955 research outputs found

    Mobility of a class of perforated polyhedra

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    A class of over-braced but typically flexible body-hinge frameworks is described. They are based on polyhedra with rigid faces where an independent subset of faces has been replaced by a set of holes. The contact polyhedron C describing the bodies (vertices of C) and their connecting joints (edges of C) is derived by subdivision of the edges of an underlying cubic polyhedron. Symmetry calculations detect flexibility not revealed by counting alone. A generic symmetry-extended version of the Grübler-Kutzbach mobility counting rule accounts for the net mobilities of infinite families of this type (based on subdivisions of prisms, wedges, barrels, and some general inflations of a parent polyhedron). The prisms with all faces even and all barrels are found to generate flexible perforated polyhedra under the subdivision construction. The investigation was inspired by a question raised by Walter Whiteley about a perforated polyhedron with a unique mechanism reducing octahedral to tetrahedral symmetry. It turns out that the perforated polyhedron with highest (OhOh) point-group symmetry based on subdivision of the cube is mechanically equivalent to the Hoberman Switch-Pitch toy. Both objects exhibit an exactly similar mechanism that preserves TdTd subgroup symmetry over a finite range; this mechanism survives in two variants suggested by Bob Connelly and Barbara Heys that have the same contact graph, but lower initial maximum symmetry.Supported by EPSRC First Grant EP/M013642/1.This is the final version of the article. It first appeared from Elsevier via https://doi.org/10.1016/j.ijsolstr.2016.02.00

    Symmetry perspectives on some auxetic body-bar frameworks

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    Scalar mobility counting rules and their symmetry extensions are reviewed for finite frameworks and also for infinite periodic frameworks of the bar-and-joint, body-joint and body-bar types. A recently published symmetry criterion for the existence of equiauxetic character of an infinite framework is applied to two long known but apparently little studied hinged-hexagon frameworks, and is shown to detect auxetic behaviour in both. In contrast, for double-link frameworks based on triangular and square tessellations, other affine deformations can mix with the isotropic expansion mode.P.W. Fowler acknowledges support from the Royal Society/Leverhulme Trust in the form of a Senior Research Fellowship for 2013. T. Tarnai is grateful for financial support under OKTA grant K81146.This is the final published version distributed under a Creative Commons Attribution License, which can also be found on the publisher's website at: http://www.mdpi.com/2073-8994/6/2/36

    Equiauxetic Hinged Archimedean Tilings

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    There is increasing interest in two-dimensional and quasi-two-dimensional materials and metamaterials for applications in chemistry, physics and engineering. Some of these applications are driven by the possible auxetic properties of such materials. Auxetic frameworks expand along one direction when subjected to a perpendicular stretching force. An equiauxetic framework has a unique mechanism of expansion (an equiauxetic mode) where the symmetry forces a Poisson’s ratio of −1. Hinged tilings offer opportunities for the design of auxetic and equiauxetic frameworks in 2D, and generic auxetic behaviour can often be detected using a symmetry extension of the scalar counting rule for mobility of periodic body-bar systems. Hinged frameworks based on Archimedean tilings of the plane are considered here. It is known that the regular hexagonal tiling, {63}, leads to an equiauxetic framework for both single-link and double-link connections between the tiles. For single-link connections, three Archimedean tilings considered as hinged body-bar frameworks are found here to be equiauxetic: these are {3.122}, {4.6.12}, and {4.82}. For double-link connections, three Archimedean tilings considered as hinged body-bar frameworks are found to be equiauxetic: these are {34.6}, {32.4.3.4}, and {3.6.3.6}.NKFI

    Identification of pannexin 1-regulated genes, interactome, and pathways in rhabdomyosarcoma and its tumor inhibitory interaction with AHNAK

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    Rhabdomyosarcoma (RMS), the most common soft tissue sarcoma in children, is an aggressive cancer with a poor prognosis. Despite current management, the 5-year survival rate for patients with metastatic RMS is ∼30%; underscoring the need to develop better treatment strategies. We have recently reported that pannexin 1 (PANX1) levels are downregulated in RMS and that restoring its expression inhibits RMS progression. Here, we have surveyed and characterized the molecular changes induced by PANX1 re-expression in RMS. We cataloged transcriptomic changes in this context by RNA sequencing. At the protein level, we unveiled PANX1 interactors using BioID, complemented by co-immunoprecipitation coupled to high-performance liquid chromatography/electrospray ionization tandem mass spectrometry performed in PANX1-enriched fractions. Using these data, we generated searchable public databases for the PANX1 interactome and changes to the RMS transcriptome occurring when PANX1 expression is restored. STRING network analyses revealed a PANX1 interactome involving plasma membrane and cytoskeleton-associated proteins including the previously undescribed interactor AHNAK. Indeed, AHNAK knockdown abrogated the PANX1-mediated reduction in RMS cell viability and migration. Using these unbiased approaches, we bring insight to the mechanisms by which PANX1 inhibits RMS progression, identifying the cell migration protein AHNAK as a key modifier of PANX1-mediated changes in RMS malignant properties

