为促进γ-TiAl叶片与Ti_(2)AlNb轮盘异种材料整体叶盘线性摩擦焊接制造技术的发展,进行了全片层γ-TiAl与Ti_(2)AlNb的线性摩擦焊接,采用扫描电镜(SEM)、EBSD及拉伸试验方法对焊态及焊后热处理态焊接接头的微观组织及力学性能进行了分...为促进γ-TiAl叶片与Ti_(2)AlNb轮盘异种材料整体叶盘线性摩擦焊接制造技术的发展,进行了全片层γ-TiAl与Ti_(2)AlNb的线性摩擦焊接,采用扫描电镜(SEM)、EBSD及拉伸试验方法对焊态及焊后热处理态焊接接头的微观组织及力学性能进行了分析。结果表明,焊合区及近区的相构成自TiAl侧至Ti_(2)AlNb侧在焊态下为γ相-α_(2)相-B2相;经过800℃/2 h AC焊后热处理后转变为γ相-α_(2)相+B2相-O+B2相;γ-TiAl侧热力影响区(TMAZ)发生了片层弯折变形,Ti_(2)AlNb侧TMAZ发生了晶粒细化及再结晶。经焊后热处理接头室温及650℃抗拉强度分别达到277 MPa和478 MPa。展开更多
Objective： The aim of our study was to determine the underlying mechanism of miR-210 on regulation of the cell cycle in nasopharyngeal carcinoma cell line CNE-1, particularly through regulation of cyclin D1, under hy...Objective： The aim of our study was to determine the underlying mechanism of miR-210 on regulation of the cell cycle in nasopharyngeal carcinoma cell line CNE-1, particularly through regulation of cyclin D1, under hypoxic conditions. Methods： The CNE-1 cell line was induced with hypoxia, and the expression levels of endogenic miR-210 and cyclin D1 were detected by real-time PCR and Western blotting. Next, the luciferase assay was used to confirm that cyclin D1 is a target gene for miR-210. Cell cycle and cell proliferation were detected in CNE-1 cells that were cultured under hypoxic conditions with either overexpression or knockout of miR-210 using flow cytometry and MTT assay, respectively. Results： Hypoxia induced the expression of miR-210, resulting in reduced mRNA and protein levels of cyclin D1 and repression of cyclin D1 in CNE-1 cells. Further analysis indicated that miR-210 directly binded to the 3＇UTR of the cyclin D1 gene, thus regulated the expression of cyclin DI. The flow cytometry assay showed that, under hypoxic conditions, miR-210 blocked CNE-1 cells in the G1 phase, and miR-210 also inhibited the proliferation of CNE-1 cells. Conclusion： Under hypoxic conditions, miR-210 directly reduced the expression of cyclin D1, leading to CNE-1 cells blocked in G1 phase.展开更多
文摘为促进γ-TiAl叶片与Ti_(2)AlNb轮盘异种材料整体叶盘线性摩擦焊接制造技术的发展,进行了全片层γ-TiAl与Ti_(2)AlNb的线性摩擦焊接,采用扫描电镜(SEM)、EBSD及拉伸试验方法对焊态及焊后热处理态焊接接头的微观组织及力学性能进行了分析。结果表明,焊合区及近区的相构成自TiAl侧至Ti_(2)AlNb侧在焊态下为γ相-α_(2)相-B2相;经过800℃/2 h AC焊后热处理后转变为γ相-α_(2)相+B2相-O+B2相;γ-TiAl侧热力影响区(TMAZ)发生了片层弯折变形,Ti_(2)AlNb侧TMAZ发生了晶粒细化及再结晶。经焊后热处理接头室温及650℃抗拉强度分别达到277 MPa和478 MPa。
基金Supported by grants from the National Natural Science Foundation of China (No.31301117,No.JCYJ20120827150357364)
文摘Objective： The aim of our study was to determine the underlying mechanism of miR-210 on regulation of the cell cycle in nasopharyngeal carcinoma cell line CNE-1, particularly through regulation of cyclin D1, under hypoxic conditions. Methods： The CNE-1 cell line was induced with hypoxia, and the expression levels of endogenic miR-210 and cyclin D1 were detected by real-time PCR and Western blotting. Next, the luciferase assay was used to confirm that cyclin D1 is a target gene for miR-210. Cell cycle and cell proliferation were detected in CNE-1 cells that were cultured under hypoxic conditions with either overexpression or knockout of miR-210 using flow cytometry and MTT assay, respectively. Results： Hypoxia induced the expression of miR-210, resulting in reduced mRNA and protein levels of cyclin D1 and repression of cyclin D1 in CNE-1 cells. Further analysis indicated that miR-210 directly binded to the 3＇UTR of the cyclin D1 gene, thus regulated the expression of cyclin DI. The flow cytometry assay showed that, under hypoxic conditions, miR-210 blocked CNE-1 cells in the G1 phase, and miR-210 also inhibited the proliferation of CNE-1 cells. Conclusion： Under hypoxic conditions, miR-210 directly reduced the expression of cyclin D1, leading to CNE-1 cells blocked in G1 phase.
