To improve the properties of Sn10Sb8Cu solder alloy, two new solders (SnSbCuAg and SnSbCuNi) were formed by adding small amounts of Ag or Ni into the solder alloy. The results show that the melting point of the SnSb...To improve the properties of Sn10Sb8Cu solder alloy, two new solders (SnSbCuAg and SnSbCuNi) were formed by adding small amounts of Ag or Ni into the solder alloy. The results show that the melting point of the SnSbCuAg solder alloy decreases by 14.1℃ and the spreading area increases by 16.5% compared to the matrix solder. The melting point of the SnSbCuNi solder alloy decreases by 5.4℃ and the spreading area is slightly less than that of the matrix solder. Microstructure analysis shows that adding trace Ag makes the melting point decline due to the dispersed distribution of SnAg phase with low melting point. Adding trace Ni, Cu6Sn5 and (Cu, Ni)6Sn5 with polyhedron shape on the copper substrate can be easily seen in the SnSbCuNi solder alloy, which makes the viscosity of the melting solder increase and the spreading property of the solder decline.展开更多
Cardiopulmonary bypass has been speculated to elicit systemic inflammation to initiate acute lung injury(ALI), including acute respiratory distress syndrome(ARDS), in patients after cardiac surgery. We previously foun...Cardiopulmonary bypass has been speculated to elicit systemic inflammation to initiate acute lung injury(ALI), including acute respiratory distress syndrome(ARDS), in patients after cardiac surgery. We previously found that post-operative patients showed an increase in endothelial cell-derived extracellular vesicles(eEVs) with components of coagulation and acute inflammatory responses. However, the mechanism underlying the onset of ALI owing to the release of e EVs after cardiopulmonary bypass, remains unclear. Plasma plasminogenactivated inhibitor-1(PAI-1) and eEV levels were measured in patients with cardiopulmonary bypass. Endothelial cells and mice(C57BL/6,Toll-like receptor 4 knockout(TLR4^(-/-))) and inducible nitric oxide synthase knockout(iNOS^(-/-)) were challenged with eEVs isolated from PAI-1-stimulated endothelial cells. Plasma PAI-1 and eEVs were remarkably enhanced after cardiopulmonary bypass. Plasma PAI-1 elevation was positively correlated with the increase in eEVs. The increase in plasma PAI-1 and eEV levels was associated with post-operative ARDS. The eEVs derived from PAI-1-stimulated endothelial cells could recognize TLR4 to stimulate a downstream signaling cascade identified as the Janus kinase 2/3(JAK2/3)-signal transducer and activator of transcription 3(STAT3)-interferon regulatory factor 1(IRF-1)pathway, along with i NOS induction, and cytokine/chemokine production in vascular endothelial cells and C57BL/6 mice, ultimately contributing to ALI. ALI could be attenuated by JAK2/3 or STAT3 inhibitors(AG490 or S3I-201, respectively), and was relieved in TLR4-/-and iNOS-/-mice. eEVs activate the TLR4/JAK3/STAT3/IRF-1 signaling pathway to induce ALI/ARDS by delivering follistatin-like protein 1(FSTL1), and FSTL1 knockdown in eEVs alleviates eEV-induced ALI/ARDS. Our data thus demonstrate that cardiopulmonary bypass may increase plasma PAI-1 levels to induce FSTL1-enriched eEVs, which target the TLR4-mediated JAK2/3/STAT3/IRF-1 signaling cascade and form a positive feedback loop, leading to ALI/ARDS after cardiac surgery. Our findings provide new insight into the molecular mechanisms and therapeutic targets for ALI/ARDS after cardiac surgery.展开更多
基金supported by the Program for Science & Technology Innovation Talents in Universities of Henan Province (No.2010HASTIT032)the City Key Technologies R & D Program of Luoyang (No.0801038A), China
文摘To improve the properties of Sn10Sb8Cu solder alloy, two new solders (SnSbCuAg and SnSbCuNi) were formed by adding small amounts of Ag or Ni into the solder alloy. The results show that the melting point of the SnSbCuAg solder alloy decreases by 14.1℃ and the spreading area increases by 16.5% compared to the matrix solder. The melting point of the SnSbCuNi solder alloy decreases by 5.4℃ and the spreading area is slightly less than that of the matrix solder. Microstructure analysis shows that adding trace Ag makes the melting point decline due to the dispersed distribution of SnAg phase with low melting point. Adding trace Ni, Cu6Sn5 and (Cu, Ni)6Sn5 with polyhedron shape on the copper substrate can be easily seen in the SnSbCuNi solder alloy, which makes the viscosity of the melting solder increase and the spreading property of the solder decline.
基金supported by the National Key Research and Development Program of China(2021YFA0805100)the National Natural Science Foundation of China(81830013,81770241,81970363,82000362,92268202,81170271,81370370,81490531,81670392,81600382)+6 种基金the National Natural Science Foundation of China Distinguished Young Scholar Grant(81325001)“973 Project”from the Ministry of Science and Technology of China(2009CB522104)Guangdong Basic and Applied Basic Research Foundation,China(2019B1515120092)the Science and Technology Planning Project of Guangzhou,China(202103000016)the Changjiang Scholars Program from the Ministry of Education of Chinathe Sun Yat-sen University Clinical Research 5010 Programthe Program of National Key Clinical Specialties。
文摘Cardiopulmonary bypass has been speculated to elicit systemic inflammation to initiate acute lung injury(ALI), including acute respiratory distress syndrome(ARDS), in patients after cardiac surgery. We previously found that post-operative patients showed an increase in endothelial cell-derived extracellular vesicles(eEVs) with components of coagulation and acute inflammatory responses. However, the mechanism underlying the onset of ALI owing to the release of e EVs after cardiopulmonary bypass, remains unclear. Plasma plasminogenactivated inhibitor-1(PAI-1) and eEV levels were measured in patients with cardiopulmonary bypass. Endothelial cells and mice(C57BL/6,Toll-like receptor 4 knockout(TLR4^(-/-))) and inducible nitric oxide synthase knockout(iNOS^(-/-)) were challenged with eEVs isolated from PAI-1-stimulated endothelial cells. Plasma PAI-1 and eEVs were remarkably enhanced after cardiopulmonary bypass. Plasma PAI-1 elevation was positively correlated with the increase in eEVs. The increase in plasma PAI-1 and eEV levels was associated with post-operative ARDS. The eEVs derived from PAI-1-stimulated endothelial cells could recognize TLR4 to stimulate a downstream signaling cascade identified as the Janus kinase 2/3(JAK2/3)-signal transducer and activator of transcription 3(STAT3)-interferon regulatory factor 1(IRF-1)pathway, along with i NOS induction, and cytokine/chemokine production in vascular endothelial cells and C57BL/6 mice, ultimately contributing to ALI. ALI could be attenuated by JAK2/3 or STAT3 inhibitors(AG490 or S3I-201, respectively), and was relieved in TLR4-/-and iNOS-/-mice. eEVs activate the TLR4/JAK3/STAT3/IRF-1 signaling pathway to induce ALI/ARDS by delivering follistatin-like protein 1(FSTL1), and FSTL1 knockdown in eEVs alleviates eEV-induced ALI/ARDS. Our data thus demonstrate that cardiopulmonary bypass may increase plasma PAI-1 levels to induce FSTL1-enriched eEVs, which target the TLR4-mediated JAK2/3/STAT3/IRF-1 signaling cascade and form a positive feedback loop, leading to ALI/ARDS after cardiac surgery. Our findings provide new insight into the molecular mechanisms and therapeutic targets for ALI/ARDS after cardiac surgery.