Polarization correlations in the two--photon decay of hydrogen--like ions

Polarization properties of the photons emitted in the two-photon decay of hydrogen-like ions are studied within the framework of the density matrix and second-order perturbation theory. In particular, we derive the polarization correlation function that gives the probability of the (two-photon) coincidence measurement performed by polarization-sensitive detectors. Detailed calculations of this function are performed for the $2s_{1/2} \to 1s_{1/2}$ transition in neutral hydrogen as well as Xe$^{53+}$ and U$^{91+}$ ions. The obtained results allow us to understand the influence of relativistic and non-dipole effects on the polarization correlations in the bound-bound two-photon transitions in heavy ions

Critical role of endothelial Notch1 signaling in postnatal angiogenesis

Notch receptors are important mediators of cell fate during embryogenesis, but their role in adult physiology, particularly in postnatal angiogenesis, remains unknown. Of the Notch receptors, only Notch1 and Notch4 are expressed in vascular endothelial cells. Here we show that blood flow recovery and postnatal neovascularization in response to hindlimb ischemia in haploinsufficient global or endothelial-specific Notch1(+/-) mice, but not Notch4(-/-) mice, were impaired compared with wild-type mice. The expression of vascular endothelial growth factor (VEGF) in response to ischemia was comparable between wild-type and Notch mutant mice, suggesting that Notch1 is downstream of VEGF signaling. Treatment of endothelial cells with VEGF increases presenilin proteolytic processing, gamma-secretase activity, Notch1 cleavage, and Hes-1 (hairy enhancer of split homolog-1) expression, all of which were blocked by treating endothelial cells with inhibitors of phosphatidylinositol 3-kinase/protein kinase Akt or infecting endothelial cells with a dominant-negative Akt mutant. Indeed, inhibition of gamma-secretase activity leads to decreased angiogenesis and inhibits VEGF-induced endothelial cell proliferation, migration, and survival. Overexpression of the active Notch1 intercellular domain rescued the inhibitory effects of gamma-secretase inhibitors on VEGF-induced angiogenesis. These findings indicate that the phosphatidylinositol 3-kinase/Akt pathway mediates gamma-secretase and Notch1 activation by VEGF and that Notch1 is critical for VEGF-induced postnatal angiogenesis. These results suggest that Notch1 may be a novel therapeutic target for improving angiogenic response and blood flow recovery in ischemic limbs

Exchange Instabilities in Semiconductor Double Quantum Well Systems

We consider various exchange-driven electronic instabilities in semiconductor double-layer systems in the absence of any external magnetic field. We establish that there is no exchange-driven bilayer to monolayer charge transfer instability in the double-layer systems. We show that, within the unrestricted Hartree-Fock approximation, the low density stable phase (even in the absence of any interlayer tunneling) is a quantum ``pseudospin rotated'' spontaneous interlayer phase coherent spin-polarized symmetric state rather than the classical Ising-like charge-transfer phase. The U(1) symmetry of the double quantum well system is broken spontaneously at this low density quantum phase transition, and the layer density develops quantum fluctuations even in the absence of any interlayer tunneling. The phase diagram for the double quantum well system is calculated in the carrier density--layer separation space, and the possibility of experimentally observing various quantum phases is discussed. The situation in the presence of an external electric field is investigated in some detail using the spin-polarized-local-density-approximation-based self-consistent technique and good agreement with existing experimental results is obtained.Comment: 24 pages, figures included. Also available at http://www-cmg.physics.umd.edu/~lzheng/preprint/ct.uu/ . Revised final version to appear in PR

Effects of macroscopic polarization in III-V nitride multi-quantum-wells

Huge built-in electric fields have been predicted to exist in wurtzite III-V nitrides thin films and multilayers. Such fields originate from heterointerface discontinuities of the macroscopic bulk polarization of the nitrides. Here we discuss the background theory, the role of spontaneous polarization in this context, and the practical implications of built-in polarization fields in nitride nanostructures. To support our arguments, we present detailed self-consistent tight-binding simulations of typical nitride QW structures in which polarization effects are dominant.Comment: 11 pages, 9 figures, uses revtex/epsf. submitted to PR

Notch signaling during human T cell development

Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

Effects of In-Plane Impurity Substitution in Sr2RuO4

We report comparative substitution effects of nonmagnetic Ti^(4+) and magnetic Ir^(4+) impurities for Ru^(4+) in the spin-triplet superconductor Sr2RuO4. We found that both impurities suppress the superconductivity completely at a concentration of approximately 0.15%, reflecting the high sensitivity to translational symmetry breaking in Sr2RuO4. In addition, a rapid enhancement of residual resistivity is in quantitative agreement with unitarity-limit scattering. Our result suggests that both nonmagnetic and magnetic impurities in Sr2RuO4 act as strong potential scatterers, similar to the nonmagnetic Zn^(2+) impurity in the high-Tc cuprates.Comment: 4 pages, 2 figures. submitted to Journal of the Physical Society of Japa

Inhibition of Fibroblast Growth by Notch1 Signaling Is Mediated by Induction of Wnt11-Dependent WISP-1