    Natural killer cells attenuate cytomegalovirus-induced hearing loss in mice

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    <div><p>Congenital cytomegalovirus (CMV) infection is the most common non-hereditary cause of sensorineural hearing loss (SNHL) yet the mechanisms of hearing loss remain obscure. Natural Killer (NK) cells play a critical role in regulating murine CMV infection via NK cell recognition of the Ly49H cell surface receptor of the viral-encoded m157 ligand expressed at the infected cell surface. This Ly49H NK receptor/m157 ligand interaction has been found to mediate host resistance to CMV in the spleen, and lung, but is much less effective in the liver, so it is not known if this interaction is important in the context of SNHL. Using a murine model for CMV-induced labyrinthitis, we have demonstrated that the Ly49H/m157 interaction mediates host resistance in the temporal bone. BALB/c mice, which lack functional Ly49H, inoculated with mCMV at post-natal day 3 developed profound hearing loss and significant outer hair cell loss by 28 days of life. In contrast, C57BL/6 mice, competent for the Ly49H/m157 interaction, had minimal hearing loss and attenuated outer hair cell loss with the same mCMV dose. Administration of Ly49H blocking antibody or inoculation with a mCMV viral strain deleted for the m157 gene rendered the previously resistant C57BL/6 mouse strain susceptible to hearing loss to a similar extent as the BALB/c mouse strain indicating a direct role of the Ly49H/m157 interaction in mCMV-dependent hearing loss. Additionally, NK cell recruitment to sites of infection was evident in the temporal bone of inoculated susceptible mouse strains. These results demonstrate participation of NK cells in protection from CMV-induced labyrinthitis and SNHL in mice.</p></div

    Identification of pannexin 1-regulated genes, interactome, and pathways in rhabdomyosarcoma and its tumor inhibitory interaction with AHNAK

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    Rhabdomyosarcoma (RMS), the most common soft tissue sarcoma in children, is an aggressive cancer with a poor prognosis. Despite current management, the 5-year survival rate for patients with metastatic RMS is ∼30%; underscoring the need to develop better treatment strategies. We have recently reported that pannexin 1 (PANX1) levels are downregulated in RMS and that restoring its expression inhibits RMS progression. Here, we have surveyed and characterized the molecular changes induced by PANX1 re-expression in RMS. We cataloged transcriptomic changes in this context by RNA sequencing. At the protein level, we unveiled PANX1 interactors using BioID, complemented by co-immunoprecipitation coupled to high-performance liquid chromatography/electrospray ionization tandem mass spectrometry performed in PANX1-enriched fractions. Using these data, we generated searchable public databases for the PANX1 interactome and changes to the RMS transcriptome occurring when PANX1 expression is restored. STRING network analyses revealed a PANX1 interactome involving plasma membrane and cytoskeleton-associated proteins including the previously undescribed interactor AHNAK. Indeed, AHNAK knockdown abrogated the PANX1-mediated reduction in RMS cell viability and migration. Using these unbiased approaches, we bring insight to the mechanisms by which PANX1 inhibits RMS progression, identifying the cell migration protein AHNAK as a key modifier of PANX1-mediated changes in RMS malignant properties

    Quantum resource estimates for computing elliptic curve discrete logarithms

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    We give precise quantum resource estimates for Shor's algorithm to compute discrete logarithms on elliptic curves over prime fields. The estimates are derived from a simulation of a Toffoli gate network for controlled elliptic curve point addition, implemented within the framework of the quantum computing software tool suite LIQUiUi|\rangle. We determine circuit implementations for reversible modular arithmetic, including modular addition, multiplication and inversion, as well as reversible elliptic curve point addition. We conclude that elliptic curve discrete logarithms on an elliptic curve defined over an nn-bit prime field can be computed on a quantum computer with at most 9n+2log2(n)+109n + 2\lceil\log_2(n)\rceil+10 qubits using a quantum circuit of at most 448n3log2(n)+4090n3448 n^3 \log_2(n) + 4090 n^3 Toffoli gates. We are able to classically simulate the Toffoli networks corresponding to the controlled elliptic curve point addition as the core piece of Shor's algorithm for the NIST standard curves P-192, P-224, P-256, P-384 and P-521. Our approach allows gate-level comparisons to recent resource estimates for Shor's factoring algorithm. The results also support estimates given earlier by Proos and Zalka and indicate that, for current parameters at comparable classical security levels, the number of qubits required to tackle elliptic curves is less than for attacking RSA, suggesting that indeed ECC is an easier target than RSA.Comment: 24 pages, 2 tables, 11 figures. v2: typos fixed and reference added. ASIACRYPT 201

    Risk of Cardiovascular Events and Death—Does Insurance Matter?

