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The atomic packing structure of Al 90.5 Y 9.5 , Al 89.5 Fe 4.5 Y 6 , Al 85.5 Ni 9.5 Y 5 , Al 89 Co 5.5 Y 5.5 and Al 85.5 Co 9.5 Y 5 metallic glasses (MGs) was studied using the extended X-ray absorption fine structure (EXAFS) technique, and the atomic packing efficiency (APE) of solute-centered clusters was calculated. The results indicated that both Co- and Y-centered clusters possess higher APE in Al 89 Co 5.5 Y 5.5 MG than in Al 85.5 Co 9.5 Y 5 MG, due to which the former has the best glass-forming ability (GFA) in Al–Co–Y system. The chemical property of transition metals (TMs) influences the medium range ordering, i.e. the connection of solute-centered clusters. As TM element changes from Fe, Co to Ni, the TM-centered clusters tend to share more and more Al atoms, resulting in the sequential increase of the concentration ratio of TM/Y in Al 89.5 Fe 4.5 Y 6 , Al 89 Co 5.5 Y 5.5 and Al 85.5 Ni 9.5 Y 5 MGs that have the best GFA in their respective alloy system. • EXAFS of several Al–Y, Al-TM-Y (TM = Fe, Ni, Co) metallic glasses are measured. • Coordination numbers of Al around TM and Y atoms and interatomic distance were determined. • Atomic packing efficiency of solute-centered clusters was evaluated. • The way for TM-centered clusters to connect depends on the type of TM. • Difference in glass-forming ability was analyzed. [ABSTRACT FROM AUTHOR]

Background: A key cause of the high mortality of cardiovascular diseases is the cardiomyocyte inability to renew after cardiac injury. As a promising strategy to supplement functional myocytes for cardiac repair, there is a pressing need to understand the cellular and molecular mechanisms of heart regeneration., Methods: Seven genetic mouse lines were used: global OSM (oncostatin M) knockout, monocyte-/macrophage-specific OSM deletion, cardiomyocyte-specific lines, including OSM receptor deletion, gp130 (glycoprotein 130) deletion, gp130 activation, and Yap (yes-associated protein) ablation with gp130 activation mice. A series of molecular signaling experiments, including RNA sequencing, immunostaining, coimmunoprecipitation, and imaging flow cytometry, were conducted. Two models of cardiac injury, apical resection and myocardial infarction operation, were performed in neonatal, juvenile, and adult mice. Heart regeneration and cardiac function were evaluated by Masson staining and echocardiography, respectively. Gene recombinant adenovirus-associated virus was constructed and infected myocardial-infarcted mice as a gene therapy., Results: OSM was identified by RNA sequencing as a key upstream regulator of cardiomyocyte proliferation during neonatal heart regeneration in mice. Cardiomyocyte proliferation and heart regeneration were suspended in neonatal mice after cardiac injury when OSM was conditionally knockout in macrophages. The cardiomyocyte-specific deficiency of the OSM receptor heterodimers, OSM receptor and gp130, individually in cardiomyocytes reduced myocyte proliferation and neonatal heart regeneration. Conditional activation of gp130 in cardiomyocytes promoted cardiomyocyte proliferation and heart regeneration in juvenile and adult mice. Using RNA sequencing and functional screening, we found that Src mediated gp130-triggered cardiomyocyte proliferation by activating Yap (yes-associated protein) with Y357 phosphorylation independently of the Hippo pathway. Cardiomyocyte-specific deletion of Yap in Myh6-gp130 ACT mice blocked the effect of gp130 activation-induced heart regeneration in juvenile mice. Gene therapy with adenovirus-associated virus encoding constitutively activated gp130 promoted cardiomyocyte proliferation and heart regeneration in adult mice after myocardial infarction., Conclusions: Macrophage recruitment is essential for heart regeneration through the secretion of OSM, which promotes cardiomyocyte proliferation. As the coreceptor of OSM, gp130 activation is sufficient to promote cardiomyocyte proliferation by activating Yap through Src during heart regeneration. gp130 is a potential therapeutic target to improve heart regeneration after cardiac injury.