Testing SUSY models of lepton flavor violation at a photon collider

The loop level lepton flavor violating signals $\gamma \gamma \to \ell \ell' (\ell=e,\mu,\tau, \ell \neq \ell^\prime)$ are studied in a scenario of low-energy, R-parity conserving, supersymmetric seesaw mechanism within the context of a high energy photon collider. Lepton flavor violation is due to off diagonal elements in the left s-lepton mass matrix induced by renormalization group equations. The average slepton masses ${\widetilde{m}}$ and the off diagonal matrix elements $\Delta m$ are treated as model independent free phenomenological parameters in order to discover regions in the parameter space where the signal cross section may be observable. At the energies of the $\gamma \gamma$ option of the future high-energy linear collider the signal has a potentially large standard model background, and therefore particular attention is paid to the study of kinematical cuts in order to reduce the latter at an acceptable level. We find, for the ($e\tau$) channel, non-negligible fractions of the parameter space ($\delta_{LL}=\Delta m^2/\widetilde{m}^2 \gtrsim 10^{-1}$) where the statistical significance ($SS$) is $SS \gtrsim 3$.Comment: 26 pages, 12 figures, Revtex

Decay of distance autocorrelation and Lyapunov exponents

This work presents numerical evidences that for discrete dynamical systems with one positive Lyapunov exponent the decay of the distance autocorrelation is always related to the Lyapunov exponent. Distinct decay laws for the distance autocorrelation are observed for different systems, namely exponential decays for the quadratic map, logarithmic for the H\'enon map and power-law for the conservative standard map. In all these cases the decay exponent is close to the positive Lyapunov exponent. For hyperbolic conservative systems, the power-law decay of the distance autocorrelation tends to be guided by the smallest Lyapunov exponent.Comment: 7 pages, 8 figure

Phagosome-lysosome fusion is a calcium-independent event in macrophages.

Phagosome-lysosome membrane fusion is a highly regulated event that is essential for intracellular killing of microorganisms. Functionally, it represents a form of polarized regulated secretion, which is classically dependent on increases in intracellular ionized calcium ([Ca2+]i). Indeed, increases in [Ca2+]i are essential for phagosome-granule (lysosome) fusion in neutrophils and for lysosomal fusion events that mediate host cell invasion by Trypanosoma cruzi trypomastigotes. Since several intracellular pathogens survive in macrophage phagosomes that do not fuse with lysosomes, we examined the regulation of phagosome-lysosome fusion in macrophages. Macrophages (M phi) were treated with 12.5 microM bis-(2-amino-S-methylphenoxy) ethane-N,N,N',N',-tetraacetic acid tetraacetoxymethyl ester (MAPT/AM), a cell-permeant calcium chelator which reduced resting cytoplasmic [Ca2+]; from 80 nM to < or = 20 nM and completely blocked increases in [Ca2+]i in response to multiple stimuli, even in the presence of extracellular calcium. Subsequently, M phi phagocytosed serum-opsonized zymosan, staphylococci, or Mycobacterium bovis. Microbes were enumerated by 4',6-diamidino-2-phenylindole, dihydrochloride (DAPI) staining, and phagosome-lysosome fusion was scored using both lysosome-associated membrane protein (LAMP-1) as a membrane marker and rhodamine dextran as a content marker for lysosomes. Confirmation of phagosome-lysosome fusion by electron microscopy validated the fluorescence microscopy findings. We found that phagosome-lysosome fusion in M phi occurs noramlly at very low [Ca2+]i (< or = 20 nM). Kinetic analysis showed that in M phi none of the steps leading from particle binding to eventual phagosome-lysosome fusion are regulated by [Ca2+]i in a rate-limiting way. Furthermore, confocal microscopy revealed no difference in the intensity of LAMP-1 immunofluorescence in phagolysosome membranes in calcium-buffered vs. control macrophages. We conclude that neither membrane recognition nor fusion events in the phagosomal pathway in macrophages are dependent on or regulated by calcium