183 research outputs found

    Intermittency and the Slow Approach to Kolmogorov Scaling

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    From a simple path integral involving a variable volatility in the velocity differences, we obtain velocity probability density functions with exponential tails, resembling those observed in fully developed turbulence. The model yields realistic scaling exponents and structure functions satisfying extended self-similarity. But there is an additional small scale dependence for quantities in the inertial range, which is linked to a slow approach to Kolmogorov (1941) scaling occurring in the large distance limit.Comment: 10 pages, 5 figures, minor changes to mirror version to appear in PR

    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

    Ranking Port Cities with High Exposure and Vulnerability to Climate Extremes

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    DOI:10.1787/011766488208This global screening study makes a first estimate of the exposure of the world's large port cities to coastal flooding due to storm surge and damage due to high winds. This assessment also investigates how climate change is likely to impact each port city's exposure to coastal flooding by the 2070s, alongside subsidence and population growth and urbanisation. The study provides a much more comprehensive analysis than earlier assessments, focusing on the 136 port cities around the world that have more than one million inhabitants in 2005. The analysis demonstrates that a large number of people are already exposed to coastal flooding in large port cities. Across all cities, about 40 million people (0.6% of the global population or roughly 1 in 10 of the total port city population in the cities considered here) are exposed to a 1 in 100 year coastal flood event. For present-day conditions (2005), the top ten cities in terms of exposed population are estimated to be Mumbai, Guangzhou, Shanghai, Miami, Ho Chi Minh City, Kolkata, Greater New York, Osaka-Kobe, Alexandria and New Orleans; almost equally split between developed and developing countries. When assets are considered, the current distribution becomes more heavily weighted towards developed countries, as the wealth of the cities becomes important. The top 10 cities in terms of assets exposed are Miami, Greater New York, New Orleans, Osaka-Kobe, Tokyo, Amsterdam, Rotterdam, Nagoya, Tampa-St Petersburg and Virginia Beach. These cities contain 60% of the total exposure, but are from only three (wealthy) countries: USA, Japan and the Netherlands. The total value of assets exposed in 2005 is across all cities considered here is estimated to be US3,000 billion; corresponding to around 5% of global GDP in 2005 (both measured in international USD)... Available at : http://www.oecd-ilibrary.org/environment/ranking-port-cities-with-high-exposure-and-vulnerability-to-climate-extremes_01176648820

    Exact Resummations in the Theory of Hydrodynamic Turbulence: III. Scenarios for Anomalous Scaling and Intermittency

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    Elements of the analytic structure of anomalous scaling and intermittency in fully developed hydrodynamic turbulence are described. We focus here on the structure functions of velocity differences that satisfy inertial range scaling laws Sn(R)RζnS_n(R)\sim R^{\zeta_n}, and the correlation of energy dissipation Kϵϵ(R)RμK_{\epsilon\epsilon}(R) \sim R^{-\mu}. The goal is to understand the exponents ζn\zeta_n and μ\mu from first principles. In paper II of this series it was shown that the existence of an ultraviolet scale (the dissipation scale η\eta) is associated with a spectrum of anomalous exponents that characterize the ultraviolet divergences of correlations of gradient fields. The leading scaling exponent in this family was denoted Δ\Delta. The exact resummation of ladder diagrams resulted in the calculation of Δ\Delta which satisfies the scaling relation Δ=2ζ2\Delta=2-\zeta_2. In this paper we continue our analysis and show that nonperturbative effects may introduce multiscaling (i.e. ζn\zeta_n not being linear in nn) with the renormalization scale being the infrared outer scale of turbulence LL. It is shown that deviations from K41 scaling of Sn(R)S_n(R) (ζnn/3\zeta_n\neq n/3) must appear if the correlation of dissipation is mixing (i.e. μ>0\mu>0). We derive an exact scaling relation μ=2ζ2ζ4\mu = 2\zeta_2-\zeta_4. We present analytic expressions for ζn\zeta_n for all nn and discuss their relation to experimental data. One surprising prediction is that the time decay constant τn(R)Rzn\tau_n(R)\propto R^{z_n} of Sn(R)S_n(R) scales independently of nn: the dynamic scaling exponent znz_n is the same for all nn-order quantities, zn=ζ2z_n=\zeta_2.Comment: PRE submitted, 22 pages + 11 figures, REVTeX. The Eps files of figures will be FTPed by request to [email protected]

    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

    Using the adaptive cycle in climate-risk insurance to design resilient futures

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    Assessing the dynamics of resilience could help insurers and governments reduce the costs of climate-risk insurance schemes and secure future insurability in the face of an increase in extreme hydro-meteorological events related to climate change

    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
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