A General Formula for Black Hole Gravitational Wave Kicks

Although the gravitational wave kick velocity in the orbital plane of coalescing black holes has been understood for some time, apparently conflicting formulae have been proposed for the dominant out-of-plane kick, each a good fit to different data sets. This is important to resolve because it is only the out-of-plane kicks that can reach more than 500 km/s and can thus eject merged remnants from galaxies. Using a different ansatz for the out-of-plane kick, we show that we can fit almost all existing data to better than 5 %. This is good enough for any astrophysical calculation, and shows that the previous apparent conflict was only because the two data sets explored different aspects of the kick parameter space.Comment: 14 pages

Tissue Inhibitor of Metalloproteinase–3 (TIMP-3) induces FAS dependent apoptosis in human vascular smooth muscle cells

Over expression of Tissue Inhibitor of Metalloproteinases-3 (TIMP-3) in vascular smooth muscle cells (VSMCs) induces apoptosis and reduces neointima formation occurring after saphenous vein interposition grafting or coronary stenting. In studies to address the mechanism of TIMP-3-driven apoptosis in human VSMCs we find that TIMP-3 increased activation of caspase-8 and apoptosis was inhibited by expression of Cytokine response modifier A (CrmA) and dominant negative FAS-Associated protein with Death Domain (FADD). TIMP-3 induced apoptosis did not cause mitochondrial depolarisation, increase activation of caspase-9 and was not inhibited by over-expression of B-cell Lymphoma 2 (Bcl2), indicating a mitochondrial independent/type-I death receptor pathway. TIMP-3 increased levels of the First Apoptosis Signal receptor (FAS) and depletion of FAS with shRNA showed TIMP-3-induced apoptosis was FAS dependent. TIMP-3 induced formation of the Death-Inducing Signalling Complex (DISC), as detected by immunoprecipitation and by immunofluorescence. Cellular-FADD-like IL-1 converting enzyme-Like Inhibitory Protein (c-FLIP) localised with FAS at the cell periphery in the absence of TIMP-3 and this localisation was lost on TIMP-3 expression with c-FLIP adopting a perinuclear localisation. Although TIMP-3 inhibited FAS shedding, this did not increase total surface levels of FAS but instead increased FAS levels within localised regions at the cell surface. A Disintegrin And Metalloproteinase 17 (ADAM17) is inhibited by TIMP-3 and depletion of ADAM17 with shRNA significantly decreased FAS shedding. However ADAM17 depletion did not induce apoptosis or replicate the effects of TIMP-3 by increasing localised clustering of cell surface FAS. ADAM17-depleted cells could activate caspase-3 when expressing levels of TIMP-3 that were otherwise sub-apoptotic, suggesting a partial role for ADAM17 mediated ectodomain shedding in TIMP-3 mediated apoptosis. We conclude that TIMP-3 induced apoptosis in VSMCs is highly dependent on FAS and is associated with changes in FAS and c-FLIP localisation, but is not solely dependent on shedding of the FAS ectodomain

Anatomy of the binary black hole recoil: A multipolar analysis

We present a multipolar analysis of the gravitational recoil computed in recent numerical simulations of binary black hole (BH) coalescence, for both unequal masses and non-zero, non-precessing spins. We show that multipole moments up to and including l=4 are sufficient to accurately reproduce the final recoil velocity (within ~2%) and that only a few dominant modes contribute significantly to it (within ~5%). We describe how the relative amplitudes, and more importantly, the relative phases, of these few modes control the way in which the recoil builds up throughout the inspiral, merger, and ringdown phases. We also find that the numerical results can be reproduced by an ``effective Newtonian'' formula for the multipole moments obtained by replacing the radial separation in the Newtonian formulae with an effective radius computed from the numerical data. Beyond the merger, the numerical results are reproduced by a superposition of three Kerr quasi-normal modes (QNMs). Analytic formulae, obtained by expressing the multipole moments in terms of the fundamental QNMs of a Kerr BH, are able to explain the onset and amount of ``anti-kick'' for each of the simulations. Lastly, we apply this multipolar analysis to help explain the remarkable difference between the amplitudes of planar and non-planar kicks for equal-mass spinning black holes.Comment: 28 pages, 20 figures, submitted to PRD; v2: minor revisions from referee repor

Modeling kicks from the merger of generic black-hole binaries

Recent numerical relativistic results demonstrate that the merger of comparable-mass spinning black holes has a maximum ``recoil kick'' of up to \sim 4000 \kms. However the scaling of these recoil velocities with mass ratio is poorly understood. We present new runs showing that the maximum possible kick perpendicular to the orbital plane does not scale as $\sim\eta^2$ (where $\eta$ is the symmetric mass ratio), as previously proposed, but is more consistent with $\sim\eta^3$, at least for systems with low orbital precession. We discuss the effect of this dependence on galactic ejection scenarios and retention of intermediate-mass black holes in globular clusters.Comment: 5 pages, 1 figure, 3 tables. Version published in Astrophys. J. Let

Elasticity Theory and Shape Transitions of Viral Shells

Recently, continuum elasticity theory has been applied to explain the shape transition of icosahedral viral capsids - single-protein-thick crystalline shells - from spherical to buckled/faceted as their radius increases through a critical value determined by the competition between stretching and bending energies of a closed 2D elastic network. In the present work we generalize this approach to capsids with non-icosahedral symmetries, e.g., spherocylindrical and conical shells. One key new physical ingredient is the role played by nonzero spontaneous curvature. Another is associated with the special way in which the energy of the twelve topologically-required five-fold sites depends on the background local curvature of the shell in which they are embedded. Systematic evaluation of these contributions leads to a shape phase diagram in which transitions are observed from icosahedral to spherocylindrical capsids as a function of the ratio of stretching to bending energies and of the spontaneous curvature of the 2D protein network. We find that the transition from icosahedral to spherocylindrical symmetry is continuous or weakly first-order near the onset of buckling, leading to extensive shape degeneracy. These results are discussed in the context of experimentally observed variations in the shapes of a variety of viral capsids.Comment: 53 pages, 17 figure