Using x-ray photoemission electron microscopy and the magneto-optical Kerr effect, we have demonstrated a perpendicular magnetic anisotropy that could be due to exchange coupling between the ferromagnetic and antiferromagnetic layers. The results of magnetic imaging and hysteresis loops show that the magnetization of Fe and permalloy (Py) films orients from the in-plane to perpendicular direction, as an Mn underlayer is above a threshold value that depends on the Fe or Py layer thickness. Their thickness-dependent behaviors can be quantitatively described by a phenomenological model that takes into account the finite-size effect of the antiferromagnet on exchange coupling. The anisotropy energy extracted from the model and the thermal stability of perpendicular magnetization enhanced with the increase of the Mn underlayer further demonstrate the exchange coupling nature.
Breast cancer cells release a large quantity of biocargo-bearing extracellular vesicles (EVs), which mediate intercellular communication within the tumour microenvironment and promote metastasis. To identify EV-bound proteins related to metastasis, we used mass spectrometry to profile EVs from highly and poorly metastatic breast cancer lines of human and mouse origins. Comparative mass spectrometry indicated that integrins, including αv and β1 subunits, are preferentially enriched in EVs of highly metastatic origin over those of poorly metastatic origin. These results are consistent with our histopathological findings, which show that integrin αv is associated with disease progression in breast cancer patients. Integrin αv colocalizes with the multivesicular-body marker CD63 at a higher frequency in the tumour and is enriched in circulating EVs of breast cancer patients at late stages when compared with circulating EVs from early-stage patients. With a magnetic bead-based flow cytometry assay, we confirmed that integrins αv and β1 are enriched in the CD63 + subsets of EVs from both human and mouse highly metastatic cells. By analysing the level of integrin αv on circulating EVs, this assay could predict the metastatic potential of a xenografted mouse model. To explore the export mechanism of integrins into EVs, we performed immunoprecipitation mass spectrometry and identified members of the galectin family as potential shuttlers of integrin αvβ1 into EVs. In particular, knockdown of galectin-3, but not galectin-1, causes a reduction in the levels of cell surface integrins β1 and αv, and decreases the colocalization of these integrins with CD63. Importantly, knockdown of galectin-3 leads to a decrease of integrin αvβ1This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Children's food approach and food avoidance are appetitive traits with genetic or biological bases. Nonetheless, parents play a critical role in children's dietary intake through parenting and feeding practices. The present study tested parents' controlling feeding practices (i.e., restriction and pressure to eat) as mediating mechanisms between child appetitive traits and child BMI in an economically and ethnically diverse sample. Participants were 139 children aged 4 to 6 years (51.8% males, M = 4.77 years, SD = 0.84) and their parents. Results showed that restriction and pressure to eat mediated the relation between child food approach or food avoidance and child BMI. Mediation effects did not differ across poverty status or ethnic groups. Also, the type of controlling feeding that parents exert related to children's weight status in diametrically different or opposite ways. Thus, food-related parenting appears to be a promising point of entry for childhood obesity prevention programs. Findings are consistent with a biopsychosocial model of the development of eating and weight in childhood which takes into account both parent and child behavior and characteristics and links child biology and behavior with psychosocial processes and environment.
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