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Alaee, R.; Albooyeh, M.; Yazdi, M.; Komjani, N.; Simovski, C.; Lederer, F.; Rockstuhl, C. We explore the optical properties of a meta-atom made of plasmonic nanopatches that possess an increasing degree of complexity. We show that if two nanopatches are strongly coupled and have a different geometrical footprint, the meta-atom exhibits a resonant magnetoelectric response, in addition to the anticipated resonant electric and magnetic response. Thus, it behaves similarly as the so-called omega particle, but with the unique advantage that frequency and strength of this magnetoelectric resonance can be independently tuned and modified with respect to the corresponding values of the electric resonance. This allows a metasurface of such meta-atoms to possess widely controlled reflection and transmission coefficients, e.g., the regimes of strongly asymmetric reflectance and perfect absorption become possible. Alternatively, an individual meta-atom of such kind can act as a directive nanoantenna with zero backscattered fields (Huygens' scatterer). Magneto-electric coupling in nonidentical plasmonic nanoparticles: Theory and applications

An indispensable role of macrophages in bone repair has been well recognized. Previous data have demonstrated the copresence of M1 macrophages and mesenchymal stem cells (MSCs) during the proinflammatory stage of bone repair. However, the exact role of M1 macrophages in MSC function and bone repair is unknown. This study aimed to define the role of M1 macrophages at bone injury sites via the function of 1,25-Dihydroxyvitamin D (1,25[OH]2D) in suppressing M1 but promoting M2 differentiation. We showed that 1,25(OH)2D suppressed M1 macrophage-mediated enhancement of MSC migration. Additionally, 1,25(OH)2D inhibited M1 macrophage secretion of osteogenic proteins (i.e., Oncostatin M, TNF-α, and IL-6). Importantly, the 1,25(OH)2D-mediated suppression of osteogenic function in M1 macrophages at the proinflammatory stage was associated with 1,25(OH)2D-mediated reduction of MSC abundance, compromised osteogenic potential of MSCs, and impairment of fracture repair. Furthermore, outside the proinflammatory stage, 1,25(OH)2D treatment did not suppress fracture repair. Accordingly, our data support 2 conclusions: (a) M1 macrophages are important for the recruitment and osteogenic priming of MSCs and, hence, are necessary for fracture repair, and (b) under vitamin D-sufficient conditions, 1,25(OH)2D treatment is unnecessary and can be detrimental if provided during the proinflammatory stage of fracture healing.

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