Fibroblasts are an integral component of stroma and important source of growth factors and extracellular matrix (ECM). They play a prominent role in maintaining tissue homeostasis and in wound healing and tumor growth. Notch signaling regulates biological function in a variety of cells. To elucidate the physiological function of Notch signaling in fibroblasts, we ablated Notch1 in mouse (Notch1Flox/Flox) embryonic fibroblasts (MEFs). Notch1-deficient (Notch1−/−) MEFs displayed faster growth and motility rate compared to Notch1Flox/Flox MEFs. Such phenotypic changes, however, were reversible by reconstitution of Notch1 activation via overexpression of the intracellular domain of Notch1 (NICD1) in Notch1-deficient MEFs. In contrast, constitutive activation of Notch1 signaling by introducing NICD1 into primary human dermal fibroblasts (FF2441), which caused pan-Notch activation, inhibited cell growth and motility, whereas cellular inhibition was relievable when the Notch activation was countered with dominant-negative mutant of Master-mind like 1 (DN-MAML-1). Functionally, “Notch-activated” stromal fibroblasts could inhibit tumor cell growth/invasion. Moreover, Notch activation induced expression of Wnt-induced secreted proteins-1 (WISP-1/CCN4) in FF2441 cells while deletion of Notch1 in MEFs resulted in an opposite effect. Notably, WISP-1 suppressed fibroblast proliferation, and was responsible for mediating Notch1's inhibitory effect since siRNA-mediated blockade of WISP-1 expression could relieve cell growth inhibition. Notch1-induced WISP-1 expression appeared to be Wnt11-dependent, but Wnt1-independent. Blockade of Wnt11 expression resulted in decreased WISP-1 expression and liberated Notch-induced cell growth inhibition. These findings indicated that inhibition of fibroblast proliferation by Notch pathway activation is mediated, at least in part, through regulating Wnt1-independent, but Wnt11-dependent WISP-1 expression

Edge states and determination of pairing symmetry in superconducting Sr2RuO4

We calculate the energy dispersion of the surface Andreev states and their contribution to tunneling conductance for the order parameters with horizontal and vertical lines of nodes proposed for superconducting Sr2RuO4. For vertical lines, we find double peaks in tunneling spectra reflecting the van Hove singularities in the density of surface states originating from the turning points in their energy dispersion. For horizontal lines, we find a single cusp-like peak at zero bias, which agrees very well with the experimental data on tunneling in Sr2RuO4.Comment: 6 pages, 6 figures. V.2: comparison with experiment added and discussion of horizontal nodes expanded. v.3: significant expansion: 1 figure and 2 pages added. v.4: acknowledgements added. Additional viewgraphs with experimental and theoretical curves superimposed are available at http://www2.physics.umd.edu/~yakovenk/talks/Sr2RuO4

Redundant Notch1 and Notch2 Signaling Is Necessary for IFNγ Secretion by T Helper 1 Cells During Infection with Leishmania major

The protective immune response to intracellular parasites involves in most cases the differentiation of IFNγ-secreting CD4+ T helper (Th) 1 cells. Notch receptors regulate cell differentiation during development but their implication in the polarization of peripheral CD4+ T helper 1 cells is not well understood. Of the four Notch receptors, only Notch1 (N1) and Notch2 (N2) are expressed on activated CD4+ T cells. To investigate the role of Notch in Th1 cell differentiation following parasite infection, mice with T cell-specific gene ablation of N1, N2 or both (N1N2ΔCD4Cre) were infected with the protozoan parasite Leishmania major. N1N2ΔCD4Cre mice, on the C57BL/6 L. major-resistant genetic background, developed unhealing lesions and uncontrolled parasitemia. Susceptibility correlated with impaired secretion of IFNγ by draining lymph node CD4+ T cells and increased secretion of the IL-5 and IL-13 Th2 cytokines. Mice with single inactivation of N1 or N2 in their T cells were resistant to infection and developed a protective Th1 immune response, showing that CD4+ T cell expression of N1 or N2 is redundant in driving Th1 differentiation. Furthermore, we show that Notch signaling is required for the secretion of IFNγ by Th1 cells. This effect is independent of CSL/RBP-Jκ, the major effector of Notch receptors, since L. major-infected mice with a RBP-Jκ deletion in their T cells were able to develop IFNγ-secreting Th1 cells, kill parasites and heal their lesions. Collectively, we demonstrate here a crucial role for RBP-Jκ-independent Notch signaling in the differentiation of a functional Th1 immune response following L. major infection

Coherent Potential Approximation for `d - wave' Superconductivity in Disordered Systems

A Coherent Potential Approximation is developed for s-wave and d-wave superconductivity in disordered systems. We show that the CPA formalism reproduces the standard pair-breaking formula, the self-consistent Born Approximation and the self-consistent T-matrix approximation in the appropriate limits. We implement the theory and compute T_c for s-wave and d-wave pairing using an attractive nearest neighbor Hubbard model featuring both binary alloy disorder and a uniform distribution of scattering site potentials. We determine the density of states and examine its consequences for low temperature heat capacity. We find that our results are in qualitative agreement with measurements on Zn doped YBCO superconductors.Comment: 35 pages, 23 figures, submitted to Phys Rev.