3,430 research outputs found

    Basins of attraction for cascading maps

    Full text link
    We study a finite uni-directional array of "cascading" or "threshold coupled" chaotic maps. Such systems have been proposed for use in nonlinear computing and have been applied to classification problems in bioinformatics. We describe some of the attractors for such systems and prove general results about their basins of attraction. In particular, we show that the basins of attraction have infinitely many path components. We show that these components always accumulate at the corners of the domain of the system. For all threshold parameters above a certain value, we show that they accumulate at a Cantor set in the interior of the domain. For certain ranges of the threshold, we prove that the system has many attractors.Comment: 15 pages, 9 figures. To appear in International Journal of Bifurcations and Chao

    Screening in Ionic Systems: Simulations for the Lebowitz Length

    Full text link
    Simulations of the Lebowitz length, ξL(T,ρ)\xi_{\text{L}}(T,\rho), are reported for t he restricted primitive model hard-core (diameter aa) 1:1 electrolyte for densi ties ρ4ρc\rho\lesssim 4\rho_c and TcT40TcT_c \lesssim T \lesssim 40T_c. Finite-size eff ects are elucidated for the charge fluctuations in various subdomains that serve to evaluate ξL\xi_{\text{L}}. On extrapolation to the bulk limit for T10TcT\gtrsim 10T_c the low-density expansions (Bekiranov and Fisher, 1998) are seen to fail badly when ρ>1/10ρc\rho > {1/10}\rho_c (with ρca30.08\rho_c a^3 \simeq 0.08). At highe r densities ξL\xi_{\text{L}} rises above the Debye length, \xi_{\text{D}} \prop to \sqrt{T/\rho}, by 10-30% (upto ρ1.3ρc\rho\simeq 1.3\rho_c); the variation is portrayed fairly well by generalized Debye-H\"{u}ckel theory (Lee and Fisher, 19 96). On approaching criticality at fixed ρ\rho or fixed TT, ξL(T,ρ)\xi_{\text{L}}(T, \rho) remains finite with ξLc0.30a1.3ξDc\xi_{\text{L}}^c \simeq 0.30 a \simeq 1.3 \xi_{\text {D}}^c but displays a weak entropy-like singularity.Comment: 4 pages 5 figure

    Galaxy Cluster Pressure Profiles as Determined by Sunyaev Zel'dovich Effect Observations with MUSTANG and Bolocam I: Joint Analysis Technique

    Get PDF
    We present a technique to constrain galaxy cluster pressure profiles by jointly fitting Sunyaev-Zel'dovich effect (SZE) data obtained with MUSTANG and Bolocam for the clusters Abell 1835 and MACS0647. Bolocam and MUSTANG probe different angular scales and are thus highly complementary. We find that the addition of the high resolution MUSTANG data can improve constraints on pressure profile parameters relative to those derived solely from Bolocam. In Abell 1835 and MACS0647, we find gNFW inner slopes of γ=0.360.21+0.33\gamma = 0.36_{-0.21}^{+0.33} and γ=0.380.25+0.20\gamma = 0.38_{-0.25}^{+0.20}, respectively when α\alpha and β\beta are constrained to 0.86 and 4.67 respectively. The fitted SZE pressure profiles are in good agreement with X-ray derived pressure profiles.Comment: 12 pages, 12 figures. Submitted to Ap

    Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.

    Get PDF
    Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA). However, the contractile sensitivity to this agent was unchanged. The increase in contractile force/cross sectional area observed in pendrin null mice was due to reduced cross sectional area of the aorta and not from increased contractile force per vessel. The pendrin-dependent increase in maximal contractile response was endothelium- and nitric oxide-independent and did not occur from changes in Ca2+ sensitivity or chronic changes in catecholamine production. However, application of 100 nM angiotensin II increased force/CSA more in aortas from pendrin null than from wild type mice. Moreover, angiotensin type 1 receptor inhibitor (candesartan) treatment in vivo eliminated the pendrin-dependent changes contractile protein abundance and changes in the contractile force/cross sectional area in response to PE. In conclusion, pendrin gene ablation increases aorta contractile force per cross sectional area in response to angiotensin II and PE due to stimulation of angiotensin type 1 receptor-dependent signaling. The angiotensin type 1 receptor-dependent increase in vascular reactivity may mitigate the fall in blood pressure observed with pendrin gene ablation
    corecore