. Results: GEPIA analysis showed that the CENPN expression in LUAD was significantly higher than that in normal lung tissue, which was negatively correlated with the prognosis. These results were consistent with our clinical data. Besides, CENPN was highly expressed in LUAD cell lines. In addition, the upregulation of CENPN amplified the cell viability, stemness and invasive ability in PC9 cells. However, the knockdown of CENPN inhibited the cell activity, stemness, invasive ability with increased cell apoptosis in A549. Furthermore, CENPN could positively regulate the phosphorylation of PI3K and AKT. The PI3K inhibitor, 740Y-P, could reverse the effect of CENPN silencing on the expression of Ki-67, cleaved caspase 3, OCT4, and snail 1. Finally, the downregulation of CENPN restrained the growth of xenograft and inactivated the PI3K/AKT pathway. Conclusion: CENPN was abnormally overexpressed in LUAD, and promoted tumor progression of LUAD by affecting PI3K/AKT pathway.

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