Flame spread in laminar mixing layers: the triple flame

In the present paper we investígate flame spread in laminar mixing layers both experimentally and numerically. First, a burner has been designed and built such that stationary triple ñames can be stabilised in a coflowing stream with well defined linear concentration gradients and well defined uniform flow velocity at the inlet to the combustión chamber. The burner itself as well as first experimental results obtained with it are presented. Second, a theoretical model is formulated for analysis of triple flames in a strained mixing laycr generated by directing a fuel stream and an oxidizer stream towards each other. Here attention is focused on the stagnation región where by means of a similarity formulation the three-dimensional flow can be described by only two spatial coordinates. To solve the governing equations for the limiting case in which a thermal-diffusional model results, a numerical solution procedure based on self-adaptive mesh refinement is developed. For the thermal-diffusional model, the structure of the triple flame and its propagation velocity are obtained by solving numerically the governing similarity equations for a wide range of strain rates

Deflagration regimes of laminar flames modeled after the ozone decomposition flame

Methods of activation-energy asymptotics are employed to investigate regimes of combustion of steady, planar, adiabatic deflagrations involving a four-step kinetic mechanism modeled after that of the ozone decomposition flame. The analysis demonstrates the occurrence of previously known regimes having flame structures that involve a nonreactive preheat zone followed by a narrow reactive-diffusive zone, in which a steady-state approximation for the reaction intermediary may or may not apply and downstream from which a recombination zone may or may not exist. In addition, a new regime is identified having a two-zone flame structure in which the intermediary is generated in a downstream zone that obeys a steady-state approximation for temperature and diffuses into an upstream zone where the primary heat release occurs. In this regime convection, diffusion, and reaction all are important in both zones, and heat release persists in the preheat zone all the way to the cold boundary. For the ozone flame new results for burning velocities are given and regimes are identified as functions of pressure, initial temperature, and initial ozone concentration

Nonlinear cellular instabilities of planar premixed flames: numerical simulations of the Reactive Navier-Stokes equations

Two-dimensional compressible Reactive Navier-Stokes numerical simulations of intrinsic planar, premixed flame instabilities are performed. The initial growth of a sinusoidally perturbed planar flame is first compared with the predictions of a recent exact linear stability analysis, and it is shown the analysis provides a necessary but not sufficient test problem for validating numerical schemes intended for flame simulations. The long-time nonlinear evolution up to the final nonlinear stationary cellular flame is then examined for numerical domains of increasing width. It is shown that for routinely computationally affordable domain widths, the evolution and final state is, in general, entirely dependent on the width of the domain and choice of numerical boundary conditions. It is also shown that the linear analysis has no relevance to the final nonlinear cell size. When both hydrodynamic and thermal-diffusive effects are important, the evolution consists of a number of symmetry breaking cell splitting and re-merging processes which results in a stationary state of a single very asymmetric cell in the domain, a flame shape which is not predicted by weakly nonlinear evolution equations. Resolution studies are performed and it is found that lower numerical resolutions, typical of those used in previous works, do not give even the qualitatively correct solution in wide domains. We also show that the long-time evolution, including whether or not a stationary state is ever achieved, depends on the choice of the numerical boundary conditions at the inflow and outflow boundaries, and on the numerical domain length and flame Mach number for the types of boundary conditions used in some previous works

Linear stability of planar premixed flames: reactive Navier-Stokes equations with finite activation energy and arbitrary Lewis number

A numerical shooting method for performing linear stability analyses of travelling waves is described and applied to the problem of freely propagating planar premixed flames. Previous linear stability analyses of premixed flames either employ high activation temperature asymptotics or have been performed numerically with finite activation temperature, but either for unit Lewis numbers (which ignores thermal-diffusive effects) or in the limit of small heat release (which ignores hydrodynamic effects). In this paper the full reactive Navier-Stokes equations are used with arbitrary values of the parameters (activation temperature, Lewis number, heat of reaction, Prandtl number), for which both thermal-diffusive and hydrodynamic effects on the instability, and their interactions, are taken into account. Comparisons are made with previous asymptotic and numerical results. For Lewis numbers very close to or above unity, for which hydrodynamic effects caused by thermal expansion are the dominant destablizing mechanism, it is shown that slowly varying flame analyses give qualitatively good but quantitatively poor predictions, and also that the stability is insensitive to the activation temperature. However, for Lewis numbers sufficiently below unity for which thermal-diffusive effects play a major role, the stability of the flame becomes very sensitive to the activation temperature. Indeed, unphysically high activation temperatures are required for the high activation temperature analysis to give quantitatively good predictions at such low Lewis numbers. It is also shown that state-insensitive viscosity has a small destabilizing effect on the cellular instability at low Lewis numbers

