Controlling the Magnetic Anisotropy of the van der Waals Ferromagnet Fe3GeTe2 through Hole Doping.

Identifying material parameters affecting properties of ferromagnets is key to optimized materials that are better suited for spintronics. Magnetic anisotropy is of particular importance in van der Waals magnets, since it not only influences magnetic and spin transport properties, but also is essential to stabilizing magnetic order in the two-dimensional limit. Here, we report that hole doping effectively modulates the magnetic anisotropy of a van der Waals ferromagnet and explore the physical origin of this effect. Fe3-xGeTe2 nanoflakes show a significant suppression of the magnetic anisotropy with hole doping. Electronic structure measurements and calculations reveal that the chemical potential shift associated with hole doping is responsible for the reduced magnetic anisotropy by decreasing the energy gain from the spin-orbit induced band splitting. Our findings provide an understanding of the intricate connection between electronic structures and magnetic properties in two-dimensional magnets and propose a method to engineer magnetic properties through doping

Phagosome Escape of Rough Mycobacterium abscessus Strains in Murine Macrophage via Phagosomal Rupture Can Lead to Type I Interferon Production and Their Cell-To-Cell Spread

Mycobacterium abscessus complex (MAB) is a rapidly growing mycobacterium(RGM) whose clinical significance as an emerging human pathogen has been increasing worldwide. It has two types of colony morphology, a smooth (S) type, producing high glycopeptidolipid (GPL) content, and a rough (R) type, which produces low levels of GPLs and is associated with increased virulence. However, the mechanism responsible for their difference in virulence is poorly known. By ultrastructural examination of murine macrophages infected, we found that MAB-R strains could replicate more actively in the macrophage phagosome than the S variants and that they could escape into cytosol via phagosomal rupture. The cytosolic access of MAB-R strains via phagosomal rupture led to enhanced Type I interferon (IFN) production and cell death, which resulted in their cell-to-cell spreading. This behavior can provide an additional niche for the survival of MAB-R strains. In addition, we found that their enhancement of cell death mediated cell spreading are dependent on Type I IFN signaling via comparison of wild-type and IFNAR1 knockout mice. In conclusion, our data indicated that a transition of MAB-S strains into MAB-R variants increased their virulence via enhanced Type I IFN production, which led to enhanced survival in infected macrophage via cell death mediated cell-to-cell spreading. This result provides not only a novel insight into the difference in virulence between MAB-R and -S variants but also hints to their treatment strategy

Metabolic engineering of a reduced-genome strain of Escherichia coli for L-threonine production

© 2009 Lee et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens