Dynamic Pattern of Finite-Pulsed Beams inside One-dimensional Photonic Band Gap Materials

The dynamics of two-dimensional electromagnetic (EM) pulses through one-dimensional photonic crystals (1DPC) has been theoretically studied. Employing the time expectation integral over the Poynting vector as the arrival time [Phys. Rev. Lett. 84, 2370, (2000)], we show that the superluminal tunneling process of EM pulses is the propagation of the net forward-going Poynting vector through the 1DPC, and the Hartman effect is due to the saturation effect of the arrival time (smaller and smaller time accumulated) of the net forward energy flow caused by the interference effect of the forward and the backward field (from the interfaces of each layer) happened in the region before the 1DPC and in the front part of the 1DPC.Comment: 18 pages, 4 figure

Emergence and reconfiguration of modular structure for synaptic neural networks during continual familiarity detection

While advances in artificial intelligence and neuroscience have enabled the emergence of neural networks capable of learning a wide variety of tasks, our understanding of the temporal dynamics of these networks remains limited. Here, we study the temporal dynamics during learning of Hebbian Feedforward (HebbFF) neural networks in tasks of continual familiarity detection. Drawing inspiration from the field of network neuroscience, we examine the network's dynamic reconfiguration, focusing on how network modules evolve throughout learning. Through a comprehensive assessment involving metrics like network accuracy, modular flexibility, and distribution entropy across diverse learning modes, our approach reveals various previously unknown patterns of network reconfiguration. In particular, we find that the emergence of network modularity is a salient predictor of performance, and that modularization strengthens with increasing flexibility throughout learning. These insights not only elucidate the nuanced interplay of network modularity, accuracy, and learning dynamics but also bridge our understanding of learning in artificial and biological realms

Abnormal magnetoresistance behavior in Nb thin film with rectangular antidot lattice

Abnormal magnetoresistance behavior is found in superconducting Nb films perforated with rectangular arrays of antidots (holes). Generally magnetoresistance were always found to increase with increasing magnetic field. Here we observed a reversal of this behavior for particular in low temperature or current density. This phenomenon is due to a strong 'caging effect' which interstitial vortices are strongly trapped among pinned multivortices.Comment: 4 pages, 2 figure

Transitions To the Long-Resident State in coupled chaotic oscillators

The behaviors of coupled chaotic oscillators before complete synchronization were investigated. We report three phenomena: (1) The emergence of long-time residence of trajectories besides one of the saddle foci; (2) The tendency that orbits of the two oscillators get close becomes faster with increasing the coupling strength; (3) The diffusion of two oscillator's phase difference is first enhanced and then suppressed. There are exact correspondences among these phenomena. The mechanism of these correspondences is explored. These phenomena uncover the route to synchronization of coupled chaotic oscillators.Comment: 3 pages, 5 figure

Constraining R-parity violating couplings from B --> PP decays using QCD improved factorization method

We investigate the role of R-parity violating interaction in the non-leptonic decays of B mesons into two light mesons B --> PP. The decay amplitudes are calculated using the QCD improved factorization method. Using the combined data on B decays from BaBar, Belle and CLEO, we obtain strong constraints on the various products of R-parity violating couplings. Many of these new constraints are stronger than the existing bounds.Comment: 19 pages including two eps figure

Lack of Tgfbr1 and Acvr1b synergistically stimulates myofibre hypertrophy and accelerates muscle regeneration

In skeletal muscle, transforming growth factor-β (TGF-β) family growth factors, TGF-β1 and myostatin, are involved in atrophy and muscle wasting disorders. Simultaneous interference with their signalling pathways may improve muscle function; however, little is known about their individual and combined receptor signalling. Here, we show that inhibition of TGF-β signalling by simultaneous muscle-specific knockout of TGF-β type I receptors Tgfbr1 and Acvr1b in mice, induces substantial hypertrophy, while such effect does not occur by single receptor knockout. Hypertrophy is induced by increased phosphorylation of Akt and p70S6K and reduced E3 ligases expression, while myonuclear number remains unaltered. Combined knockout of both TGF-β type I receptors increases the number of satellite cells, macrophages and improves regeneration post cardiotoxin-induced injury by stimulating myogenic differentiation. Extra cellular matrix gene expression is exclusively elevated in muscle with combined receptor knockout. Tgfbr1 and Acvr1b are synergistically involved in regulation of myofibre size, regeneration, and collagen deposition