Stability of Relativistic Matter with Magnetic Fields for Nuclear Charges up to the Critical Value

We give a proof of stability of relativistic matter with magnetic fields all the way up to the critical value of the nuclear charge $Z\alpha=2/\pi$.Comment: LaTeX2e, 12 page

The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier

Podocytes form the outer part of the glomerular filter, where they have to withstand enormous transcapillary filtration forces driving glomerular filtration. Detachment of podocytes from the glomerular basement membrane precedes most glomerular diseases. However, little is known about the regulation of podocyte adhesion in vivo. Thus, we systematically screened for podocyte-specific focal adhesome (FA) components, using genetic reporter models in combination with iTRAQ-based mass spectrometry. This approach led to the identification of FERM domain protein EPB41L5 as a highly enriched podocyte-specific FA component in vivo. Genetic deletion of Epb41l5 resulted in severe proteinuria, detachment of podocytes, and development of focal segmental glomerulosclerosis. Remarkably, by binding and recruiting the RhoGEF ARGHEF18 to the leading edge, EPB41L5 directly controls actomyosin contractility and subsequent maturation of focal adhesions, cell spreading, and migration. Furthermore, EPB41L5 controls matrix-dependent outside-in signaling by regulating the focal adhesome composition. Thus, by linking extracellular matrix sensing and signaling, focal adhesion maturation, and actomyosin activation EPB41L5 ensures the mechanical stability required for podocytes at the kidney filtration barrier. Finally, a diminution of EPB41L5-dependent signaling programs appears to be a common theme of podocyte disease, and therefore offers unexpected interventional therapeutic strategies to prevent podocyte loss and kidney disease progression

Single cell sequencing reveals endothelial plasticity with transient mesenchymal activation after myocardial infarction.

Endothelial cells play a critical role in the adaptation of tissues to injury. Tissue ischemia induced by infarction leads to profound changes in endothelial cell functions and can induce transition to a mesenchymal state. Here we explore the kinetics and individual cellular responses of endothelial cells after myocardial infarction by using single cell RNA sequencing. This study demonstrates a time dependent switch in endothelial cell proliferation and inflammation associated with transient changes in metabolic gene signatures. Trajectory analysis reveals that the majority of endothelial cells 3 to 7 days after myocardial infarction acquire a transient state, characterized by mesenchymal gene expression, which returns to baseline 14 days after injury. Lineage tracing, using the Cdh5-CreERT2;mT/mG mice followed by single cell RNA sequencing, confirms the transient mesenchymal transition and reveals additional hypoxic and inflammatory signatures of endothelial cells during early and late states after injury. These data suggest that endothelial cells undergo a transient mes-enchymal activation concomitant with a metabolic adaptation within the first days after myocardial infarction but do not acquire a long-term mesenchymal fate. This mesenchymal activation may facilitate endothelial cell migration and clonal expansion to regenerate the vascular network

Accumulation of α-synuclein mediates podocyte injury in Fabry nephropathy

Current therapies for Fabry disease are based on reversing intracellular accumulation of globotriaosylceramide (Gb3) by enzyme replacement therapy (ERT) or chaperone-mediated stabilization of the defective enzyme, thereby alleviating lysosomal dysfunction. However, their effect in the reversal of end-organ damage, like kidney injury and chronic kidney disease, remains unclear. In this study, ultrastructural analysis of serial human kidney biopsies showed that long-term use of ERT reduced Gb3 accumulation in podocytes but did not reverse podocyte injury. Then, a CRISPR/Cas9–mediated α-galactosidase knockout podocyte cell line confirmed ERT-mediated reversal of Gb3 accumulation without resolution of lysosomal dysfunction. Transcriptome-based connectivity mapping and SILAC-based quantitative proteomics identified α-synuclein (SNCA) accumulation as a key event mediating podocyte injury. Genetic and pharmacological inhibition of SNCA improved lysosomal structure and function in Fabry podocytes, exceeding the benefits of ERT. Together, this work reconceptualizes Fabry-associated cell injury beyond Gb3 accumulation, and introduces SNCA modulation as a potential intervention, especially for patients with Fabry nephropathy.publishedVersio