119 research outputs found

    Fluctuations in the Irreversible Decay of Turbulent Energy

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    A fluctuation law of the energy in freely-decaying, homogeneous and isotropic turbulence is derived within standard closure hypotheses for 3D incompressible flow. In particular, a fluctuation-dissipation relation is derived which relates the strength of a stochastic backscatter term in the energy decay equation to the mean of the energy dissipation rate. The theory is based on the so-called ``effective action'' of the energy history and illustrates a Rayleigh-Ritz method recently developed to evaluate the effective action approximately within probability density-function (PDF) closures. These effective actions generalize the Onsager-Machlup action of nonequilibrium statistical mechanics to turbulent flow. They yield detailed, concrete predictions for fluctuations, such as multi-time correlation functions of arbitrary order, which cannot be obtained by direct PDF methods. They also characterize the mean histories by a variational principle.Comment: 26 pages, Latex Version 2.09, plus seceq.sty, a stylefile for sequential numbering of equations by section. This version includes new discussion of the physical interpretation of the formal Rayleigh-Ritz approximation. The title is also change

    Holder exponents of irregular signals and local fractional derivatives

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    It has been recognized recently that fractional calculus is useful for handling scaling structures and processes. We begin this survey by pointing out the relevance of the subject to physical situations. Then the essential definitions and formulae from fractional calculus are summarized and their immediate use in the study of scaling in physical systems is given. This is followed by a brief summary of classical results. The main theme of the review rests on the notion of local fractional derivatives. There is a direct connection between local fractional differentiability properties and the dimensions/ local Holder exponents of nowhere differentiable functions. It is argued that local fractional derivatives provide a powerful tool to analyse the pointwise behaviour of irregular signals and functions.Comment: 20 pages, Late

    Adult Drosophila melanogaster evolved for antibacterial defense invest in infection-induced expression of both humoral and cellular immunity genes

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    <p>Abstract</p> <p>Background</p> <p>While the transcription of innate immunity genes in response to bacterial infection has been well-characterised in the Drosophila model, we recently demonstrated the capacity for such transcription to evolve in flies selected for improved antibacterial defense. Here we use this experimental system to examine how insects invest in constitutive versus infection-induced transcription of immunity genes. These two strategies carry with them different consequences with respect to energetic and pleiotropic costs and may be more or less effective in improving defense depending on whether the genes contribute to humoral or cellular aspects of immunity.</p> <p>Findings</p> <p>Contrary to expectation we show that selection preferentially increased the infection-induced expression of both cellular and humoral immunity genes. Given their functional roles, infection induced increases in expression were expected for the humoral genes, while increases in constitutive expression were expected for the cellular genes. We also report a restricted ability to improve transcription of immunity genes that is on the order of 2-3 fold regardless of total transcription level of the gene.</p> <p>Conclusions</p> <p>The evolved increases in infection-induced expression of the cellular genes may result from specific cross talk with humoral pathways or from generalised strategies for enhancing immunity gene transcription. A failure to see improvements in constitutive expression of the cellular genes suggests either that increases might come at too great a cost or that patterns of expression in adults are decoupled from the larval phase where increases would be most effective. The similarity in fold change increase across all immunity genes may suggest a shared mechanism for the evolution of increased transcription in small, discrete units such as duplication of <it>cis</it>-regulatory elements.</p

    Track E Implementation Science, Health Systems and Economics

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138412/1/jia218443.pd

    Use of anticoagulants and antiplatelet agents in stable outpatients with coronary artery disease and atrial fibrillation. International CLARIFY registry

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    Desastres naturais: convivência com o risco

