Enhancement of the ν=5/2\nu = 5/2 Fractional Quantum Hall State in a Small In-Plane Magnetic Field

Using a 50-nm width, ultra-clean GaAs/AlGaAs quantum well, we have studied the Landau level filling factor $\nu = 5/2$ fractional quantum Hall effect in a perpendicular magnetic field $B \sim$ 1.7 T and determined its dependence on tilted magnetic fields. Contrary to all previous results, the 5/2 resistance minimum and the Hall plateau are found to strengthen continuously under an increasing tilt angle $0 < \theta < 25^\circ$ (corresponding to an in-plane magnetic field 0 $<$ $B_\parallel$ $< 0.8$ T). In the same range of $\theta$ the activation gaps of both the 7/3 and the 8/3 states are found to increase with tilt. The 5/2 state transforms into a compressible Fermi liquid upon tilt angle $\theta > 60^\circ$, and the composite fermion series [2+$p/(2p\pm1)$], $p =$ 1, 2 can be identified. Based on our results, we discuss the relevance of a Skyrmion spin texture at $\nu = 5/2$ associated with small Zeeman energy in wide quantum wells, as proposed by W$\acute{\text o}$js $et$ $al$., Phys. Rev. Lett. 104, 086801 (2010).Comment: 5+ pages, 3 figures, accepted for by Phy. Rev. Let

The Environments of Supernovae in Post-Refurbishment Hubble Space Telescope Images

The locations of supernovae in the local stellar and gaseous environment in galaxies contain important clues to their progenitor stars. Access to this information, however, has been hampered by the limited resolution achieved by ground-based observations. High spatial resolution Hubble Space Telescope (HST) images of galaxy fields in which supernovae had been observed can improve the situation considerably. We have examined the immediate environments of a few dozen supernovae using archival post-refurbishment HST images. Although our analysis is limited due to signal-to-noise ratio and filter bandpass considerations, the images allow us for the first time to resolve individual stars in, and to derive detailed color-magnitude diagrams for, several environments. We are able to place more rigorous constraints on the masses of these supernovae. A search was made for late-time emission from supernovae in the archival images, and for the progenitor stars in presupernova images of the host galaxies. We have detected SN 1986J in NGC 891 and, possibly, SN 1981K in NGC 4258. We have also identified the progenitor of the Type IIn SN 1997bs in NGC 3627. By removing younger resolved stars in the environments of SNe Ia, we can measure the colors of the unresolved stellar background and attribute these colors generally to an older, redder population. HST images ``accidentally'' caught the Type Ia SN 1994D in NGC 4526 shortly after its outburst; we measure its brightness. Finally, we add to the statistical inferences that can be made from studying the association of SNe with recent star-forming regions.Comment: 20 pages, 29 figures, to appear in A

E7(7) formulation of N=2 backgrounds

In this paper we reformulate N=2 supergravity backgrounds arising in type II string theory in terms of quantities transforming under the U-duality group E7(7). In particular we combine the Ramond--Ramond scalar degrees of freedom together with the O(6,6) pure spinors which govern the Neveu-Schwarz sector by considering an extended version of generalised geometry. We give E7(7)-invariant expressions for the Kahler and hyperkahler potentials describing the moduli space of vector and hypermultiplets, demonstrating that both correspond to standard E7(7) coset spaces. We also find E7(7) expressions for the Killing prepotentials defining the scalar potential, and discuss the equations governing N=1 vacua in this formalism.Comment: 40 pages, final version to appear in JHE

A Comprehensive Analysis in Terms of Molecule-Intrinsic, Quasi-Atomic Orbitals. II. Strongly Correlated MCSCF Wave Functions

