Cu/Al bar clad material was fabricated by a drawing process and a subsequent heat treatment.During these processes,intermetallic compounds have been formed at the interface of Cu/Al and have affected its bonding prope...Cu/Al bar clad material was fabricated by a drawing process and a subsequent heat treatment.During these processes,intermetallic compounds have been formed at the interface of Cu/Al and have affected its bonding property.Microstructures of Cu/Al interfaces were observed by OM,SEM and EDX Analyser in order to investigate the bonding properties of the material.According to the microstructure a series of diffusion layers were observed at the interface and the thicknesses of diffusion layers have increased with aging time as a result of the diffusion bonding.The interfaces were composed of 3-ply diffusion layers and their compositions were changed with aging time at 400 °C.These compositional compounds were revealed to be η2,(θ+η2),(α+θ) intermetallic phases.It is evident from V-notch impact tests that the growth of the brittle diffusion layers with the increasing aging time directly influenced delamination distance between the Cu sleeve and the Al core.It is suggested that the proper holding time at 400 °C for aging as post heat treatment of a drawn Cu/Al bar clad material would be within 1 h.展开更多
Apoptotic cell clearance by phagocytes is essential in tissue homeostasis.We demonstrated that conditioned medium(CM)from macrophages exposed to apoptotic cancer cells inhibits the TGFβ1-induced epithelial–mesenchym...Apoptotic cell clearance by phagocytes is essential in tissue homeostasis.We demonstrated that conditioned medium(CM)from macrophages exposed to apoptotic cancer cells inhibits the TGFβ1-induced epithelial–mesenchymal transition(EMT),migration,and invasion of cancer cells.Apoptotic 344SQ(ApoSQ)cell-induced PPARγactivity in macrophages increased the levels of PTEN,which was secreted in exosomes.Exosomal PTEN was taken up by recipient lung cancer cells.ApoSQ-exposed CM from PTEN knockdown cells failed to enhance PTEN in 344SQ cells,restore cellular polarity,or exert anti-EMT and anti-invasive effects.The CM that was deficient in PPARγligands,including 15-HETE,lipoxin A4,and 15d-PGJ2,could not reverse the suppression of PPARγactivity or the PTEN increase in 344SQ cells and consequently failed to prevent the EMT process.Moreover,a single injection of ApoSQ cells inhibited lung metastasis in syngeneic immunocompetent mice with enhanced PPARγ/PTEN signaling both in tumorassociated macrophages and in tumor cells.PPARγantagonist GW9662 reversed the signaling by PPARγ/PTEN;the reduction in EMT-activating transcription factors,such as Snai1 and Zeb1;and the antimetastatic effect of the ApoSQ injection.Thus,the injection of apoptotic lung cancer cells may offer a new strategy for the prevention of lung metastasis.展开更多
基金Project supported by the Fundamental Materials Development funded by the Korean Ministry of Knowledge Economy
文摘Cu/Al bar clad material was fabricated by a drawing process and a subsequent heat treatment.During these processes,intermetallic compounds have been formed at the interface of Cu/Al and have affected its bonding property.Microstructures of Cu/Al interfaces were observed by OM,SEM and EDX Analyser in order to investigate the bonding properties of the material.According to the microstructure a series of diffusion layers were observed at the interface and the thicknesses of diffusion layers have increased with aging time as a result of the diffusion bonding.The interfaces were composed of 3-ply diffusion layers and their compositions were changed with aging time at 400 °C.These compositional compounds were revealed to be η2,(θ+η2),(α+θ) intermetallic phases.It is evident from V-notch impact tests that the growth of the brittle diffusion layers with the increasing aging time directly influenced delamination distance between the Cu sleeve and the Al core.It is suggested that the proper holding time at 400 °C for aging as post heat treatment of a drawn Cu/Al bar clad material would be within 1 h.
基金supported by the Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Science,ICT,Future Planning(2015R1A2A1A15053112,2017R1A2B2004864,and 2010-0027945).
文摘Apoptotic cell clearance by phagocytes is essential in tissue homeostasis.We demonstrated that conditioned medium(CM)from macrophages exposed to apoptotic cancer cells inhibits the TGFβ1-induced epithelial–mesenchymal transition(EMT),migration,and invasion of cancer cells.Apoptotic 344SQ(ApoSQ)cell-induced PPARγactivity in macrophages increased the levels of PTEN,which was secreted in exosomes.Exosomal PTEN was taken up by recipient lung cancer cells.ApoSQ-exposed CM from PTEN knockdown cells failed to enhance PTEN in 344SQ cells,restore cellular polarity,or exert anti-EMT and anti-invasive effects.The CM that was deficient in PPARγligands,including 15-HETE,lipoxin A4,and 15d-PGJ2,could not reverse the suppression of PPARγactivity or the PTEN increase in 344SQ cells and consequently failed to prevent the EMT process.Moreover,a single injection of ApoSQ cells inhibited lung metastasis in syngeneic immunocompetent mice with enhanced PPARγ/PTEN signaling both in tumorassociated macrophages and in tumor cells.PPARγantagonist GW9662 reversed the signaling by PPARγ/PTEN;the reduction in EMT-activating transcription factors,such as Snai1 and Zeb1;and the antimetastatic effect of the ApoSQ injection.Thus,the injection of apoptotic lung cancer cells may offer a new strategy for the prevention of lung metastasis.
