154 research outputs found

    Dynamical Organization around Turbulent Bursts

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    The detailed dynamics around intermittency bursts is investigated in turbulent shell models. We observe that the amplitude of the high wave number velocity modes vanishes before each burst, meaning that the fixed point in zero and not the Kolmogorov fixed point determines the intermittency. The phases of the field organize during the burst, and after a burst the field oscillates back to the laminar level. We explain this behavior from the variations in the values of the dissipation and the advection around the zero fixed point.Comment: 4 pages, REVTex, 3 figures in one ps-fil

    Inertial- and Dissipation-Range Asymptotics in Fluid Turbulence

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    We propose and verify a wave-vector-space version of generalized extended self similarity and broaden its applicability to uncover intriguing, universal scaling in the far dissipation range by computing high-order (\leq 20\/) structure functions numerically for: (1) the three-dimensional, incompressible Navier Stokes equation (with and without hyperviscosity); and (2) the GOY shell model for turbulence. Also, in case (2), with Taylor-microscale Reynolds numbers 4 \times 10^{4} \leq Re_{\lambda} \leq 3 \times 10^{6}\/, we find that the inertial-range exponents (\zeta_{p}\/) of the order - p\/ structure functions do not approach their Kolmogorov value p/3\/ as Re_{\lambda}\/ increases.Comment: RevTeX file, with six postscript figures. epsf.tex macro is used for figure insertion. Packaged using the 'uufiles' utilit

    Statistics of Dissipation and Enstrophy Induced by a Set of Burgers Vortices

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    Dissipation and enstropy statistics are calculated for an ensemble of modified Burgers vortices in equilibrium under uniform straining. Different best-fit, finite-range scaling exponents are found for locally-averaged dissipation and enstrophy, in agreement with existing numerical simulations and experiments. However, the ratios of dissipation and enstropy moments supported by axisymmetric vortices of any profile are finite. Therefore the asymptotic scaling exponents for dissipation and enstrophy induced by such vortices are equal in the limit of infinite Reynolds number.Comment: Revtex (4 pages) with 4 postscript figures included via psfi

    PPARα siRNA–Treated Expression Profiles Uncover the Causal Sufficiency Network for Compound-Induced Liver Hypertrophy

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    Uncovering pathways underlying drug-induced toxicity is a fundamental objective in the field of toxicogenomics. Developing mechanism-based toxicity biomarkers requires the identification of such novel pathways and the order of their sufficiency in causing a phenotypic response. Genome-wide RNA interference (RNAi) phenotypic screening has emerged as an effective tool in unveiling the genes essential for specific cellular functions and biological activities. However, eliciting the relative contribution of and sufficiency relationships among the genes identified remains challenging. In the rodent, the most widely used animal model in preclinical studies, it is unrealistic to exhaustively examine all potential interactions by RNAi screening. Application of existing computational approaches to infer regulatory networks with biological outcomes in the rodent is limited by the requirements for a large number of targeted permutations. Therefore, we developed a two-step relay method that requires only one targeted perturbation for genome-wide de novo pathway discovery. Using expression profiles in response to small interfering RNAs (siRNAs) against the gene for peroxisome proliferator-activated receptor α (Ppara), our method unveiled the potential causal sufficiency order network for liver hypertrophy in the rodent. The validity of the inferred 16 causal transcripts or 15 known genes for PPARα-induced liver hypertrophy is supported by their ability to predict non-PPARα–induced liver hypertrophy with 84% sensitivity and 76% specificity. Simulation shows that the probability of achieving such predictive accuracy without the inferred causal relationship is exceedingly small (p < 0.005). Five of the most sufficient causal genes have been previously disrupted in mouse models; the resulting phenotypic changes in the liver support the inferred causal roles in liver hypertrophy. Our results demonstrate the feasibility of defining pathways mediating drug-induced toxicity from siRNA-treated expression profiles. When combined with phenotypic evaluation, our approach should help to unleash the full potential of siRNAs in systematically unveiling the molecular mechanism of biological events

    Transcriptional and phenotypic comparisons of Ppara knockout and siRNA knockdown mice

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    RNA interference (RNAi) has great potential as a tool for studying gene function in mammals. However, the specificity and magnitude of the in vivo response to RNAi remains to be fully characterized. A molecular and phenotypic comparison of a genetic knockout mouse and the corresponding knockdown version would help clarify the utility of the RNAi approach. Here, we used hydrodynamic delivery of small interfering RNA (siRNA) to knockdown peroxisome proliferator activated receptor alpha (Ppara), a gene that is central to the regulation of fatty acid metabolism. We found that Ppara knockdown in the liver results in a transcript profile and metabolic phenotype that is comparable to those of Ppara(−/−) mice. Combining the profiles from mice treated with the PPARα agonist fenofibrate, we confirmed the specificity of the RNAi response and identified candidate genes proximal to PPARα regulation. Ppara knockdown animals developed hypoglycemia and hypertriglyceridemia, phenotypes observed in Ppara(−/−) mice. In contrast to Ppara(−/−) mice, fasting was not required to uncover these phenotypes. Together, these data validate the utility of the RNAi approach and suggest that siRNA can be used as a complement to classical knockout technology in gene function studies

    Prospect theory, mitigation and adaptation to climate change

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    Climate change is one of the most pressing challenges in current environmental policy. Appropriate policies intended to stimulate efficient adaptation and mitigation should not exclusively rely on the assumption of the homo oeconomicus, but take advantage of well-researched alternative behavioural patterns. Prospect theory provides a number of climate-relevant insights, such as the notion that evaluations of outcomes are reference dependent, and the relevance of perceived certainty of outcomes. This paper systematically reviews what prospect theory can offer to analyse mitigation and adaptation. It is shown that accounting for reference dependence and certainty effects contributes to a better understanding of some well-known puzzles in the climate debate, including (but not limited to) the different uptake of mitigation and adaptation amongst individuals and nations, the role of technical vs. financial adaptation, and the apparent preference for hard protection measures in coastal adaptation. Finally, concrete possibilities for empirical research on these effects are proposed
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