Enriching rare variants using family-specific linkage information

Genome-wide association studies have been successful in identifying common variants for common complex traits in recent years. However, common variants have generally failed to explain substantial proportions of the trait heritabilities. Rare variants, structural variations, and gene-gene and gene-environment interactions, among others, have been suggested as potential sources of the so-called missing heritability. With the advent of exome-wide and whole-genome next-generation sequencing technologies, finding rare variants in functionally important sites (e.g., protein-coding regions) becomes feasible. We investigate the role of linkage information to select families enriched for rare variants using the simulated Genetic Analysis Workshop 17 data. In each replicate of simulated phenotypes Q1 and Q2 on 697 subjects in 8 extended pedigrees, we select one pedigree with the largest family-specific LOD score. Across all 200 replications, we compare the probability that rare causal alleles will be carried in the selected pedigree versus a randomly chosen pedigree. One example of successful enrichment was exhibited for gene VEGFC. The causal variant had minor allele frequency of 0.0717% in the simulated unrelated individuals and explained about 0.1% of the phenotypic variance. However, it explained 7.9% of the phenotypic variance in the eight simulated pedigrees and 23.8% in the family that carried the minor allele. The carrier’s family was selected in all 200 replications. Thus our results show that family-specific linkage information is useful for selecting families for sequencing, thus ensuring that rare functional variants are segregating in the sequencing samples

Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression

<p>Abstract</p> <p>Background</p> <p>Lipopolysaccharide (LPS) is a cell wall component of Gram-negative bacteria with proved role in pathogenesis of sepsis. Brain injury was observed with both patients dead from sepsis and animal septic models. However, <it>in vitro </it>administration of LPS has not shown obvious cell damage to astrocytes and other relative cell lines while it does cause endothelial cell death <it>in vitro</it>. These observations make it difficult to understand the role of LPS in brain parenchymal injury.</p> <p>Results</p> <p>To test the hypothesis that LPS may cause biological changes in astrocytes and make the cells to become vulnerable to reactive oxygen species, a recently developed highly sensitive and highly specific system for large-scale gene expression profiling was used to examine the gene expression profile of a group of 1,135 selected genes in a cell line, T98G, a derivative of human glioblastoma of astrocytic origin. By pre-treating T98G cells with different dose of LPS, it was found that LPS treatment caused a broad alteration in gene expression profile, but did not cause obvious cell death. However, after short exposure to H₂O₂, cell death was dramatically increased in the LPS pretreated samples. Interestingly, cell death was highly correlated with down-regulated expression of antioxidant genes such as cytochrome b561, glutathione s-transferase a4 and protein kinase C-epsilon. On the other hand, expression of genes encoding growth factors was significantly suppressed. These changes indicate that LPS treatment may suppress the anti-oxidative machinery, decrease the viability of the T98G cells and make the cells more sensitive to H₂O₂stress.</p> <p>Conclusion</p> <p>These results provide very meaningful clue for further exploring and understanding the mechanism underlying astrocyte injury in sepsis <it>in vivo</it>, and insight for why LPS could cause astrocyte injury <it>in vivo</it>, but not <it>in vitro</it>. It will also shed light on the therapeutic strategy of sepsis.</p

Constraints on the phase γ\gamma and new physics from B→KπB\to K\pi Decays

Recent results from CLEO on $B\to K\pi$ indicate that the phase $\gamma$ may be substantially different from that obtained from other fit to the KM matrix elements in the Standard Model. We show that $\gamma$ extracted using $B\to K\pi, \pi\pi$ is sensitive to new physics occurring at loop level. It provides a powerful method to probe new physics in electroweak penguin interactions. Using effects due to anomalous gauge couplings as an example, we show that within the allowed ranges for these couplings information about $\gamma$ obtained from $B\to K \pi, \pi\pi$ can be very different from the Standard Model prediction.Comment: Revised version with analysis done using new data from CLEO. RevTex, 11 Pages with two figure