3,536 research outputs found

    Prescription for healthy communities: community development finance

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    Public health - Economic aspects ; Community development

    Orbital Magnetism of Graphene Nanostructures: Bulk and Confinement Effects

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    We consider the orbital magnetic properties of non-interacting charge carriers in graphene-based nanostructures in the low-energy regime. The magnetic response of such systems results both, frombulk contributions and from confinement effects that can be particularly strong in ballistic quantum dots. First we provide a comprehensive study of the magnetic susceptibility χ\chi of bulk graphene in a magnetic field for the different regimes arising from the relative magnitudes of the energy scales involved, i.e. temperature, Landau level spacing and chemical potential. We show that for finite temperature or chemical potential, χ\chi is not divergent although the diamagnetic contribution χ0\chi_{0} from the filled valance band exhibits the well-known B1/2-B^{-1/2} dependence. We further derive oscillatory modulations of χ\chi, corresponding to de Haas-van Alphen oscillations of conventional two-dimensional electron gases. These oscillations can be large in graphene, thereby compensating the diamagnetic contribution χ0\chi_{0} and yielding a net paramagnetic susceptibility for certain energy and magnetic field regimes. Second, we predict and analyze corresponding strong, confinement-induced susceptibility oscillations in graphene-based quantum dots with amplitudes distincly exceeding the corresponding bulk susceptibility. Within a semiclassical approach we derive generic expressions for orbital magnetism of graphene quantum dots with regular classical dynamics. Graphene-specific features can be traced back to pseudospin interference along the underlying periodic orbits. We demonstrate the quality of the semiclassical approximation by comparison with quantum mechanical results for two exemplary mesoscopic systems, a graphene disk with infinite mass-type edges and a rectangular graphene structure with armchair and zigzag edges, using numerical tight-binding calculations in the latter case.Comment: 21 pages, 16 figure

    Containing a firestorm: adaptive policies needed to address changing foreclosure landscape

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    Like a wildfire leaving devastation in its path, the foreclosure crisis continues to wreak havoc on many families and communities throughout the Fourth District, especially in the largest urban areas. Only a year ago the primary reason for foreclosures centered on subprime mortgages. Today, the primary driver is unemployment, further widening the consumption arc of this blaze.Foreclosure

    Maintenance of cell type-specific connectivity and circuit function requires Tao kinase

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    Sensory circuits are typically established during early development, yet how circuit specificity and function are maintained during organismal growth has not been elucidated. To gain insight we quantitatively investigated synaptic growth and connectivity in the Drosophila nociceptive network during larval development. We show that connectivity between primary nociceptors and their downstream neurons scales with animal size. We further identified the conserved Ste20-like kinase Tao as a negative regulator of synaptic growth required for maintenance of circuit specificity and connectivity. Loss of Tao kinase resulted in exuberant postsynaptic specializations and aberrant connectivity during larval growth. Using functional imaging and behavioral analysis we show that loss of Tao-induced ectopic synapses with inappropriate partner neurons are functional and alter behavioral responses in a connection-specific manner. Our data show that fine-tuning of synaptic growth by Tao kinase is required for maintaining specificity and behavioral output of the neuronal network during animal growth

    Extending the first-order post-Newtonian scheme in multiple systems to the second-order contributions to light propagation

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    In this paper, we extend the first-order post-Newtonian scheme in multiple systems presented by Damour-Soffel-Xu to the second-order contribution to light propagation without changing the virtueof the scheme on the linear partial differential equations of the potential and vector potential. The spatial components of the metric are extended to second order level both in a global coordinates (qij/c4q_{ij}/ c^4) and a local coordinates (Qab/c4Q_{ab}/ c^4). The equations of qijq_{ij} (or QabQ_{ab}) are obtained from the field equations.The relationship between qijq_{ij} and QabQ_{ab} are presented in this paper also. In special case of the solar system (isotropic condition is applied (qij=δijqq_{ij} = \delta_{ij} q )), we obtain the solution of qq. Finally, a further extension of the second-order contributions in the parametrized post-Newtonian formalism is discussed.Comment: Latex2e; 6 pages PS fil

