Wall turbulence control

A variety of wall turbulence control devices which were experimentally investigated are discussed; these include devices for burst control, alteration of outer flow structures, large eddy substitution, increased heat transfer efficiency, and reduction of wall pressure fluctuations. Control of pre-burst flow was demonstrated with a single, traveling surface depression which is phase-locked to elements of the burst production process. Another approach to wall turbulence control is to interfere with the outer layer coherent structures. A device in the outer part of a boundary layer was shown to suppress turbulence and reduce drag by opposing both the mean and unsteady vorticity in the boundary layer. Large eddy substitution is a method in which streamline curvature is introduced into the boundary layer in the form of streamwise vortices. Riblets, which were already shown to reduce turbulent drag, were also shown to exhibit superior heat transfer characteristics. Heat transfer efficiency as measured by the Reynolds Analogy Factor was shown to be as much as 36 percent greater than a smooth flat plate in a turbulent boundary layer. Large Eddy Break-Up (LEBU) which are also known to reduce turbulent drag were shown to reduce turbulent wall pressure fluctuation

Modelling the effect of gap junctions on tissue-level cardiac electrophysiology

When modelling tissue-level cardiac electrophysiology, continuum approximations to the discrete cell-level equations are used to maintain computational tractability. One of the most commonly used models is represented by the bidomain equations, the derivation of which relies on a homogenisation technique to construct a suitable approximation to the discrete model. This derivation does not explicitly account for the presence of gap junctions connecting one cell to another. It has been seen experimentally [Rohr, Cardiovasc. Res. 2004] that these gap junctions have a marked effect on the propagation of the action potential, specifically as the upstroke of the wave passes through the gap junction. In this paper we explicitly include gap junctions in a both a 2D discrete model of cardiac electrophysiology, and the corresponding continuum model, on a simplified cell geometry. Using these models we compare the results of simulations using both continuum and discrete systems. We see that the form of the action potential as it passes through gap junctions cannot be replicated using a continuum model, and that the underlying propagation speed of the action potential ceases to match up between models when gap junctions are introduced. In addition, the results of the discrete simulations match the characteristics of those shown in Rohr 2004. From this, we suggest that a hybrid model -- a discrete system following the upstroke of the action potential, and a continuum system elsewhere -- may give a more accurate description of cardiac electrophysiology.Comment: In Proceedings HSB 2012, arXiv:1208.315

Mechanism of Magainin 2a Induced Permeabilization of Phospholipid Vesicles

The magainins, peptide antibiotics secreted by the frog Xenopus laevis, have previously been shown to permeabilize phospholipid vesicles. To elucidate the mechanism of permeabilization, we have conducted detailed kinetic studies of magainin 2 amide (mgn2a)hduced release of 6-carboxyfluorescein from vesicles of phosphatidylserine. The results show that dye release occurs in (at least) two stages-an initial rapid phase, with t1/2 ≈ 3 s, followed by a much slower phase that approaches zero leakage rate before all the dye is released. Light-scattering studies showed that mgn2a does not cause gross changes in vesicle structure. The peptide was found to rapidly equilibrate between vesicles; this was demonstrated by determining a binding isotherm for the peptidelipid interaction, and by showing that addition of unloaded vesicles rapidly quenches peptide-induced leakage from loaded vesicles. Transient dye release in the presence of an equilibrating peptide can be explained in two ways: (1) the peptide exists only transiently in an active form; (2) the vesicles are only transiently leaky. Preincubation of mgn2a at assay concentrations in buffer alone or with unloaded vesicles did not inactivate the peptide. Therefore, rapid leakage is probably due to transient destabilization of the vesicle upon addition of mgn2a

Mechanism of Magainin 2a Induced Permeabilization of Phospholipid Vesicles

The magainins, peptide antibiotics secreted by the frog Xenopus laevis, have previously been shown to permeabilize phospholipid vesicles. To elucidate the mechanism of permeabilization, we have conducted detailed kinetic studies of magainin 2 amide (mgn2a)hduced release of 6-carboxyfluorescein from vesicles of phosphatidylserine. The results show that dye release occurs in (at least) two stages-an initial rapid phase, with t1/2 ≈ 3 s, followed by a much slower phase that approaches zero leakage rate before all the dye is released. Light-scattering studies showed that mgn2a does not cause gross changes in vesicle structure. The peptide was found to rapidly equilibrate between vesicles; this was demonstrated by determining a binding isotherm for the peptidelipid interaction, and by showing that addition of unloaded vesicles rapidly quenches peptide-induced leakage from loaded vesicles. Transient dye release in the presence of an equilibrating peptide can be explained in two ways: (1) the peptide exists only transiently in an active form; (2) the vesicles are only transiently leaky. Preincubation of mgn2a at assay concentrations in buffer alone or with unloaded vesicles did not inactivate the peptide. Therefore, rapid leakage is probably due to transient destabilization of the vesicle upon addition of mgn2a

Impact of electronic reminders on venous thromboprophylaxis after admissions and transfers

