An observationally-driven kinetic approach to coronal heating

Coronal heating through the explosive release of magnetic energy remains an open problem in solar physics. Recent hydrodynamical models attempt an investigation by placing swarms of 'nanoflares' at random sites and times in modeled one-dimensional coronal loops. We investigate the problem in three dimensions, using extrapolated coronal magnetic fields of observed solar active regions. We apply a nonlinear force-free field extrapolation above an observed photospheric magnetogram of NOAA active region (AR) 11158. We then determine the locations, energy contents, and volumes of 'unstable' areas, namely areas prone to releasing magnetic energy due to locally accumulated electric current density. Statistical distributions of these volumes and their fractal dimension are inferred, investigating also their dependence on spatial resolution. Further adopting a simple resistivity model, we infer the properties of the fractally distributed electric fields in these volumes. Next, we monitor the evolution of 10^5 particles (electrons and ions) obeying an initial Maxwellian distribution with a temperature of 10 eV, by following their trajectories and energization when subjected to the resulting electric fields. For computational convenience, the length element of the magnetic-field extrapolation is 1 arcsec, much coarser than the particles collisional mean free path in the low corona. The presence of collisions traps the bulk of the plasma around the unstable volumes, or current sheets (UCS), with only a tail of the distribution gaining substantial energy. Assuming that the distance between UCS is similar to the collisional mean free path we find that the low active-region corona is heated to 100-200 eV, corresponding to temperatures exceeding 2 MK, within tens of seconds for electrons and thousands of seconds for ions. Fractally distributed, nanoflare-triggening fragmented UCS ...Comment: accepted by A&

Particle Acceleration in Multiple Dissipation Regions

The sharp magnetic discontinuities which naturally appear in solar magnetic flux tubes driven by turbulent photospheric motions are associated with intense currents. \citet{Par83} proposed that these currents can become unstable to a variety of microscopic processes, with the net result of dramatically enhanced resistivity and heating (nanoflares). The electric fields associated with such ``hot spots'' are also expected to enhance particle acceleration. We test this hypothesis by exact relativistic orbit simulations in strong random phase magnetohydrodynamic (MHD) turbulence which is forming localized super-Dreicer Ohm electric fields ($E_\Omega/E_D$ = $10^2 ... 10^5$) occurring in 2..15 % of the volume. It is found that these fields indeed yield a large amplification of acceleration of electrons and ions, and can effectively overcome the injection problem. We suggest in this article that nanoflare heating will be associated with sporadic particle acceleration.Comment: 12 pages, 5 figures, to appear in ApJ

Serum Amyloid A induces toll-like receptor 2-dependent inflammatory cytokine expression and atrophy in C2C12 skeletal muscle myotubes

Background Skeletal muscle wasting is an important comorbidity of Chronic Obstructive Pulmonary Disease (COPD) and is strongly correlated with morbidity and mortality. Patients who experience frequent acute exacerbations of COPD (AECOPD) have more severe muscle wasting and reduced recovery of muscle mass and function after each exacerbation. Serum levels of the pro-inflammatory acute phase protein Serum Amyloid A (SAA) can rise more than 1000-fold in AECOPD and are predictively correlated with exacerbation severity. The direct effects of SAA on skeletal muscle are poorly understood. Here we have examined SAA effects on pro-inflammatory cachectic cytokine expression (IL-6 and TNFα) and atrophy in C2C12 myotubes. Results SAA increased IL-6 (31-fold) and TNFα (6.5-fold) mRNA levels compared to control untreated cells after 3h of SAA treatment, and increased secreted IL-6 protein at 24h. OxPAPC, a dual TLR2 and TLR4 inhibitor, reduced the response to SAA by approximately 84% compared to SAA alone, and the TLR2 neutralising antibody T2.5 abolished SAA-induced expression of IL-6, indicating that SAA signalling in C2C12 myotubes is primarily via TLR2. SAA also reduced myotube width by 10-13% and induced a 2.5-fold increase in the expression of the muscle atrophy gene Atrogin-1, suggesting direct effects of SAA on muscle wasting. Blocking of TLR2 inhibited the SAA-induced decrease in myotube width and Atrogin-1 gene expression, indicating that SAA induces atrophy through TLR2. Conclusions These data demonstrate that SAA stimulates a robust pro-inflammatory response in skeletal muscle myotubes via the TLR2-dependent release of IL-6 and TNFα. Furthermore, the observed atrophy effects indicate that SAA could also be directly contributing to the wasting and poor recovery of muscle mass. Therapeutic strategies targeting this SAA-TLR2 axis may therefore ameliorate muscle wasting in AECOPD and a range of other inflammatory conditions associated with loss of m

Are Coronae of Magnetically Active Stars Heated by Flares? III. Analytical Distribution of Superimposed Flares