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    Estudos sobre riscos de desastres naturais têm-se aprimorado de uma abordagem fisicalista para uma perspectiva socioambiental. No entanto, planejamento e gestão ainda seguem o paradigma antropocêntrico da superioridade humana e do poder ilimitado da ciência e tecnologia. Evidencia-se uma incapacidade cognitiva, cultural e de ação por parte de especialistas, científicos e tomadores de decisão (claimmakers) para identificar e atuar sobre as causas sociais da produção de risco. Frente a uma ciência cartesiana e positivista na resolução de problemas, baseada na segurança e controle sobre o mundo natural, propõe-se uma ciência pós-normal que considera os riscos e incertezas do conhecimento científico e das problemáticas ambientais. Essa nova proposta também incide sobre a participação e o diálogo entre stakeholders como referência para ampliar a qualidade do saber científico e o entendimento da complexidade das questões ambientais. Este artigo discute a necessidade de se promover um salto epistemológico sobre a forma de pensar e produzir conhecimentos, bem como implementar a gestão dos riscos de desastres, tendo como objeto de estudo processos de comunicação e educação para prevenção de desastres.Studies on the risks of natural disasters have improved from a physicalist approach to a social and environmental perspective. However, planning and management still follow the anthropocentric paradigm of human superiority and the unlimited power of science and technology, evincing a cognitive, cultural and action inability on the part of experts, scientists and decision makers (or, rather, claim makers) to identify and act upon the social causes of risk production. In view of the Cartesian and Positivist science used to solve problems, based on security and on control over the natural world, a post-normal science has been proposed that considers the risks and uncertainties of scientific knowledge and environmental issues. This new approach encompasses participation and dialogue among stakeholders as a means to increase the quality of scientific knowledge and acknowledge the complexity of environmental issues. This article discusses the need for an epistemological leap on how we think and produce knowledge, as well as for implementing the management of disaster risk. Its objects of study are communication processes and education for disaster prevention

    Case reports: Misdiagnosed herpes zoster

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    Anti-metastatic treatment in colorectal cancer: targeting signaling pathways

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    Colorectal cancer is one of the most common cancers worldwide and one of the leading causes of cancer-related death in the Western world. Tumor progression towards metastasis affects a large number of patients with colorectal cancer and seriously affects their clinical outcome. Therefore, considerable effort has been made towards the development of therapeutic strategies that can decrease or prevent colorectal cancer metastasis. Standard treatment of metastatic colorectal cancer with chemotherapy has been improved in the last 10 years by the addition of new targeted agents. The currently used antibodies bevacizumab, cetuximab and panitumumab target the VEGF and EGFR signaling pathways, which are crucial for tumor progression and metastasis. These antibodies have shown relevant efficacy in both first- and second-line treatment of metastatic colorectal cancer. Additionally, other signaling pathways, including the Wnt and HGF/Met pathways, have a well-established role in colorectal cancer progression and metastasis and constitute, therefore, promising targets for new therapeutic approaches. Several new drugs targeting these pathways, including different antibodies and small-molecule tyrosine kinase inhibitors, are currently being developed and tested in clinical trials. In this review, we summarize the new developments in this field, focusing on the inhibitors that show more promising results for use in colorectal cancer patients

    Promoter identification and transcriptional regulation of the metastasis gene MACC1 in colorectal cancer

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    MACC1, Metastasis associated in colon cancer 1, is a newly identified prognostic biomarker for colorectal cancer metastasis and patient survival, when determined in the primary tumor or patient blood. MACC1 induces cell motility and proliferation in cell culture and metastasis in mouse models. MACC1 acts as a transcriptional regulator of the receptor tyrosine kinase gene Met via binding to its promoter. However, no information about the promoter of the MACC1 gene and its transcriptional regulation has been reported so far. Here we report the identification of the MACC1 promoter using a promoter luciferase construct that directs transcription of MACC1. To gain insights into the essential domains within this promoter region, we constructed 5' truncated deletion constructs. Our results show that the region from -426 to -18 constitutes the core promoter and harbors functional motifs for the binding of AP-1, Sp1, and C/EBP transcription factors as validated by site directed mutagenesis study. Using electrophoretic mobility shift assay and chromatin immunoprecipitation assay, we demonstrated the physical interaction of these transcription factors to a minimal essential MACC1 core promoter sequence. Knock down of these transcription factors using RNAi strategy reduced MACC1 expression (P < 0.001), and resulted in decrease of cell migration (P < 0.01) which could be specifically rescued by ectopic overexpression of MACC1. In human colorectal tumors, expression levels of c-Jun and Sp1 correlated significantly to MACC1 (P = 0.0007 and P = 0.02, respectively). Importantly, levels of c-Jun and Sp1 also showed significant correlation to development of metachronous metastases (P = 0.01 and P = 0.001, respectively). This is the first study identifying the MACC1 promoter and its transcriptional regulation by AP-1 and Sp1. Knowledge of the transcriptional regulation of the MACC1 gene will implicate in enhanced understanding of its role in cancer progression and metastasis
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