    Baseline UT measurements for armor inspection

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    Some prototype armor panels are fabricated from several layers of dissimilar material bonded together. These may include ceramics, graphite composites, fiberglass composites and rubber. The ultrasonic properties of these layers influence inspections for armor defects. In this paper we describe measurements of ultrasonic velocity, attenuation, sound beam distortion and signal fluctuations for the individual layers comprising one armor prototype. We then discuss how knowledge of these properties can be used when choosing an optimum frequency for an ultrasonic pitch∕catch immersion inspection. In our case an effective inspection frequency near 1.5 MHz affords: (1) adequate strength of through‐transmitted signals in unflawed armor; (2) adequate lateral resolution for detecting small disbonds at interfaces; and (3) low levels of UT signal fluctuations due to the natural inhomogeneity of certain armor layers. The utility of this approach is demonstrated using armor panels containing artificial disbonds at selected interfaces

    Immune Boost, Early Pandemic

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    Immune Boost, Early Pandemic by Lisa Richte

    HDAC1 is a Required Cofactor of CBFβ-SMMHC and a Therapeutic Target in Inversion 16 Acute Myeloid Leukemia

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    Acute myeloid leukemia (AML) is a neoplastic disease characterized by the uncontrolled proliferation and accumulation of immature myeloid cells. A common mutation in AML is the inversion of chromosome 16 [inv(16)], which generates a fusion between the genes for core binding factor beta (CBFB) and smooth muscle myosin heavy chain (MYH11), forming the oncogene CBFB-MYH11. The expressed protein, CBFβ-SMMHC, forms a heterodimer with the key hematopoietic transcription factor RUNX1. Although CBFβ-SMMHC was previously thought to dominantly repress RUNX1, recent work suggests that CBFβ-SMMHC functions together with RUNX1 to activate transcription of specific target genes. Targeting the activity of CBFβ-SMMHC is a promising approach for treating inv(16) AML, although currently there are no inhibitors of CBFβ-SMMHC ready for clinical use. An alternative approach is to indirectly target the fusion protein by inhibiting the activity of other proteins which are recruited to CBFβ-SMMHC and are required for its activity. One possible target is the epigenetic regulator histone deacetylase 1 (HDAC1), which was previously shown to colocalize with CBFβ-SMMHC on gene promoters. We hypothesized that HDAC1 was recruited to the CBFβ-SMMHC:RUNX1 complex and inhibitors of HDAC1 could be used to indirectly target its leukemogenic activity. In this study, we demonstrate that HDAC1 forms a complex with CBFβ-SMMHC, confirmed its colocalization with RUNX1 and CBFβ-SMMHC on the promoters of known fusion protein target genes, and determined that Hdac1 is required for expression of these genes. These results imply that HDAC1 is an important component of the CBFβ-SMMHC transcriptional complex, and that leukemia cells expressing the fusion protein may be sensitive to treatment with HDAC1 inhibitors. Both Hdac1 knockdown and treatment with the HDAC1 selective inhibitor entinostat in vitro results in a decrease in colony-forming ability and an increase in differentiation in CBFβ-SMMHC+ cells, implying that HDAC1 is required to maintain the differentiation block in the leukemia cells. Using a knock-in mouse model expressing CBFβ-SMMHC, we found that in vivo treatment with entinostat decreased leukemic burden and induced differentiation and apoptosis of leukemia cells. Importantly, entinostat treatment specifically targeted the leukemia cells with minimal toxicity to normal cells. We also tested the same treatment strategy on survival of the mice but found that leukemia cells were able to continue to grow after cessation of treatment. Overall, our results demonstrate the strict requirement for HDAC1 in CBFβ-SMMHC+ cells and reveal that it is a promising therapeutic target for treatment of inv(16) AML
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