Objective Clinical decision support has the potential to improve prevention of venous thromboembolism (VTE). The purpose of this prospective study was to analyze the effect of electronic reminders on thromboprophylaxis rates in wards to which patients were admitted and transferred. The latter was of particular interest since patient handoffs are considered to be critical safety issues. Methods The trial involved two study periods in the six departments of a university hospital, three of which were randomly assigned to the intervention group displaying reminders during the second period. At 6 h after admission or transfer, the algorithm checked for prophylaxis orders within 0-30 h of the patient's arrival, increasing the specificity of the displayed reminders. Results The significant impact of the reminders could be seen by prophylaxis orders placed 6-24 h after admission (increasing from 8.6% (223/2579) to 12% (307/2555); p<0.0001) and transfer (increasing from 2.4% (39/1616) to 3.7% (63/1682); p=0.034). In admission wards, the rate of thromboprophylaxis increased from 62.4% to 67.7% (p<0.0001), and in transfer wards it increased from 80.2% to 84.3% (p=0.0022). Overall, the rate of prophylaxis significantly increased in the intervention group from 69.2% to 74.3% (p<0.0001). No significant changes were observed in the control group. Postponing prophylaxis checks to 6 h after admissions and transfers reduced the number of reminders by 62% and thereby minimized the risk of alert fatigue. Conclusions The reminders improved awareness of VTE prevention in both admission and transfer wards. This approach may contribute to better quality of care and safer patient handoff

Evidence for tuning adipocytes ICER levels for obesity care.

Abnormal adipokine production, along with defective uptake and metabolism of glucose within adipocytes, contributes to insulin resistance and altered glucose homeostasis. Recent research has highlighted one of the mechanisms that accounts for impaired production of adiponectin (ADIPOQ) and adipocyte glucose uptake in obesity. In adipocytes of human obese subjects and mice fed with a high fat diet, the level of the inducible cAMP early repressor (ICER) is diminished. Reduction of ICER elevates the cAMP response element binding protein (CREB) activity, which in turn increases the repressor activating transcription factor 3. In fine, the cascade triggers reduction in the ADIPOQ and GLUT4 levels, which ultimately hampers insulin-mediated glucose uptake. The c-Jun N-terminal kinase (JNK) interacting-protein 1, also called islet brain 1 (IB1), is a target of CREB/ICER that promotes JNK-mediated insulin resistance in adipocytes. A rise in IB1 and c-Jun levels accompanies the drop of ICER in white adipose tissues of obese mice when compared with mice fed with a chow diet. Other than the expression of ADIPOQ and glucose transport, decline in ICER expression might impact insulin signaling. Impairment of ICER is a critical issue that will need major consideration in future therapeutic purposes

Combining polynomial chaos expansions and genetic algorithm for the coupling of electrophysiological models

The number of computational models in cardiac research has grown over the last decades. Every year new models with di erent assumptions appear in the literature dealing with di erences in interspecies cardiac properties. Generally, these new models update the physiological knowledge using new equations which reect better the molecular basis of process. New equations require the fi tting of parameters to previously known experimental data or even, in some cases, simulated data. This work studies and proposes a new method of parameter adjustment based on Polynomial Chaos and Genetic Algorithm to nd the best values for the parameters upon changes in the formulation of ionic channels. It minimizes the search space and the computational cost combining it with a Sensitivity Analysis. We use the analysis of di ferent models of L-type calcium channels to see that by reducing the number of parameters, the quality of the Genetic Algorithm dramatically improves. In addition, we test whether the use of the Polynomial Chaos Expansions improves the process of the Genetic Algorithm search. We conclude that it reduces the Genetic Algorithm execution in an order of 103 times in the case studied here, maintaining the quality of the results. We conclude that polynomial chaos expansions can improve and reduce the cost of parameter adjustment in the development of new models.Peer ReviewedPostprint (author's final draft

Raman Spectroscopy of Synthetic Antimicrobial Frog Peptides Magainin 2a and PGLa

Magainin and PGLa are 23- and 21-residue peptides isolated from the skin of the African clawed frog Xenopus lueuis. They protect the frog from infection and exhibit a broad-spectrum antimicrobial activity in vitro. The mechanism of this activity involves the interaction of magainin with microbial membranes. We have measured the secondary structure and membrane-perturbing ability of these peptides to obtain information about this mechanism. Our results show that mgn2a forms a helix with an average length of less than 20 Å upon binding to liposomes. At high concentrations (50 mg/mL) mgn2a spontaneously solubilizes phosphatidylcholine liposomes at temperatures above the gel-liquid-crystalline phase transition. Mgn2a appears to bind to the surface of liposomes made of negatively charged lipids without spontaneously penetrating the bilayer. Finally, mgn2a and PGLa interact together with liposomes in a synergistic way that enhances the helix content of one or both of the peptides and allows the peptides to more easily penetrate the bilayer. PGLa mixed with a small nonperturbing amount of magainin 2 amide is 25-43 times as potent as PGLa alone at inducing the release of carboxyfluorescein from liposomes. The results suggest that the mechanism of antimicrobial activity does not involve a channel formed by transmembrane helical peptides

Effect of Off-Body Laser Discharge on Drag Reduction of Hemisphere Cylinder in Supersonic Flow-Part II

The interaction of on-axis and o -axis laser discharge in front of a hemisphere cylinder in Mach 2.0 ow is investigated numerically. Details of the physics of the interaction of the laser-induced shock and the heated region with the bow shock and its e ect on drag reduction are included. The energetic eciency of the laser discharge in reducing drag is calculated