Slowdown and splitting of gap solitons in apodized Bragg gratings

We study the motion of gap solitons in two models of apodized nonlinear fiber Bragg gratings (BGs), with the local reflectivity (LR) varying along the fiber. A single step of LR, and a periodic array of alternating steps with opposite signs (a "Bragg superstructure") are considered. A challenging possibility is to slow down and eventually halt the soliton by passing it through the step of increasing reflectivity, thus capturing a pulse of standing light. First, we develop an analytical approach, assuming adiabatic evolution of the soliton, and making use of the energy conservation and balance equation for the momentum. Comparison with simulations shows that the analytical approximation is quite accurate (unless the inhomogeneity is too steep): the soliton is either transmitted across the step or bounces back. If the step is narrow, systematic simulations demontrate that the soliton splits into transmitted and reflected pulses (splitting of a BG soliton which hits a chirped grating was observed in experiments). Moving through the periodic "superstructure", the soliton accummulates distortion and suffers radiation loss if the structure is composed of narrow steps. The soliton moves without any loss or irreversible deformation through the array of sufficiently broad steps.Comment: to appear in a special issue on Wave-Optical Engineering, Journal of Modern Optic

Medium Resolution Near-Infrared Spectra of the Host Galaxies of Nearby Quasars

We present medium resolution near-infrared host galaxy spectra of low redshift quasars, PG 0844 + 349 (z=0.064), PG 1226 + 023 (z=0.158), and PG 1426+015 (z=0.086). The observations were done by using the Infrared Camera and Spectrograph (IRCS) at the Subaru 8.2 m telescope. The full width at half maximum of the point spread function was about 0.3 arcsec by operations of an adaptive optics system, which can effectively resolve the quasar spectra from the host galaxy spectra. We spent up to several hours per target and developed data reduction methods to reduce the systematic noises of the telluric emissions and absorptions. From the obtained spectra, we identified absorption features of Mg I (1.503 um), Si I (1.589 um) and CO (6-3) (1.619 um), and measured the velocity dispersions of PG 0844 + 349 to be 132+/-110 km s-1 and PG 1426 + 015 to be 264+/-215 km s-1. By using an M_BH-sigma relation of elliptical galaxies, we derived the black hole (BH) mass of PG 0844+349, log(M_BH/M_SUN) = 7.7+/-5.5 and PG 1426+015, log(M_BH/M_SUN) = 9.0+/-7.5. These values are consistent with the BH mass values from broad emission lines with an assumption of a virial factor of 5.5.Comment: 16 pages, 5 figure

Profiles of inflated surfaces

We study the shape of inflated surfaces introduced in \cite{B1} and \cite{P1}. More precisely, we analyze profiles of surfaces obtained by inflating a convex polyhedron, or more generally an almost everywhere flat surface, with a symmetry plane. We show that such profiles are in a one-parameter family of curves which we describe explicitly as the solutions of a certain differential equation.Comment: 13 pages, 2 figure

Strong scaling of general-purpose molecular dynamics simulations on GPUs

We describe a highly optimized implementation of MPI domain decomposition in a GPU-enabled, general-purpose molecular dynamics code, HOOMD-blue (Anderson and Glotzer, arXiv:1308.5587). Our approach is inspired by a traditional CPU-based code, LAMMPS (Plimpton, J. Comp. Phys. 117, 1995), but is implemented within a code that was designed for execution on GPUs from the start (Anderson et al., J. Comp. Phys. 227, 2008). The software supports short-ranged pair force and bond force fields and achieves optimal GPU performance using an autotuning algorithm. We are able to demonstrate equivalent or superior scaling on up to 3,375 GPUs in Lennard-Jones and dissipative particle dynamics (DPD) simulations of up to 108 million particles. GPUDirect RDMA capabilities in recent GPU generations provide better performance in full double precision calculations. For a representative polymer physics application, HOOMD-blue 1.0 provides an effective GPU vs. CPU node speed-up of 12.5x.Comment: 30 pages, 14 figure

Quantitative assessment of cell fate decision between autophagy and apoptosis

Abstract Autophagy and apoptosis are cellular processes that regulate cell survival and death, the former by eliminating dysfunctional components in the cell, the latter by programmed cell death. Stress signals can induce either process, and it is unclear how cells ‘assess’ cellular damage and make a ‘life’ or ‘death’ decision upon activating autophagy or apoptosis. A computational model of coupled apoptosis and autophagy is built here to analyze the underlying signaling and regulatory network dynamics. The model explains the experimentally observed differential deployment of autophagy and apoptosis in response to various stress signals. Autophagic response dominates at low-to-moderate stress; whereas the response shifts from autophagy (graded activation) to apoptosis (switch-like activation) with increasing stress intensity. The model reveals that cytoplasmic Ca2+ acts as a rheostat that fine-tunes autophagic and apoptotic responses. A G-protein signaling-mediated feedback loop maintains cytoplasmic Ca2+ level, which in turn governs autophagic response through an AMP-activated protein kinase (AMPK)-mediated feedforward loop. Ca2+/calmodulin-dependent kinase kinase β (CaMKKβ) emerges as a determinant of the competing roles of cytoplasmic Ca2+ in autophagy regulation. The study demonstrates that the proposed model can be advantageously used for interrogating cell regulation events and developing pharmacological strategies for modulating cell decisions

Blockade of adenosine A2A receptors prevents protein phosphorylation in the striatum induced by cortical stimulation

©2006 Society for NeurosciencePrevious studies have shown that cortical stimulation selectively activates extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and immediate early gene expression in striatal GABAergic enkephalinergic neurons. In the present study, we demonstrate that blockade of adenosine A2A receptors with caffeine or a selective A2A receptor antagonist counteracts the striatal activation of cAMP– protein kinase A cascade (phosphorylation of the Ser845 residue of the glutamate receptor 1 subunit of the AMPA receptor) and mitogenactivated protein kinase (ERK1/2 phosphorylation) induced by the in vivo stimulation of corticostriatal afferents. The results indicate that A2A receptors strongly modulate the efficacy of glutamatergic synapses on striatal enkephalinergic neurons.This work was supported by the Intramural Research Program of the National Institutes of Health, National Institute on Drug Abuse, Department of Health and Human Services