Kink stability, propagation, and length scale competition in the periodically modulated sine-Gordon equation

We have examined the dynamical behavior of the kink solutions of the one-dimensional sine-Gordon equation in the presence of a spatially periodic parametric perturbation. Our study clarifies and extends the currently available knowledge on this and related nonlinear problems in four directions. First, we present the results of a numerical simulation program which are not compatible with the existence of a radiative threshold, predicted by earlier calculations. Second, we carry out a perturbative calculation which helps interpret those previous predictions, enabling us to understand in depth our numerical results. Third, we apply the collective coordinate formalism to this system and demonstrate numerically that it accurately reproduces the observed kink dynamics. Fourth, we report on a novel occurrence of length scale competition in this system and show how it can be understood by means of linear stability analysis. Finally, we conclude by summarizing the general physical framework that arises from our study.Comment: 19 pages, REVTeX 3.0, 24 figures available from A S o

Towards hardware acceleration of neuroevolution for multimedia processing applications on mobile devices

This paper addresses the problem of accelerating large artificial neural networks (ANN), whose topology and weights can evolve via the use of a genetic algorithm. The proposed digital hardware architecture is capable of processing any evolved network topology, whilst at the same time providing a good trade off between throughput, area and power consumption. The latter is vital for a longer battery life on mobile devices. The architecture uses multiple parallel arithmetic units in each processing element (PE). Memory partitioning and data caching are used to minimise the effects of PE pipeline stalling. A first order minimax polynomial approximation scheme, tuned via a genetic algorithm, is used for the activation function generator. Efficient arithmetic circuitry, which leverages modified Booth recoding, column compressors and carry save adders, is adopted throughout the design

HIV-1 Evolutionary Patterns Associated with Metastatic Kaposi's Sarcoma during AIDS.

Kaposi's sarcoma (KS) in HIV-infected individuals can have a wide range of clinical outcomes, from indolent skin tumors to a life-threatening visceral cancer. KS tumors contain endothelial-related cells and inflammatory cells that may be HIV-infected. In this study we tested if HIV evolutionary patterns distinguish KS tumor relatedness and progression. Multisite autopsies from participants who died from HIV-AIDS with KS prior to the availability of antiretroviral therapy were identified at the AIDS and Cancer Specimen Resource (ACSR). Two patients (KS1 and KS2) died predominantly from non-KS-associated disease and KS3 died due to aggressive and metastatic KS within one month of diagnosis. Skin and visceral tumor and nontumor autopsy tissues were obtained (n = 12). Single genome sequencing was used to amplify HIV RNA and DNA, which was present in all tumors. Independent HIV tumor clades in phylogenies differentiated KS1 and KS2 from KS3, whose sequences were interrelated by both phylogeny and selection. HIV compartmentalization was confirmed in KS1 and KS2 tumors; however, in KS3, no compartmentalization was observed among sampled tissues. While the sample size is small, the HIV evolutionary patterns observed in all patients suggest an interplay between tumor cells and HIV-infected cells which provides a selective advantage and could promote KS progression

Renormalization Group Theory for a Perturbed KdV Equation

We show that renormalization group(RG) theory can be used to give an analytic description of the evolution of a perturbed KdV equation. The equations describing the deformation of its shape as the effect of perturbation are RG equations. The RG approach may be simpler than inverse scattering theory(IST) and another approaches, because it dose not rely on any knowledge of IST and it is very concise and easy to understand. To the best of our knowledge, this is the first time that RG has been used in this way for the perturbed soliton dynamics.Comment: 4 pages, no figure, revte

Annealing schedule from population dynamics

We introduce a dynamical annealing schedule for population-based optimization algorithms with mutation. On the basis of a statistical mechanics formulation of the population dynamics, the mutation rate adapts to a value maximizing expected rewards at each time step. Thereby, the mutation rate is eliminated as a free parameter from the algorithm.Comment: 6 pages RevTeX, 4 figures PostScript; to be published in Phys. Rev.

Virtual Immortality: Reanimating Characters from TV Shows.

The objective of this work is to build virtual talking avatars of characters fully automatically from TV shows. From this unconstrained data, we show how to capture a character's style of speech, visual appearance and language in an e ort to construct an interactive avatar of the person and e ectively immortalize them in a computational model. We make three contributions (i) a complete framework for producing a generative model of the audiovisual and language of characters from TV shows; (ii) a novel method for aligning transcripts to video using the audio; and (iii) a fast audio segmentation system for silencing nonspoken audio from TV shows. Our framework is demonstrated using all 236 episodes from the TV series Friends [34] ( 97hrs of video) and shown to generate novel sentences as well as character specific speech and video

HIV-1 Evolutionary Patterns Associated with Metastatic Kaposi’s Sarcoma during AIDS

