Resonant recoil in extreme mass ratio binary black hole mergers

The inspiral and merger of a binary black hole system generally leads to an asymmetric distribution of emitted radiation, and hence a recoil of the remnant black hole directed opposite to the net linear momentum radiated. The recoil velocity is generally largest for comparable mass black holes and particular spin configurations, and approaches zero in the extreme mass ratio limit. It is generally believed that for extreme mass ratios eta<<1, the scaling of the recoil velocity is V {\propto} eta^2, where the proportionality coefficient depends on the spin of the larger hole and the geometry of the system (e.g. orbital inclination). Here we show that for low but nonzero inclination prograde orbits and very rapidly spinning large holes (spin parameter a*>0.9678) the inspiralling binary can pass through resonances where the orbit-averaged radiation-reaction force is nonzero. These resonance crossings lead to a new contribution to the kick, V {\propto} eta^{3/2}. For these configurations and sufficiently extreme mass ratios, this resonant recoil is dominant. While it seems doubtful that the resonant recoil will be astrophysically significant, its existence suggests caution when extrapolating the results of numerical kick results to extreme mass ratios and near-maximal spins.Comment: fixed references; matches PRD accepted version (minor revision); 9 pages, 2 figure

The Earth Effect in the MSW Analysis of the Solar Neutrino Experiments

We consider the Earth effect in the MSW analysis of the Homestake, Kamiokande, GALLEX, and SAGE solar neutrino experiments. Using the time-averaged data and assuming two-flavor oscillations, the large-angle region of the combined fit extends to much smaller angles (to $\sin^22\theta \simeq 0.1$) than when the Earth effect is ignored. However, the additional constraint from the Kamiokande II day-night data excludes most of the parameter space sensitive to the Earth effect independent of astrophysical uncertainties, and leaves only a small large-angle region close to maximal mixing at 90\% C.L. The nonadiabatic solution remains unaffected by the Earth effect and is still preferred. Both theoretical and experimental uncertainties are included in the analysis.Comment: (11 pages, Revtex 3.0 (can be changed to Latex), 3 postscript figures included, UPR-0570T

Periodic Oscillations of Josephson-Vortex Flow Resistance in Oxygen-Deficient Y1Ba2Cu3Ox

We measured the Josephson vortex flow resistance as a function of magnetic field applied parallel to the ab-planes using annealed Y1Ba2Cu3Ox intrinsic Josephson junctions having high anisotropy (around 40) by oxygen content reduction. Periodic oscillations were observed in magnetic fields above 45-58 kOe, corresponding to dense-dilute boundary for Josephson vortex lattice. The observed period of oscillations, agrees well with the increase of one fluxon per two junctions ($H_{p}$\textit{=$\Phi$}$_{0}$\textit{/2Ls}), may correspond to formation of a triangular lattice of Josephson vortices as has been reported by Ooi et al. for highly anisotropic (larger than 200) Bi-2212 intrinsic Josephson junctions.Comment: 5 pages, 4 figure

Glutamate induces autophagy via the two-pore channels in neural cells

NAADP (nicotinic acid adenine dinucleotide phosphate) has been proposed as a second messenger for glutamate in neuronal and glial cells via the activation of the lysosomal Ca2+ channels TPC1 and TPC2. However, the activities of glutamate that are mediated by NAADP remain unclear. In this study, we evaluated the effect of glutamate on autophagy in astrocytes at physiological, non-toxic concentration. We found that glutamate induces autophagy at similar extent as NAADP. By contrast, the NAADP antagonist NED-19 or SiRNA-mediated inhibition of TPC1/2 decreases autophagy induced by glutamate, confirming a role for NAADP in this pathway. The involvement of TPC1/2 in glutamate-induced autophagy was also confirmed in SHSY5Y neuroblastoma cells. Finally, we show that glutamate leads to a NAADP-dependent activation of AMPK, which is required for autophagy induction, while mTOR activity is not affected by this treatment. Taken together, our results indicate that glutamate stimulates autophagy via NAADP/TPC/AMPK axis, providing new insights of how Ca2+ signalling glutamate-mediated can control the cell metabolism in the central nervous system