315 research outputs found

    Statistics of Conductances and Subleading Corrections to Scaling near the Integer Quantum Hall Plateau Transition

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    We study the critical behavior near the integer quantum Hall plateau transition by focusing on the multifractal (MF) exponents XqX_q describing the scaling of the disorder-average moments of the point contact conductance TT between two points of the sample, within the Chalker-Coddington network model. Past analytical work has related the exponents XqX_q to the MF exponents Δq\Delta_q of the local density of states (LDOS). To verify this relation, we numerically determine the exponents XqX_q with high accuracy. We thereby provide, at the same time, independent numerical results for the MF exponents Δq\Delta_q for the LDOS. The presence of subleading corrections to scaling makes such determination directly from scaling of the moments of TT virtually impossible. We overcome this difficulty by using two recent advances. First, we construct pure scaling operators for the moments of TT which have precisely the same leading scaling behavior, but no subleading contributions. Secondly, we take into account corrections to scaling from irrelevant (in the renormalization group sense) scaling fields by employing a numerical technique ("stability map") recently developed by us. We thereby numerically confirm the relation between the two sets of exponents, XqX_q (point contact conductances) and Δq\Delta_q (LDOS), and also determine the leading irrelevant (corrections to scaling) exponent yy as well as other subleading exponents. Our results suggest a way to access multifractality in an experimental setting.Comment: 7 pages and 4 figures, plus Supplemental materia

    Dissertatio inauguralis de usu loquendi

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    2 kirja Karl Morgensternile, Riga

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    http://tartu.ester.ee/record=b1817657~S1*es

    Structural insights into Cullin4-RING ubiquitin ligase remodelling by Vpr from simian immunodeficiency viruses

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    Viruses have evolved means to manipulate the host's ubiquitin-proteasome system, in order to down-regulate antiviral host factors. The Vpx/Vpr family of lentiviral accessory proteins usurp the substrate receptor DCAF1 of host Cullin4-RING ligases (CRL4), a family of modular ubiquitin ligases involved in DNA replication, DNA repair and cell cycle regulation. CRL4DCAF1 specificity modulation by Vpx and Vpr from certain simian immunodeficiency viruses (SIV) leads to recruitment, poly-ubiquitylation and subsequent proteasomal degradation of the host restriction factor SAMHD1, resulting in enhanced virus replication in differentiated cells. To unravel the mechanism of SIV Vpr-induced SAMHD1 ubiquitylation, we conducted integrative biochemical and structural analyses of the Vpr protein from SIVs infecting Cercopithecus cephus (SIVmus). X-ray crystallography reveals commonalities between SIVmus Vpr and other members of the Vpx/Vpr family with regard to DCAF1 interaction, while cryo-electron microscopy and cross-linking mass spectrometry highlight a divergent molecular mechanism of SAMHD1 recruitment. In addition, these studies demonstrate how SIVmus Vpr exploits the dynamic architecture of the multi-subunit CRL4DCAF1 assembly to optimise SAMHD1 ubiquitylation. Together, the present work provides detailed molecular insight into variability and species-specificity of the evolutionary arms race between host SAMHD1 restriction and lentiviral counteraction through Vpx/Vpr proteins

    Creating ecologically sound buildings by integrating ecology, architecture and computational design

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    1. Research is revealing an increasing number of positive effects of nature for humans. At the same time, biodiversity in cities, where most humans live, is often low or in decline. Tangible solutions are needed to increase urban biodiversity. 2. Architecture is a key discipline that has considerable influence on the built-up area of cities, thereby influencing urban biodiversity. In general, architects do not design for biodiversity. Conversely, urban conservation planning generally focuses on the limited space free of buildings and does not embrace architecture as an important discipline for the creation of urban green infrastructure. 3. In this paper, we argue that the promotion of biodiversity needs to become a key driving force of architectural design. This requires a new multi-species design paradigm that considers both human and non-human needs. Such a design approach needs to maintain the standards of the architectural profession, including the aim to increase the well-being of humans in buildings. Yet, it also needs to add other stakeholders, organisms such as animals, plants and even microbiota. New buildings designed for humans and other inhabitants can then increase biodiversity in cities and also increase the benefits that humans can derive from close proximity to nature. 4. We review the challenges that this new design approach poses for both architecture and ecology and show that multi-species-design goes beyond existing approaches in architecture and ecology. The new design approach needs to make ecological knowledge available to the architectural design process, enabling practitioners to find architectural solutions that can facilitate synergies from a multi-species perspective. 5. We propose that a first step in creating such a multi-species habitat is the design of buildings with an ecolope, a multi criteria-designed building envelope that takes into account the needs of diverse organisms. Because there is no framework to design such an ecolope, we illustrate how multi-species design needs to draw on knowledge from ecology, as well as architecture, and design computation. 6. We discuss how architectures designed via a multi-species approach can be an important step in establishing beneficial human-nature relationships in cities, and contribute to human well-being and biodiversity conservation.Read the free Plain Language Summary for this article on the Journal blog

    Atorvastatin added to interferon beta for relapsing multiple sclerosis: a randomized controlled trial

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    Statins have anti-inflammatory and immunomodulatory properties in addition to lipid-lowering effects. The present study evaluated the effect of atorvastatin added to interferon beta-1b in multiple sclerosis (MS) in a multicenter, randomized, parallel-group, rater-blinded study performed in eight Swiss hospitals. Seventy-seven patients with relapsing-remitting MS started interferon beta-1b every other day. After 3months, they were randomized 1:1 to receive atorvastatin 40mg/day or not in addition to interferon beta-1b until month 15. The primary endpoint was the proportion of patients with new lesions on T2-weighted images at month 15 compared to baseline at month three. At study end, the proportion of patients with new lesions on T2-weighted images was equal in both groups (odds ratio 1.14; 95% CI 0.36-3.56; p=0.81). All predefined secondary endpoints including number of new lesions and total lesion volume on T2-weighted images, total number of new Gd-enhancing lesions on T1-weighted images, total brain volume, volume of grey matter, volume of white matter, EDSS, MSFC, relapse rate, time to first relapse, number of relapse-free patients and neutralizing antibodies did not show any significant differences (all p values >0.1). Transient elevations of liver enzymes were more frequent with atorvastatin (p=0.02). In conclusion, atorvastatin 40mg/day in addition to interferon beta-1b did not have a beneficial effect on relapsing-remitting MS compared to interferon beta-1b monotherapy over a 12-month perio
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