Kaposi’s sarcoma (KS) in HIV-infected individuals can have a wide range of clinical outcomes, from indolent skin tumors to a life-threatening visceral cancer. KS tumors contain endothelial-related cells and inflammatory cells that may be HIV-infected. In this study we tested if HIV evolutionary patterns distinguish KS tumor relatedness and progression. Multisite autopsies from participants who died from HIV-AIDS with KS prior to the availability of antiretroviral therapy were identified at the AIDS and Cancer Specimen Resource (ACSR). Two patients (KS1 and KS2) died predominantly from non-KS-associated disease and KS3 died due to aggressive and metastatic KS within one month of diagnosis. Skin and visceral tumor and nontumor autopsy tissues were obtained (n=12). Single genome sequencing was used to amplify HIV RNA and DNA, which was present in all tumors. Independent HIV tumor clades in phylogenies differentiated KS1 and KS2 from KS3, whose sequences were interrelated by both phylogeny and selection. HIV compartmentalization was confirmed in KS1 and KS2 tumors; however, in KS3, no compartmentalization was observed among sampled tissues. While the sample size is small, the HIV evolutionary patterns observed in all patients suggest an interplay between tumor cells and HIV-infected cells which provides a selective advantage and could promote KS progression

Genioglossal muscle response to CO2 stimulation during NREM sleep

STUDY OBJECTIVES: The objective was to evaluate the responsiveness of upper airway muscles to hypercapnia with and without intrapharyngeal negative pressure during non-rapid eye movement (NREM) sleep and wakefulness. DESIGN: We assessed the genioglossal muscle response to CO2 off and on continuous positive airway pressure (CPAP) (to attenuate negative pressure) during stable NREM sleep and wakefulness in the supine position. SETTING: Laboratory of the Sleep Medicine Division, Brigham and Women's Hospital. PATIENTS OR PARTICIPANTS: Eleven normal healthy subjects. INTERVENTIONS: During wakefulness and NREM sleep, we measured genioglossal electromyography (EMG) on and off CPAP at the normal eupneic level and at levels 5 and 10 mm Hg above the awake eupneic level. MEASUREMENTS AND RESULTS: We observed that CO2 could increase upper-airway muscle activity during NREM sleep and wakefulness in the supine position with and without intrapharyngeal negative pressure. The application of nasal CPAP significantly decreased genioglossal EMG at all 3 levels of PETCO2 during NREM sleep (13.0 +/- 4.9% vs. 4.6 +/- 1.6% of maximal EMG, 14.6 +/- 5.6% vs. 7.1 +/- 2.3% of maximal EMG, and 17.3 +/- 6.3% vs. 10.2 +/- 3.1% of maximal EMG, respectively). However, the absence of negative pressure in the upper airway did not significantly affect the slope of the pharyngeal airway dilator muscle response to hypercapnia during NREM sleep (0.72 +/- 0.30% vs. 0.79 +/- 0.27% of maximal EMG per mm Hg PCO2, respectively, off and on CPAP). CONCLUSIONS: We conclude that both chemoreceptive and negative pressure reflex inputs to this upper airway dilator muscle are still active during stable NREM sleep

Agonist-Specific Desensitization of PGE2-Stimulated cAMP Signaling due to upregulated Phosphodiesterase Expression in Human Lung Fibroblasts

Pulmonary fibrosis is characterized by fibroblasts persisting in an activated form, producing excessive fibrous material that destroys alveolar structure. The second messenger molecule cyclic 3′,5′-adenosine monophosphate (cAMP) has antifibrotic properties, and prostaglandin E2 (PGE2) can stimulate cAMP production through prostaglandin E (EP)2 and EP4 receptors. Although EP receptors are attractive therapeutic targets, the effects of long-term exposure to PGE2 have not been characterized. To determine the effects of long-term exposure of lung fibroblasts to PGE2, human fetal lung (HFL)-1 cells were treated for 24 h with 100 nM PGE2 or other cAMP-elevating agents. cAMP levels stimulated by acute exposure to PGE2 were measured using a fluorescent biosensor. Pretreatment for 24 h with PGE2 shifted the concentration-response curve to PGE2 rightward by approximately 22-fold but did not affect responses to the beta-adrenoceptor agonist isoproterenol. Neither isoproterenol nor forskolin pretreatment altered PGE2 responses, implying that other cAMP-elevating agents do not induce desensitization. Use of EP2- and EP4-selective agonists and antagonists suggested that PGE2-stimulated cAMP responses in HFL-1 cells are mediated by EP2 receptors. EP2 receptors are resistant to classical mechanisms of agonist-specific receptor desensitization, so we hypothesized that increased PDE activity mediates the loss of signaling after PGE2 pretreatment. PGE2 treatment upregulated messenger RNA for PDE3A, PDE3B, PDE4B, and PDE4D and increased overall PDE activity. The PDE4 inhibitor rolipram partially reversed PGE2- mediated desensitization and PDE4 activity was increased, but rolipram did not alter responses to isoproterenol. The PDE3 inhibitor cilostazol had minimal effect. These results show that long-term exposure to PGE2 causes agonist-specific desensitization of EP2 receptor-stimulated cAMP signaling through the increased expression of PDE isozymes, most likely of the PDE4 family