(abridged) We study the hypothesis that observed X-ray/extreme ultraviolet emission from coronae of magnetically active stars is entirely (or to a large part) due to the superposition of flares, using an analytic approach to determine the amplitude distribution of flares in light curves. The flare-heating hypothesis is motivated by time series that show continuous variability suggesting the presence of a large number of superimposed flares with similar rise and decay time scales. We rigorously relate the amplitude distribution of stellar flares to the observed histograms of binned counts and photon waiting times, under the assumption that the flares occur at random and have similar shapes. Applying these results to EUVE/DS observations of the flaring star AD Leo, we find that the flare amplitude distribution can be represented by a truncated power law with a power law index of 2.3 +/- 0.1. Our analytical results agree with existing Monte Carlo results of Kashyap et al. (2002) and Guedel et al. (2003). The method is applicable to a wide range of further stochastically bursting astrophysical sources such as cataclysmic variables, Gamma Ray Burst substructures, X-ray binaries, and spatially resolved observations of solar flares.Comment: accepted for publication in Ap

Random walk through fractal environments

We analyze random walk through fractal environments, embedded in 3-dimensional, permeable space. Particles travel freely and are scattered off into random directions when they hit the fractal. The statistical distribution of the flight increments (i.e. of the displacements between two consecutive hittings) is analytically derived from a common, practical definition of fractal dimension, and it turns out to approximate quite well a power-law in the case where the dimension D of the fractal is less than 2, there is though always a finite rate of unaffected escape. Random walks through fractal sets with D less or equal 2 can thus be considered as defective Levy walks. The distribution of jump increments for D > 2 is decaying exponentially. The diffusive behavior of the random walk is analyzed in the frame of continuous time random walk, which we generalize to include the case of defective distributions of walk-increments. It is shown that the particles undergo anomalous, enhanced diffusion for D_F < 2, the diffusion is dominated by the finite escape rate. Diffusion for D_F > 2 is normal for large times, enhanced though for small and intermediate times. In particular, it follows that fractals generated by a particular class of self-organized criticality (SOC) models give rise to enhanced diffusion. The analytical results are illustrated by Monte-Carlo simulations.Comment: 22 pages, 16 figures; in press at Phys. Rev. E, 200

Presence of antiphospholipid antibodies is associated with increased implantation failure following in vitro fertilization technique and embryo transfer: A systematic review and meta-analysis

PURPOSE: A systematic review and meta-analysis was conducted comparing the presence of anti-phospholipid (anti-PL) antibodies between women of reproductive age, without diagnosis of antiphospholipid syndrome, who experienced at least two implantation failures following in vitro fertilization and embryo transfer (IVF-ET), and either women who had a successful implantation after IVF-ET or women with at least one successful spontaneous pregnancy or unselected healthy fertile women with no history of IVF-ET. METHODS: Systematic search of the literature and meta-analysis of the relevant studies studying presence of antiphospholipid antibodies in women experiencing at least two implantation failures in IVF-ET as compared to either women who had a successful implantation after IVF-ET or/and women with at least one successful spontaneous pregnancy or unselected healthy fertile women with no history of IVF-ET. Six hundred ninety-four published reports were retrieved; 17 of them fulfilled the inclusion criteria set. RESULTS: Presence of either any type of anti-phospholipid or anticardiolipin antibodies or lupus-anticoagulant in women experiencing at least two implantation failures in IVF-ET was associated with increased implantation failure compared to women who had a successful implantation after IVF-ET (relative risk, RR: 3.06, 5.06 and 5.81, respectively). Presence of either anticardiolipin or lupus-anticoagulant or anti-beta(2) glycoprotein-I or anti-phosphatidylserine antibodies in women experiencing at least two implantation failures in IVF-EΤ was associated with increased implantation failure compared to unselected healthy fertile women with no history of IVF-ET (RR:13.92, 6.37, 15.04 and 164.58, respectively). CONCLUSION: The prevalence of antiphospholipid antibodies, particularly that of anti-beta(2) glycoprotein-I and anti-phosphatidylserine antibodies, in women experiencing at least two implantation failures in IVF-ET without diagnosis of antiphospholipid syndrome is significantly greater than either in women who had a successful implantation after IVF-ET or women with at least one successful spontaneous pregnancy or unselected healthy fertile women with no history of IVF-ET. TRIAL REGISTRATION NUMBER: PROSPERO ID: CRD4201808145

Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress

Influenza A virus infection is an ongoing clinical problem and thus, there is an urgent need to understand the mechanisms that regulate the lung inflammation in order to unravel novel generic pharmacological strategies. Evidence indicates that the Nox2-containing NADPH oxidase enzyme promotes influenza A virus-induced lung oxidative stress, inflammation and dysfunction via ROS generation. In addition, lung epithelial and endothelial cells express the Nox1 isoform of NADPH oxidase, placing this enzyme at key sites to regulate influenza A virus-induced lung inflammation. The aim of this study was to investigate whether Nox1 oxidase regulates the inflammatory response and the oxidative stress to influenza infection in vivo in mice. Male WT and Nox1-deficient (Nox1−/y) mice were infected with the moderately pathogenic HkX-31 (H3N2, 1×104 PFU) influenza A virus for analysis of bodyweight, airways inflammation, oxidative stress, viral titre, lung histopathology, and cytokine/chemokine expression at 3 and 7 days post infection. HkX-31 virus infection of Nox1−/y mice resulted in significantly greater: loss of bodyweight (Day 3); BALF neutrophilia, peri-bronchial, peri-vascular and alveolar inflammation; Nox2-dependent inflammatory cell ROS production and peri-bronchial, epithelial and endothelial oxidative stress. The expression of pro-inflammatory cytokines including CCL2, CCL3, CXCL2, IL-1β, IL-6, GM-CSF and TNF-α was higher in Nox1−/y lungs compared to WT mice at Day 3, however, the expression of CCL2, CCL3, CXCL2, IFN-γ and the anti-inflammatory cytokine IL-10 were lower in lungs of Nox1−/y mice vs. WT mice at Day 7. Lung viral titre, and airways infiltration of active CD8+ and CD4+ T lymphocytes, and of Tregs were similar between WT and Nox1−/y mice. In conclusion, Nox1 oxidase suppresses influenza A virus induced lung inflammation and oxidative stress in mice particularly at the early phases of the infection. Nox1 and Nox2 oxidases appear to have opposing roles in the regulation of inflammation caused by influenza A viruses

The Effect of Coherent Structures on Stochastic Acceleration in MHD Turbulence

We investigate the influence of coherent structures on particle acceleration in the strongly turbulent solar corona. By randomizing the Fourier phases of a pseudo-spectral simulation of isotropic MHD turbulence (Re $\sim 300$), and tracing collisionless test protons in both the exact-MHD and phase-randomized fields, it is found that the phase correlations enhance the acceleration efficiency during the first adiabatic stage of the acceleration process. The underlying physical mechanism is identified as the dynamical MHD alignment of the magnetic field with the electric current, which favours parallel (resistive) electric fields responsible for initial injection. Conversely, the alignment of the magnetic field with the bulk velocity weakens the acceleration by convective electric fields - \bfu \times \bfb at a non-adiabatic stage of the acceleration process. We point out that non-physical parallel electric fields in random-phase turbulence proxies lead to artificial acceleration, and that the dynamical MHD alignment can be taken into account on the level of the joint two-point function of the magnetic and electric fields, and is therefore amenable to Fokker-Planck descriptions of stochastic acceleration.Comment: accepted for publication in Ap

The Emission of Electromagnetic Radiation from Charges Accelerated by Gravitational Waves and its Astrophysical Implications

We provide calculations and theoretical arguments supporting the emission of electromagnetic radiation from charged particles accelerated by gravitational waves (GWs). These waves have significant indirect evidence to support their existence, yet they interact weakly with ordinary matter. We show that the induced oscillations of charged particles interacting with a GW, which lead to the emission of electromagnetic radiation, will also result in wave attenuation. These ideas are supported by a small body of literature, as well as additional arguments for particle acceleration based on GW memory effects. We derive order of magnitude power calculations for various initial charge distributions accelerated by GWs. The resulting power emission is extremely small for all but very strong GWs interacting with large quantities of charge. If the results here are confirmed and supplemented, significant consequences such as attenuation of early universe GWs could result. Additionally, this effect could extend GW detection techniques into the electromagnetic regime. These explorations are worthy of study to determine the presence of such radiation, as it is extremely important to refine our theoretical framework in an era of active GW astrophysics.Comment: Appears in Gravitational Wave Astrophysics, Editor C.F. Sopuerta, Astrophysics and Space Science Proceedings, Volume 40. ISBN 978-3-319-10487-4. Springer International Publishing Switzerland, 2015, p. 30

Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette smoke-induced lung inflammation in mice

Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). Interleukin-17A (IL-17A) is a pivotal cytokine that regulates lung immunity and inflammation. The aim of this study was to investigate how IL-17A regulates CS-induced lung inflammation in vivo . IL-17A KO mice and neutralisation of IL-17A in WT mice reduced macrophage and neutrophil recruitment and CCL2, CCL3 and MMP-12 mRNA expression in response to acute CS exposure. IL-17A expression was increased in NOD SCID mice with non-functional B and T cells over a 4 week CS exposure period, where macrophages accumulated to the same extent as WT mice. Gene expression analysis by QPCR of isolated immune cell subsets detected increased levels of IL-17A transcript in macrophages, neutrophils and NK/NKT cells in the lungs of CS-exposed mice. In order to further explore the relative contribution of innate immune cellular sources, intracellular IL-17A staining was performed. Here, we demonstrate that CS exposure primes NK, NKT and γδ T cells to produce more IL-17A protein and CS alone increased the frequency of IL17+ γδ T cells in the lung, whereas IL-17A protein was not detected in macrophages and neutrophils. Our data suggest that activation of innate cellular sources of IL-17A is an essential mediator of macrophage accumulation in CS-exposed lungs. Targeting non-conventional T cell sources of IL-17A may offer an alternative strategy to reduce pathogenic macrophages in COPD