Improved Lagrangian mixing models for passive scalars in isotropic turbulence

Lagrangian data for velocity, scalars, and energy and scalar dissipation from direct numerical simulations are used to validate Lagrangian mixing models for inert passive scalars in stationary isotropic turbulence. The scalar fluctuations are nearly Gaussian, and, as a result of production by uniform mean gradients, statistically stationary. Comparisons are made for Taylor-scale Reynolds numbers in the range 38 to about 240 and Schmidt numbers in the range 1/8 to 1. Model predictions for one-point, one-time Eulerian statistics ~Eulerian correspondence! and one-particle, two-time Lagrangian statistics ~Lagrangian correspondence! are examined. Two scalar mixing models, namely the Lagrangian Fokker–Planck model and the Lagrangian colored-noise ~LCN! model, are proposed and written in terms of stochastic differential equations ~SDE! with specified drift and diffusion terms. Both of these models rely on statistics of the scalar field conditioned upon the energy dissipation, as provided by the Lagrangian spectral relaxation ~LSR! model. With the exception of the scalar dissipation, the models are shown to capture the Reynolds and Schmidt-number dependence of the Lagrangian integral time scales. However, the LCN model provides a more realistic description of the Lagrangian scalar fluctuations as differentiable time series having the correct form of the scalar autocorrelation function. Further extensions of the new mixing models to non-Gaussian scalars are conceptually straightforward, but require a closure for the scalar-conditioned scalar dissipation rate matrix. Likewise, accurate prediction of joint statistics for differential diffusion between different scalars with unequal molecular diffusivities will require the formulation of a multiscale SDE similar to the LSR model

Can Deflagration-Detonation-Transitions occur in Type Ia Supernovae?

The mechanism for deflagration-detonation-transition (DDT) by turbulent preconditioning, suggested to explain the possible occurrence of delayed detonations in Type Ia supernova explosions, is argued to be conceptually inconsistent. It relies crucially on diffusive heat losses of the burned material on macroscopic scales. Regardless of the amplitude of turbulent velocity fluctuations, the typical gradient scale for temperature fluctuations is shown to be the laminar flame width or smaller, rather than the factor of thousand more required for a DDT. Furthermore, thermonuclear flames cannot be fully quenched in regions much larger than the laminar flame width as a consequence of their simple ``chemistry''. Possible alternative explosion scenarios are briefly discussed.Comment: 8 pages, uses aastex; added references. Accepted by ApJ Letter

The Thermonuclear Explosion Of Chandrasekhar Mass White Dwarfs

The flame born in the deep interior of a white dwarf that becomes a Type Ia supernova is subject to several instabilities. We briefly review these instabilities and the corresponding flame acceleration. We discuss the conditions necessary for each of the currently proposed explosion mechanisms and the attendant uncertainties. A grid of critical masses for detonation in the range $10^7$ - $2 \times 10^9$ g cm$^{-3}$ is calculated and its sensitivity to composition explored. Prompt detonations are physically improbable and appear unlikely on observational grounds. Simple deflagrations require some means of boosting the flame speed beyond what currently exists in the literature. ``Active turbulent combustion'' and multi-point ignition are presented as two plausible ways of doing this. A deflagration that moves at the ``Sharp-Wheeler'' speed, $0.1 g_{\rm eff} t$, is calculated in one dimension and shows that a healthy explosion is possible in a simple deflagration if the front moves with the speed of the fastest floating bubbles. The relevance of the transition to the ``distributed burning regime'' is discussed for delayed detonations. No model emerges without difficulties, but detonation in the distributed regime is plausible, will produce intermediate mass elements, and warrants further study.Comment: 28 pages, 4 figures included, uses aaspp4.sty. Submitted to Ap

Non-Gaussian Distributions in Extended Dynamical Systems

We propose a novel mechanism for the origin of non-Gaussian tails in the probability distribution functions (PDFs) of local variables in nonlinear, diffusive, dynamical systems including passive scalars advected by chaotic velocity fields. Intermittent fluctuations on appropriate time scales in the amplitude of the (chaotic) noise can lead to exponential tails. We provide numerical evidence for such behavior in deterministic, discrete-time passive scalar models. Different possibilities for PDFs are also outlined.Comment: 12 pages and 6 figs obtainable from the authors, LaTex file, OSU-preprint-

The role of cell-cell adhesion in wound healing

We present a stochastic model which describes fronts of cells invading a wound. In the model cells can move, proliferate, and experience cell-cell adhesion. We find several qualitatively different regimes of front motion and analyze the transitions between them. Above a critical value of adhesion and for small proliferation large isolated clusters are formed ahead of the front. This is mapped onto the well-known ferromagnetic phase transition in the Ising model. For large adhesion, and larger proliferation the clusters become connected (at some fixed time). For adhesion below the critical value the results are similar to our previous work which neglected adhesion. The results are compared with experiments, and possible directions of future work are proposed.Comment: to appear in Journal of Statistical Physic

