Silicon surface with giant spin-splitting

We demonstrate the induction of a giant Rashba-type spin-splitting on a semiconducting substrate by means of a Bi trimer adlayer on a Si(111) wafer. The in-plane inversion symmetry is broken so that the in-plane potential gradient induces a giant spin-splitting with a Rashba energy of about 140 meV, which is more than an order of magnitude larger than what has previously been reported for any semiconductor heterostructure. The separation of the electronic states is larger than their lifetime broadening, which has been directly observed with angular resolved photoemission spectroscopy. The experimental results are confirmed by relativistic first-principles calculations. We envision important implications for basic phenomena as well as for the semiconductor based technology

Tight-binding study of high-pressure phase transitions in titanium: alpha to omega and beyond

We use a tight-binding total energy method, with parameters determined from a fit to first-principles calculations, to examine the newly discovered gamma phase of titanium. Our parameters were adjusted to accurately describe the alpha Ti-omega Ti phase transition, which is misplaced by density functional calculations. We find a transition from omega Ti to gamma Ti at 102 GPa, in good agreement with the experimental value of 116 GPa. Our results suggest that current density functional calculations will not reproduce the omega Ti-gamma Ti phase transition, but will instead predict a transition from omega Ti to the bcc beta Ti phase.Comment: 3 encapsulated Postscript figures, submitted to Phyical Review Letter

A density functional study of pressure induced superconductivity in P and its implication for spintronics

The stability of high-pressure phases of P has been studied using density functional theory and the local density approximation. Using a linear response technique, we have calculated the phonon spectrum and electron-phonon interaction for bcc P and predict it to be superconducting with $T_c$ of 19 K. We propose that this phase might be realized in epitaxial thin films using templates such as V(100), Fe(100) or Cr(100) relevant to spintronics applications.Comment: 4 pages, 4 figure

The hyperfine properties of a hydrogenated Fe/V superlattice

: We study the effect of hydrogen on the electronic, magnetic and hyperfine structures of an iron-vanadium superlattice consisting of three Fe monolayers and nine V monolayers. The contact charge density ({\rho}), the contact hyperfine field (Bhf) and the electronic field gradient (EFG) at the Fe sites for different H locations and H fillings are calculated using the first principle full-potential linear-augmented-plane-wave (FP-LAPW) method . It is found that sizeable changes in the hyperfine properties are obtained only when H is in the interface region.Comment: 6 pages, 2 figures, 3 tables, ICAME 2011 conference (Kobe, Japan

HVEM Signalling Promotes Colitis

Background Tumor necrosis factor super family (TNFSF) members regulate important processes involved in cell proliferation, survival and differentiation and are therefore crucial for the balance between homeostasis and inflammatory responses. Several members of the TNFSF are closely associated with inflammatory bowel disease (IBD). Thus, they represent interesting new targets for therapeutic treatment of IBD. Methodology/Principal Findings We have used mice deficient in TNFSF member HVEM in experimental models of IBD to investigate its role in the disease process. Two models of IBD were employed: i) chemical-induced colitis primarily mediated by innate immune cells; and ii) colitis initiated by CD4+CD45RBhigh T cells following their transfer into immuno-deficient RAG1-/- hosts. In both models of disease the absence of HVEM resulted in a significant reduction in colitis and inflammatory cytokine production. Conclusions These data show that HVEM stimulatory signals promote experimental colitis driven by innate or adaptive immune cells

Expression of genes of cytokines, transcription factors and differentiation antigens in human dendritic cells activated by double-stranded DNA

