27 research outputs found

    A physical model for state transitions in black hole X-ray binaries

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    We present an accretion cycle which can explain state transitions and other observed phenomena in black hole X-ray binaries. This model is based on the process of disc tearing, where individual rings of gas break off the disc and precess effectively independently. This occurs when the Lense-Thirring effect is stronger than the local disc viscosity. We discuss implications of this model for quasi-periodic oscillations and the disc-jet-corona coupling. We also speculate on applying this model to active galactic nuclei and other accreting systems.Comment: 6 pages, 3 figures. Accepted to MNRA

    Quantifying energetics and dissipation in magnetohydrodynamic turbulence

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    We perform a suite of two- and three-dimensional magnetohydrodynamic (MHD) simulations with the Athena code of the non-driven Kelvin-Helmholtz instability in the subsonic, weak magnetic field limit. Focusing the analysis on the non-linear turbulent regime, we quantify energy transfer on a scale-by-scale basis and identify the physical mechanisms responsible for energy exchange by developing the diagnostic known as spectral energy transfer function analysis. At late times when the fluid is in a state of MHD turbulence, magnetic tension mediates the dominant mode of energy injection into the magnetic reservoir, whereby turbulent fluid motions twist and stretch the magnetic field lines. This generated magnetic energy turbulently cascades to smaller scales, while being exchanged backwards and forwards with the kinetic energy reservoir, until finally being dissipated. Incorporating explicit dissipation pushes the dissipation scale to larger scales than if the dissipation were entirely numerical. For scales larger than the dissipation scale, we show that the physics of energy transfer in decaying MHD turbulence is robust to numerical effects.Comment: 23 pages, 20 figures, 4 tables, Accepted for publication in MNRA

    Shock Speed, Cosmic Ray Pressure, and Gas Temperature in the Cygnus Loop

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    Upper limits on the shock speeds in supernova remnants can be combined with post-shock temperatures to obtain upper limits on the ratio of cosmic ray to gas pressure (P_CR / P_G) behind the shocks. We constrain shock speeds from proper motions and distance estimates, and we derive temperatures from X-ray spectra. The shock waves are observed as faint H-alpha filaments stretching around the Cygnus Loop supernova remnant in two epochs of the Palomar Observatory Sky Survey (POSS) separated by 39.1 years. We measured proper motions of 18 non-radiative filaments and derived shock velocity limits based on a limit to the Cygnus Loop distance of 576 +/- 61 pc given by Blair et al. for a background star. The PSPC instrument on-board ROSAT observed the X-ray emission of the post-shock gas along the perimeter of the Cygnus Loop, and we measure post-shock electron temperature from spectral fits. Proper motions range from 2.7 arcseconds to 5.4 arcseconds over the POSS epochs and post-shock temperatures range from kT ~ 100-200 eV. Our analysis suggests a cosmic ray to post-shock gas pressure consistent with zero, and in some positions P_CR is formally smaller than zero. We conclude that the distance to the Cygnus Loop is close to the upper limit given by the distance to the background star and that either the electron temperatures are lower than those measured from ROSAT PSPC X-ray spectral fits or an additional heat input for the electrons, possibly due to thermal conduction, is required.Comment: Submitted to ApJ, 7 color figure

    Intranasal Delivery of Caspase-9 Inhibitor Reduces Caspase-6-Dependent Axon/Neuron Loss and Improves Neurological Function after Stroke

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    Despite extensive research to develop an effective neuroprotective strategy for the treatment of ischemic stroke, therapeutic options remain limited. Although caspase-dependent death is thought to play a prominent role in neuronal injury, direct evidence of active initiator caspases in stroke and the functional relevance of this activity have not previously been shown. Using an unbiased caspase-trapping technique in vivo, we isolated active caspase-9 from ischemic rat brain within 1 h of reperfusion. Pathogenic relevance of active caspase-9 was shown by intranasal delivery of a novel cell membrane-penetrating highly specific inhibitor for active caspase-9 at 4 h postreperfusion (hpr). Caspase-9 inhibition provided neurofunctional protection and established caspase-6 as its downstream target. The temporal and spatial pattern of expression demonstrates that neuronal caspase-9 activity induces caspase-6 activation, mediating axonal loss by 12 hpr followed by neuronal death within 24 hpr. Collectively, these results support selective inhibition of these specific caspases as an effective therapeutic strategy for stroke.C.M.T.wassupported bythe American Heart Association and National Institutes of Health (NIH)GrantsNS035933 and NS43089. G.S.S. and S.J.S. were supported by NIH Grant CA69381. E.S.C. was supported by NIH Grant NS40409.Peer reviewe
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