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    BACKGROUND: Many Americans lack health insurance. Despite good evidence that lack of insurance compromises access to care, few prospective studies examine its relationship to health outcomes. OBJECTIVE: To determine the relationship between insurance and cardiovascular outcomes and the relationship between insurance and selected process measures. DESIGN AND PARTICIPANTS: We used data from 15,792 participants in the Atherosclerosis Risk in Communities Study, a prospective cohort study. Participants were enrolled in 1987–1989 and returned for follow-up visits every 3 years, for a total of 4 visits. MAIN OUTCOME MEASURES: We estimated the hazard of myocardial infarction, stroke, and death associated with insurance status using Cox proportional hazard modeling. We used generalized estimating equations to examine the association between insurance status and risk of (1) reporting no routine physical examinations, (2) being unaware of a personal cardiovascular risk condition, and (3) inadequate control of cardiovascular risk conditions. RESULTS: Persons without insurance had higher rates of stroke (adjusted hazard ratio, 95% CI 1.22–2.22) and death (adjusted hazard ratio 1.26, 95% CI 1.03–1.53), but not myocardial infarction, than those who were insured. The uninsured were less likely to report routine physical examinations (adjusted risk ratio 1.13, 95% CI 1.08–1.18); more likely to be unaware of hypertension (adjusted risk ratio 1.12, 95% CI 1.00–1.25) and hyperlipidemia (adjusted risk ratio 1.11, 95% CI 1.03–1.19); and more likely to have poor blood pressure control (adjusted risk ratio 1.23, 95% CI 1.08–1.39). CONCLUSIONS: Lack of health insurance is associated with increased rates of stroke and death and with less awareness and control of cardiovascular risk conditions. Health insurance may improve cardiovascular risk factor awareness, control and outcomes

    The genome sequence of <i>Trypanosoma brucei gambiense</i>, causative agent of chronic Human African Trypanosomiasis

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    &lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; &lt;i&gt;Trypanosoma brucei gambiense&lt;/i&gt; is the causative agent of chronic Human African Trypanosomiasis or sleeping sickness, a disease endemic across often poor and rural areas of Western and Central Africa. We have previously published the genome sequence of a &lt;i&gt;T. b. brucei&lt;/i&gt; isolate, and have now employed a comparative genomics approach to understand the scale of genomic variation between &lt;i&gt;T. b. gambiense&lt;/i&gt; and the reference genome. We sought to identify features that were uniquely associated with &lt;i&gt;T. b. gambiense&lt;/i&gt; and its ability to infect humans.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods and findings:&lt;/b&gt; An improved high-quality draft genome sequence for the group 1 &lt;i&gt;T. b. gambiense&lt;/i&gt; DAL 972 isolate was produced using a whole-genome shotgun strategy. Comparison with &lt;i&gt;T. b. brucei&lt;/i&gt; showed that sequence identity averages 99.2% in coding regions, and gene order is largely collinear. However, variation associated with segmental duplications and tandem gene arrays suggests some reduction of functional repertoire in &lt;i&gt;T. b. gambiense&lt;/i&gt; DAL 972. A comparison of the variant surface glycoproteins (VSG) in &lt;i&gt;T. b. brucei&lt;/i&gt; with all &lt;i&gt;T. b. gambiense&lt;/i&gt; sequence reads showed that the essential structural repertoire of VSG domains is conserved across &lt;i&gt;T. brucei&lt;/i&gt;.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions:&lt;/b&gt; This study provides the first estimate of intraspecific genomic variation within &lt;i&gt;T. brucei&lt;/i&gt;, and so has important consequences for future population genomics studies. We have shown that the &lt;i&gt;T. b. gambiense&lt;/i&gt; genome corresponds closely with the reference, which should therefore be an effective scaffold for any &lt;i&gt;T. brucei&lt;/i&gt; genome sequence data. As VSG repertoire is also well conserved, it may be feasible to describe the total diversity of variant antigens. While we describe several as yet uncharacterized gene families with predicted cell surface roles that were expanded in number in &lt;i&gt;T. b. brucei&lt;/i&gt;, no &lt;i&gt;T. b. gambiense&lt;/i&gt;-specific gene was identified outside of the subtelomeres that could explain the ability to infect humans.&lt;/p&gt

    Blind topological measurement-based quantum computation

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    Blind quantum computation is a novel secure quantum-computing protocol that enables Alice, who does not have sufficient quantum technology at her disposal, to delegate her quantum computation to Bob, who has a fully fledged quantum computer, in such a way that Bob cannot learn anything about Alice's input, output and algorithm. A recent proof-of-principle experiment demonstrating blind quantum computation in an optical system has raised new challenges regarding the scalability of blind quantum computation in realistic noisy conditions. Here we show that fault-tolerant blind quantum computation is possible in a topologically protected manner using the Raussendorf-Harrington-Goyal scheme. The error threshold of our scheme is 0.0043, which is comparable to that (0.0075) of non-blind topological quantum computation. As the error per gate of the order 0.001 was already achieved in some experimental systems, our result implies that secure cloud quantum computation is within reach.Comment: 17 pages, 5 figure
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