One of the most important properties of extracellular double-stranded DNA related to the treatment of various diseases is its ability to activate effector cells of the immune system (anti-tumor and vaccinal immunity) through dendritic cells (DCs). The stimulatory effect of DNA on DCs is mediated by the TLR9 signaling pathway and/or through a system of cytosolic sensors and is manifested by increased expression of MHC class II antigens and costimulatory molecules and by increased synthesis of immunoregulatory cytokines. In this work, the expression of cytokines, differentiation antigens and transcription factor genes has been investigated in DCs activated by double-stranded human DNA (i) without any additional factors, (ii) using a lipophilic agent, and (iii) by blocking TLR9 with chloroquine. Evaluation of the DNA effect was carried out after the 6- and 24-hour exposure. It was found that the preparation of double-stranded DNA transfected by Lipofectamine 2000 boosts DCs at the same level as Poly(dA : dT), a synthetic equivalent of double-stranded DNA. It was discovered that combined application of DNA and chloroquine enhances expression of the IFN-α, IFN-β, IFN-γ, IL­8, МСР1, VEGF, CD25, and CD83 genes by hour 24 of incubation. It was for the first time shown that genomic “self” double-stranded DNA as a mono agent activates mRNA synthesis of cytokines IFN-α, IFN-β, IFN-γ, IL­8, IL­10, and VEGF in DCs at 6 hours of induction

Evaluation of a strategy for tumor-initiating stem cell eradication in primary human glioblastoma cultures as a model

Primary cultures of human glioblastoma were obtained from the surgical material of patients K. (female, 61 years, Ds: relapse of glioblastoma) and Zh. (female, 60 years, Ds: relapse of glioblastoma). The effectiveness of a new therapeutic approach aimed at destroying the cancer cell community was evaluated on the primary cell lines of human glioblastoma culture by employing a new strategy of tumor-initiating stem cell synchronization and a domestic strategy of their eradication "3+1". The key elements of the strategy were the following indicator results: (1) evaluation of the presence of tumor-initiating stem cells in a population of cells from analyzed cultures by their ability to internalize double-stranded labeled DNA (TAMRA+ cells); (2) determination of the reference time points of the repair cycle of DNA interstrand cross-links induced by cross-linking cytostatic mitomycin C; (3) evaluation of cell cycle synchronization; (4) determination of the time (day after therapy initiation) when TAMRA+ cells were synchronously present in phase G1/S of the cell cycle, sensitive to the therapy; and (5) establishment of the TAMRA+ (tumor-initiating stem cells) eradication schedule. The cultures were treated with cross-linking cytostatic mitomycin C and a compositional DNA preparation. After the treatments, cell division slows down, and the cultures degrade. The K cell line completely degraded within 30 days of observation. The cell number of the Zh culture fell to nearly one-third of the starting value by day 15 of observation. On day 15, this indicator constituted 1/7.45 for mitomycin C and 1/10.28 for mitomycin C + DNA with reference to the control. The main target of the mitomycin C + DNA regimen was TAMRA+ tumor-initiating stem cells of the glioblastoma cell populations. The action of mitomycin C alone or in the combination with DNA demonstrated effective elimination of TAMRA+ tumor-initiating stem cells and the whole primary cultures of human glioblastomas

An intestinal epithelial defect conferring ER stress results in inflammation involving both innate and adaptive immunity

We recently characterized Winnie mice carrying a missense mutation in Muc2, leading to severe endoplasmic reticulum stress in intestinal goblet cells and spontaneous colitis. In this study, we characterized the immune responses due to this intestinal epithelial dysfunction. In Winnie, there was a fourfold increase in activated dendritic cells (DCs; CD11c+ major histocompatibility complex (MHC) class IIhi) in the colonic lamina propria accompanied by decreased colonic secretion of an inhibitor of DC activation, thymic stromal lymphopoietin (TSLP). Winnie also displayed a significant increase in mRNA expression of the mucosal TH17 signature genes Il17a, IL17f, Tgfb, and Ccr6, particularly in the distal colon. Winnie mesenteric lymph node leukocytes secreted multiple TH1, TH2, and TH17 cytokines on activation, with a large increase in interleukin-17A (IL-17A) progressively with age. A major source of mucosal IL-17A in Winnie was CD4+ T lymphocytes. Loss of T and B lymphocytes in Rag1-/- × Winnie (RaW) crosses did not prevent spontaneous inflammation but did prevent progression with age in the colon but not the cecum. Adoptive transfer of naive T cells into RaW mice caused more rapid and severe colitis than in Rag1-/-, indicating that the epithelial defect results in an intestinal microenvironment conducive to T-cell activation. Thus, the Winnie primary epithelial defect results in complex multicytokine-mediated colitis involving both innate and adaptive immune components with a prominent IL-23/TH17 response, similar to that of human ulcerative colitis