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To design a promising Al—Si filler alloy with a relatively low melting-point, good strength and plasticity for the Cu/Al joint, the Cu, Ni, Zr and Er elements were innovatively added to modify the traditional Al—Si eutectic filler. The microstructure and mechanical properties of filler alloys and Cu/Al joints were investigated. The result indicated that the Al—Si—Ni—Cu filler alloys mainly consisted of Al(s,s), Al2(Cu,Ni) and Si(s,s). The Al—10Si—2Ni—6Cu filler alloy exhibited relatively low solidus (521 °C) and liquidus (577 °C) temperature, good tensile strength (305.8 MPa) and fracture elongation (8.5%). The corresponding Cu/Al joint brazed using Al—10Si—2Ni—6Cu filler was mainly composed of Al8(Mn,Fe)2Si, Al2(Cu,Ni)3, Al(Cu,Ni), Al2(Cu,Ni) and Al(s,s), yielding a shear strength of (90.3±10.7) MPa. The joint strength was further improved to (94.6±2.5) MPa when the joint was brazed using the Al—10Si—2Ni—6Cu—0.2Er—0.2Zr filler alloy. Consequently, the (Cu, Ni, Zr, Er)-modified Al—Si filler alloy was suitable for obtaining high-quality Cu/Al brazed joints.

Background: Breast Cancer (BC) is the leading cause of cancer-related deaths among women. As such, novel chemotherapeutic agents are urgently needed, especially for Triple-Negative Breast Cancer (TNBC). Hydroxytyrosol (HT) and Oleuropein (OL) are rich in olive oil, which is associated with a low occurrence of BC. However, the effects and mechanisms of action of HT and OL in BC cells are still unclear. This study aimed to explore the molecular mechanisms underlying the antitumor effect of HT and OL in TNBC. Methods: TNBC MDA-MB-231 cells were treated with HT and OL in combination with Hepatocyte Growth Factor (HGF), rapamycin (Rapa, an inducer of autophagy) or 3-methyladenine (3-MA, an inhibitor of autophagy). Cell viability, migration, invasion, and autophagy signaling were analyzed by scratch assays, transwell migration assays, and Western blot analysis. Results: Treatment with HT or OL reduced MDA-MB-231 cell viability in a dose-dependent manner. MDAMB- 231 cells were more sensitive to HT treatment than OL treatment. Rapa treatment could significantly block HGF-induced MDA-MB-231 cell migration and invasion, suggesting that inhibition of autophagy could promote migration and invasion. Moreover, HT or OL treatment significantly suppressed HGF or 3-MA induced cell migration and invasion by reversing LC3-II/LC3-I and Beclin-1 downregulation and reversing p62 upregulation. Conclusion: These data indicated that HT and OL may inhibit migration and invasion of TNBC cells by activating autophagy. These findings provide potential therapeutic strategies that target autophagy to limit the pathogenesis and progression of BC.