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Topological surface-states can acquire an energy gap when time-reversal symmetry is broken by interfacing with a magnetic insulator. This gap has yet to be measured. Such topological-magnetic insulator heterostructures can host a quantized anomalous Hall effect and can allow the control of the magnetic state of the insulator in a spintronic device. In this work, we observe the energy gap of topological surface-states in proximity to a magnetic insulator using magnetooptical Landau level spectroscopy. We measure Pb1-xSnxSe–EuSe heterostructures grown by molecular beam epitaxy exhibiting a record mobility and low Fermi energy. Through temperature dependent measurements and theoretical calculations, we show this gap is likely due to quantum confinement and conclude that the magnetic proximity effect is weak in this system. This weakness is disadvantageous for the realization of the quantum anomalous Hall effect, but favorable for spintronic devices which require the preservation of spin-momentum locking at the Fermi level. The proximity coupling of topological insulators with magnetic materials can give rise to exotic phenomenon such as the quantum anomalous Hall effect. Here, the authors use magneto-optical Landau level spectroscopy to investigate Pb1-xSnxSe-EuSe heterostructures finding evidence of a quantum confinement induced energy gaps in the topological surface states, that overshadow the magnetic proximity effects. [ABSTRACT FROM AUTHOR]

Interactions of leukocytes with the vascular endothelium culminating in their diapedesis represent not only a crucial event in immune surveillance and defense but are also critically involved in the pathogenesis of many inflammatory diseases, including atherosclerosis. Our previous in vitro studies using atomic force microscopy measurement of monocyte-endothelial cell interaction have demonstrated that a cyclic arginine-glycine-aspartic acid peptide (cRGD) inhibited their adhesion through very late antigen (α4β1-integrin; VLA4)-vascular cell adhesion molecule-i by 60% with the IC50 = 100 nM. To elucidate the potential efficacy of this peptide in vivo in preventing atherogenesis, experiments were performed in apolipoprotein E (ApoE)-deficient (-/-) mice fed a Western diet and receiving chronic treatment with cRGD peptide for 2-4 wk. In addition, some animals were subjected to a temporary carotid artery ligation while receiving the above treatment. Formation of fatty streaks and infiltration of the vascular wall with macrophages were not affected by cRGD treatment. Infiltration of the carotid artery postligation was significantly reduced in the cRGD-treated animals, as was the lipid accumulation. Furthermore, cRGD-treated ApoE-/- mice exhibited significantly lesser macrophage infiltration and lipid accumulation in the kidneys, the site of the highest expression of VLA4, These data demonstrated that cRGD peptide is a potent inhibitor of monocyte/macrophage infiltration of the injured macrovasculature and of the renal microvasculature, where it results in the attenuation of lipid accumulation. Formation of fatty streaks in the aortic root was not inhibitable by this treatment. [ABSTRACT FROM AUTHOR]