Toward a structural understanding of turbulent drag reduction: nonlinear coherent states in viscoelastic shear flows

Nontrivial steady flows have recently been found that capture the main structures of the turbulent buffer layer. We study the effects of polymer addition on these "exact coherent states" (ECS) in plane Couette flow. Despite the simplicity of the ECS flows, these effects closely mirror those observed experimentally: Structures shift to larger length scales, wall-normal fluctuations are suppressed while streamwise ones are enhanced, and drag is reduced. The mechanism underlying these effects is elucidated. These results suggest that the ECS are closely related to buffer layer turbulence.Comment: 5 pages, 3 figures, published version, Phys. Rev. Lett. 89, 208301 (2002

Stretching of polymers in a random three-dimensional flow

Behavior of a dilute polymer solution in a random three-dimensional flow with an average shear is studied experimentally. Polymer contribution to the shear stress is found to be more than two orders of magnitude higher than in a laminar shear flow. The results indicate that the polymer molecules get strongly stretched by the random motion of the fluid.Comment: 4 pages, 3 figure

Polymer transport in random flow

The dynamics of polymers in a random smooth flow is investigated in the framework of the Hookean dumbbell model. The analytical expression of the time-dependent probability density function of polymer elongation is derived explicitly for a Gaussian, rapidly changing flow. When polymers are in the coiled state the pdf reaches a stationary state characterized by power-law tails both for small and large arguments compared to the equilibrium length. The characteristic relaxation time is computed as a function of the Weissenberg number. In the stretched state the pdf is unstationary and exhibits multiscaling. Numerical simulations for the two-dimensional Navier-Stokes flow confirm the relevance of theoretical results obtained for the delta-correlated model.Comment: 28 pages, 6 figure

Crude incidence in two-phase designs in the presence of competing risks.

BackgroundIn many studies, some information might not be available for the whole cohort, some covariates, or even the outcome, might be ascertained in selected subsamples. These studies are part of a broad category termed two-phase studies. Common examples include the nested case-control and the case-cohort designs. For two-phase studies, appropriate weighted survival estimates have been derived; however, no estimator of cumulative incidence accounting for competing events has been proposed. This is relevant in the presence of multiple types of events, where estimation of event type specific quantities are needed for evaluating outcome.MethodsWe develop a non parametric estimator of the cumulative incidence function of events accounting for possible competing events. It handles a general sampling design by weights derived from the sampling probabilities. The variance is derived from the influence function of the subdistribution hazard.ResultsThe proposed method shows good performance in simulations. It is applied to estimate the crude incidence of relapse in childhood acute lymphoblastic leukemia in groups defined by a genotype not available for everyone in a cohort of nearly 2000 patients, where death due to toxicity acted as a competing event. In a second example the aim was to estimate engagement in care of a cohort of HIV patients in resource limited setting, where for some patients the outcome itself was missing due to lost to follow-up. A sampling based approach was used to identify outcome in a subsample of lost patients and to obtain a valid estimate of connection to care.ConclusionsA valid estimator for cumulative incidence of events accounting for competing risks under a general sampling design from an infinite target population is derived

Hysteresis phenomenon in turbulent convection

Coherent large-scale circulations of turbulent thermal convection in air have been studied experimentally in a rectangular box heated from below and cooled from above using Particle Image Velocimetry. The hysteresis phenomenon in turbulent convection was found by varying the temperature difference between the bottom and the top walls of the chamber (the Rayleigh number was changed within the range of $10^7 - 10^8$). The hysteresis loop comprises the one-cell and two-cells flow patterns while the aspect ratio is kept constant ($A=2 - 2.23$). We found that the change of the sign of the degree of the anisotropy of turbulence was accompanied by the change of the flow pattern. The developed theory of coherent structures in turbulent convection (Elperin et al. 2002; 2005) is in agreement with the experimental observations. The observed coherent structures are superimposed on a small-scale turbulent convection. The redistribution of the turbulent heat flux plays a crucial role in the formation of coherent large-scale circulations in turbulent convection.Comment: 10 pages, 9 figures, REVTEX4, Experiments in Fluids, 2006, in pres

Neandertal and Denisovan DNA from Pleistocene sediments.

Although a rich record of Pleistocene human-associated archaeological assemblages exists, the scarcity of hominin fossils often impedes the understanding of which hominins occupied a site. Using targeted enrichment of mitochondrial DNA we show that cave sediments represent a rich source of ancient mammalian DNA that often includes traces of hominin DNA, even at sites and in layers where no hominin remains have been discovered. By automation-assisted screening of numerous sediment samples we detect Neandertal DNA in eight archaeological layers from four caves in Eurasia. In Denisova Cave we retrieved Denisovan DNA in a Middle Pleistocene layer near the bottom of the stratigraphy. Our work opens the possibility to detect the presence of hominin groups at sites and in areas where no skeletal remains are found

Drug-gene interactions of antihypertensive medications and risk of incident cardiovascular disease: a pharmacogenomics study from the CHARGE consortium

Background Hypertension is a major risk factor for a spectrum of cardiovascular diseases (CVD), including myocardial infarction, sudden death, and stroke. In the US, over 65 million people have high blood pressure and a large proportion of these individuals are prescribed antihypertensive medications. Although large long-term clinical trials conducted in the last several decades have identified a number of effective antihypertensive treatments that reduce the risk of future clinical complications, responses to therapy and protection from cardiovascular events vary among individuals. Methods Using a genome-wide association study among 21,267 participants with pharmaceutically treated hypertension, we explored the hypothesis that genetic variants might influence or modify the effectiveness of common antihypertensive therapies on the risk of major cardiovascular outcomes. The classes of drug treatments included angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, each study performed array-based genome-wide genotyping, imputed to HapMap Phase II reference panels, and used additive genetic models in proportional hazards or logistic regression models to evaluate drug-gene interactions for each of four therapeutic drug classes. We used meta-analysis to combine study-specific interaction estimates for approximately 2 million single nucleotide polymorphisms (SNPs) in a discovery analysis among 15,375 European Ancestry participants (3,527 CVD cases) with targeted follow-up in a case-only study of 1,751 European Ancestry GenHAT participants as well as among 4,141 African-Americans (1,267 CVD cases). Results Although drug-SNP interactions were biologically plausible, exposures and outcomes were well measured, and power was sufficient to detect modest interactions, we did not identify any statistically significant interactions from the four antihypertensive therapy meta-analyses (Pinteraction > 5.0×10−8). Similarly, findings were null for meta-analyses restricted to 66 SNPs with significant main effects on coronary artery disease or blood pressure from large published genome-wide association studies (Pinteraction ≥ 0.01). Our results suggest that there are no major pharmacogenetic influences of common SNPs on the relationship between blood pressure medications and the risk of incident CVD