Intrinsic spin Hall effect in monolayers of group-VI dichalcogenides: A first-principles study

Using first-principles calculations within density functional theory, we investigate the intrinsic spin Hall effect in monolayers of group-VI transition-metal dichalcogenides MX2 (M = Mo, W and X = S, Se). MX2 monolayers are direct band-gap semiconductors with two degenerate valleys located at the corners of the hexagonal Brillouin zone. Because of the inversion symmetry breaking and the strong spin-orbit coupling, charge carriers in opposite valleys carry opposite Berry curvature and spin moment, giving rise to both a valley- and a spin-Hall effect. The intrinsic spin Hall conductivity (ISHC) in p-doped samples is found to be much larger than the ISHC in n-doped samples due to the large spin-splitting at the valence band maximum. We also show that the ISHC in inversion-symmetric bulk dichalcogenides is an order of magnitude smaller compared to monolayers. Our result demonstrates monolayer dichalcogenides as an ideal platform for the integration of valleytronics and spintronics.Comment: published version (7 pages, 6 figures

Strain tuning of topological band order in cubic semiconductors

We theoretically explore the possibility of tuning the topological order of cubic diamond/zinc-blende semiconductors with external strain. Based on the tight-binding model, we analyze the evolution of the cubic semiconductor band structure under hydrostatic or biaxial lattice expansion, by which a generic guiding principle is established that lattice \emph{expansion} can induce a topological phase transition of small band-gap cubic semiconductors via a band inversion, and further breaking of the cubic symmetry leads to a topological insulating phase. Using density functional theory calculations, we demonstrate that a prototype topological trivial semiconductor, InSb, is converted to a nontrivial topological semiconductor with a 2%-3% biaxial lattice expansion.Comment: 4 pages, 3 figure

Half-Heusler Compounds as a New Class of Three-Dimensional Topological Insulators

Using first-principles calculations within density functional theory, we explore the feasibility of converting ternary half-Heusler compounds into a new class of three-dimensional topological insulators (3DTI). We demonstrate that the electronic structure of unstrained LaPtBi as a prototype system exhibits distinct band-inversion feature. The 3DTI phase is realized by applying a uniaxial strain along the [001] direction, which opens a bandgap while preserving the inverted band order. A definitive proof of the strained LaPtBi as a 3DTI is provided by directly calculating the topological Z2 invariants in systems without inversion symmetry. We discuss the implications of the present study to other half-Heusler compounds as 3DTI, which, together with the magnetic and superconducting properties of these materials, may provide a rich platform for novel quantum phenomena.Comment: 4 pages, 5 figures; Phys. Rev. Lett. (in press

Estrogen Modulates NFκB Signaling by Enhancing IκBα Levels and Blocking p65 Binding at the Promoters of Inflammatory Genes via Estrogen Receptor-β

NFκB signaling is critical for expression of genes involved in the vascular injury response. We have shown that estrogen (17β-estradiol, E2) inhibits expression of these genes in an estrogen receptor (ER)-dependent manner in injured rat carotid arteries and in tumor necrosis factor (TNF)-α treated rat aortic smooth muscle cells (RASMCs). This study tested whether E2 inhibits NFκB signaling in RASMCs and defined the mechanisms.TNF-α treated RASMCs demonstrated rapid degradation of IκBα (10-30 min), followed by dramatic increases in IκBα mRNA and protein synthesis (40-60 min). E2 enhanced TNF-α induced IκBα synthesis without affecting IκBα degradation. Chromatin immunoprecipitation (ChIP) assays revealed that E2 pretreatment both enhanced TNF-α induced binding of NFκB p65 to the IκBα promoter and suppressed TNF-α induced binding of NFκB p65 to and reduced the levels of acetylated histone 3 at promoters of monocyte chemotactic protein (MCP)-1 and cytokine-induced neutrophil chemoattractant (CINC)-2β genes. ChIP analyses also demonstrated that ERβ can be recruited to the promoters of MCP-1 and CINC-2β during co-treatment with TNF-α and E2.These data demonstrate that E2 inhibits inflammation in RASMCs by two distinct mechanisms: promoting new synthesis of IκBα, thus accelerating a negative feedback loop in NFκB signaling, and directly inhibiting binding of NFκB to the promoters of inflammatory genes. This first demonstration of multifaceted modulation of NFκB signaling by E2 may represent a novel mechanism by which E2 protects the vasculature against inflammatory injury

Ferritin Light Chain Confers Protection Against Sepsis-Induced Inflammation and Organ Injury

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Cardiomyopathy and Response to Enzyme Replacement Therapy in a Male Mouse Model for Fabry Disease

Fabry disease is an X-linked disorder of glycosphingolipid metabolism that results in progressive accumulation of neutral glycosphingolipids, (predominately globotriaosylceramide; GL-3) in lysosomes, as well as other cellular compartments and the extracellular space. Our aim was to characterize the cardiac phenotype of male knock-out mice that are deficient in alpha-galactosidase A activity, as a model for Fabry disease and test the efficacy of Enzyme Replacement Therapy with agalsidase-beta. Male mice (3–4 months of age) were characterized with awake blood pressure and heart rate measurements, cardiac echocardiography and electrocardiography measurements under light anesthesia, histological studies and molecular studies with real-time polymerase chain reaction. The Fabry knock-out mouse has bradycardia and lower blood pressure than control wild type (CB7BL/6J) mice. In Fabry knock-out mice, the cardiomyopathy associated mild hypertrophy at echography with normal systolic LV function and mild diastolic dysfunction. Premature atrial contractions were more frequent in without conduction defect. Heart weight normalized to tibial length was increased in Fabry knock-out mice. Ascending aorta dilatation was observed. Molecular studies were consistent with early stages of cardiac remodeling. A single dose of agalsidase-beta (3 mg/kg) did not affect the LV hypertrophy, function or heart rate, but did improve the mRNA signals of early cardiac remodeling. In conclusion, the alpha-galactosidase A deficient mice at 3 to 4 months of age have cardiac and vascular alterations similar to that described in early clinical stage of Fabry disease in children and adolescents. Enzyme replacement therapy affects cardiac molecular remodeling after a single dose