A methodology is developed for the quantitative identification of the quasi-atomic orbitals that are embedded in a strongly correlated molecular wave function. The wave function is presumed to be generated from configurations in an internal orbital space whose dimension is equal to (or slightly larger) than that of the molecular minimal basis set. The quasi-atomic orbitals are found to have large overlaps with corresponding orbitals on the free atoms. They separate into bonding and nonbonding orbitals. From the bonding quasi-atomic orbitals, localized bonding and antibonding molecular orbitals are formed. The resolution of molecular density matrices in terms of these orbitals furnishes a basis for analyzing the interatomic bonding patterns in molecules and the changes in these bonding patterns along reaction paths. A new bond strength measure, the kinetic bond order, is introduced.Reprinted (adapted) with permission from Journal of Physical Chemistry A 119 (2015): 10360, doi:10.1021/acs.jpca.5b03399. Copyright 2015 American Chemical Society.</p

Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming

Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors

Cheating on the Edge

We present the results of an individual agent-based model of antibiotic resistance in bacteria. Our model examines antibiotic resistance when two strategies exist: “producers”–who secrete a substance that breaks down antibiotics–and nonproducers (“cheats”) who do not secrete, or carry the machinery associated with secretion. The model allows for populations of up to 10,000, in which bacteria are affected by their nearest neighbors, and we assume cheaters die when there are no producers in their neighborhood. Each of 10,000 slots on our grid (a torus) could be occupied by a producer or a nonproducer, or could (temporarily) be unoccupied. The most surprising and dramatic result we uncovered is that when producers and nonproducers coexist at equilibrium, nonproducers are almost always found on the edges of clusters of producers

Hospital characteristics associated with highly automated and usable clinical information systems in Texas, United States

<p>Abstract</p> <p>Background</p> <p>A hospital's clinical information system may require a specific environment in which to flourish. This environment is not yet well defined. We examined whether specific hospital characteristics are associated with highly automated and usable clinical information systems.</p> <p>Methods</p> <p>This was a cross-sectional survey of 125 urban hospitals in Texas, United States using the Clinical Information Technology Assessment Tool (CITAT), which measures a hospital's level of automation based on physician interactions with the information system. Physician responses were used to calculate a series of CITAT scores: automation and usability scores, four automation sub-domain scores, and an overall clinical information technology (CIT) score. A multivariable regression analysis was used to examine the relation between hospital characteristics and CITAT scores.</p> <p>Results</p> <p>We received a sufficient number of physician responses at 69 hospitals (55% response rate). Teaching hospitals, hospitals with higher IT operating expenses (>$1 million annually), IT capital expenses (>$75,000 annually) and hospitals with larger IT staff (≥ 10 full-time staff) had higher automation scores than hospitals that did not meet these criteria (p < 0.05 in all cases). These findings held after adjustment for bed size, total margin, and ownership (p < 0.05 in all cases). There were few significant associations between the hospital characteristics tested in this study and usability scores.</p> <p>Conclusion</p> <p>Academic affiliation and larger IT operating, capital, and staff budgets are associated with more highly automated clinical information systems.</p

Loss of RhoB Expression Enhances the Myelodysplastic Phenotype of Mammalian Diaphanous-Related Formin mDia1 Knockout Mice

Myelodysplastic syndrome (MDS) is characterized by ineffective hematopoiesis and hyperplastic bone marrow. Complete loss or interstitial deletions of the long arm of chromosome 5 occur frequently in MDS. One candidate tumor suppressor on 5q is the mammalian Diaphanous (mDia)-related formin mDia1, encoded by DIAPH1 (5q31.3). mDia-family formins act as effectors for Rho-family small GTP-binding proteins including RhoB, which has also been shown to possess tumor suppressor activity. Mice lacking the Drf1 gene that encodes mDia1 develop age-dependent myelodysplastic features. We crossed mDia1 and RhoB knockout mice to test whether the additional loss of RhoB expression would compound the myelodysplastic phenotype. Drf1−/−RhoB−/− mice are fertile and develop normally. Relative to age-matched Drf1−/−RhoB+/− mice, the age of myelodysplasia onset was earlier in Drf1−/−RhoB−/− animals—including abnormally shaped erythrocytes, splenomegaly, and extramedullary hematopoiesis. In addition, we observed a statistically significant increase in the number of activated monocytes/macrophages in both the spleen and bone marrow of Drf1−/−RhoB−/− mice relative to Drf1−/−RhoB+/− mice. These data suggest a role for RhoB-regulated mDia1 in the regulation of hematopoietic progenitor cells