Prospective, multicenter study of managing lower extremity venous ulcers

Seventy patients with 90 venous ulcers were randomly assigned to hydrocolloid or conventional dressing and compression therapy at four study centers. The ulcers had been present for a mean of 47.8 in the control and 46.2 weeks in the treatment group and 42% of all patients had recurrent ulcers. Ulcers treated with hydrocolloid dressings reduced 71% and control treated wounds reduced 43% in area after 7.2 weeks of treatment. Thirty-four percent of all ulcers healed. Mean time to healing was 7 weeks for the hydrocolloid dressing group and 8 weeks for the control group. Most ulcers were less painful at final evaluation, but reduction in pain was more pronounced in hydrocolloid-dressed ulcers ( p =0.03). At baseline as well as during follow-up, significant differences between study centers were observed. Ulcers in patients in the United Kingdom were larger and less likely to heal ( p =0.001). Size of the ulcer at baseline was associated with treatment response and time to healing ( p =0.002). Percent reduction in ulcer area after 2 weeks was also correlated with treatment outcome ( p =0.004) and time to healing ( p =0.002). When all treatment outcome predictors were analyzed together, only percent reduction in area after 2 weeks remained statistically significant ( p =0.002), with percent reduction during the first 2 weeks of treatment >30% predicting healing .Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41373/1/10016_2005_Article_BF02132997.pd

On LEM/LES methodology for two-phase flows

A two-phase subgrid combustion model developed earlier has been evaluated for applicability in large-eddy simulations (LES). Direct Numerical Simulations (DNS) of two-phase isotropic turbulence in the presence of passive, momentum-coupled and vaporizing droplets has been extensively studied to form a base-line database. Current DNS results agree with earlier studies and show that the presence of droplets increase the kinetic energy and dissipation at the small scales. LES for these same cases were also carried out to investigate what modifications are needed to incorporate the small-scale turbulence modifications seen in DNS of two-phase flows. LES subgrid modeling for two-phase mixing within the context of the new subgrid combustion model is also addressed

Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation

Background: The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials. Main body: We suggest that this may be because classical inflammation only represents part of the story, with activation of neurogenic inflammation potentially one of the key initiating inflammatory events following TBI. Indeed, evidence suggests that the transient receptor potential cation channels (TRP channels), TRPV1 and TRPA1, are polymodal receptors that are activated by a variety of stimuli associated with TBI, including mechanical shear stress, leading to the release of neuropeptides such as substance P (SP). SP augments many aspects of the classical inflammatory response via activation of microglia and astrocytes, degranulation of mast cells, and promoting leukocyte migration. Furthermore, SP may initiate the earliest changes seen in blood-brain barrier (BBB) permeability, namely the increased transcellular transport of plasma proteins via activation of caveolae. This is in line with reports that alterations in transcellular transport are seen first following TBI, prior to decreases in expression of tight-junction proteins such as claudin-5 and occludin. Indeed, the receptor for SP, the tachykinin NK1 receptor, is found in caveolae and its activation following TBI may allow influx of albumin and other plasma proteins which directly augment the inflammatory response by activating astrocytes and microglia. Conclusions: As such, the neurogenic inflammatory response can exacerbate classical inflammation via a positive feedback loop, with classical inflammatory mediators such as bradykinin and prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition of neuroinflammation following TBI may require the inhibition of both classical and neurogenic inflammatory pathways.Frances Corrigan, Kimberley A. Mander, Anna V. Leonard and Robert Vin

Pharmacologic prophylaxis for atrial fibrillation following cardiac surgery: a systematic review

Atrial Fibrillation (AF) is the most common arrhythmia occurring after cardiac surgery. Its incidence varies depending on type of surgery. Postoperative AF may cause hemodynamic deterioration, predispose to stroke and increase mortality. Effective treatment for prophylaxis of postoperative AF is vital as reduces hospitalization and overall morbidity. Beta - blockers, have been proved to prevent effectively atrial fibrillation following cardiac surgery and should be routinely used if there are no contraindications. Sotalol may be more effective than standard b-blockers for the prevention of AF without causing an excess of side effects. Amiodarone is useful when beta-blocker therapy is not possible or as additional prophylaxis in high risk patients. Other agents such as magnesium, calcium channels blocker or non-antiarrhythmic drugs as glycose-insulin - potassium, non-steroidal anti-inflammatory drugs, corticosteroids, N-acetylcysteine and statins have been studied as alternative treatment for postoperative AF prophylaxis