3,713 research outputs found

    Faster is More Different: Mean-Field Dynamics of Innovation Diffusion

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    Based on a recent model of paradigm shifts by Bornholdt et al., we studied mean-field opinion dynamics in an infinite population where an infinite number of ideas compete simultaneously with their values publicly known. We found that a highly innovative society is not characterized by heavy concentration in highly valued ideas: Rather, ideas are more broadly distributed in a more innovative society with faster progress, provided that the rate of adoption is constant, which suggests a positive correlation between innovation and technological disparity. Furthermore, the distribution is generally skewed in such a way that the fraction of innovators is substantially smaller than has been believed in conventional innovation-diffusion theory based on normality. Thus, the typical adoption pattern is predicted to be asymmetric with slow saturation in the ideal situation, which is compared with empirical data sets.Comment: 11 pages, 4 figure

    Percolation on hyperbolic lattices

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    The percolation transitions on hyperbolic lattices are investigated numerically using finite-size scaling methods. The existence of two distinct percolation thresholds is verified. At the lower threshold, an unbounded cluster appears and reaches from the middle to the boundary. This transition is of the same type and has the same finite-size scaling properties as the corresponding transition for the Cayley tree. At the upper threshold, on the other hand, a single unbounded cluster forms which overwhelms all the others and occupies a finite fraction of the volume as well as of the boundary connections. The finite-size scaling properties for this upper threshold are different from those of the Cayley tree and two of the critical exponents are obtained. The results suggest that the percolation transition for the hyperbolic lattices forms a universality class of its own.Comment: 17 pages, 18 figures, to appear in Phys. Rev.

    Anomalous response in the vicinity of spontaneous symmetry breaking

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    We propose a mechanism to induce negative AC permittivity in the vicinity of a ferroelectric phase transition involved with spontaneous symmetry breaking. This mechanism makes use of responses at low frequency, yielding a high gain and a large phase delay, when the system jumps over the free-energy barrier with the aid of external fields. We illustrate the mechanism by analytically studying spin models with the Glauber-typed dynamics under periodic perturbations. Then, we show that the scenario is supported by numerical simulations of mean-field as well as two-dimensional spin systems.Comment: 6 pages, 5 figure

    Residual discrete symmetry of the five-state clock model

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    It is well-known that the qq-state clock model can exhibit a Kosterlitz-Thouless (KT) transition if qq is equal to or greater than a certain threshold, which has been believed to be five. However, recent numerical studies indicate that helicity modulus does not vanish in the high-temperature phase of the five-state clock model as predicted by the KT scenario. By performing Monte Carlo calculations under the fluctuating twist boundary condition, we show that it is because the five-state clock model does not have the fully continuous U(1) symmetry even in the high-temperature phase while the six-state clock model does. We suggest that the upper transition of the five-state clock model is actually a weaker cousin of the KT transition so that it is q6q \ge 6 that exhibits the genuine KT behavior.Comment: 13 pages, 17 figure

    Proinflammatory Role of Vascular Endothelial Growth Factor in the Pathogenesis of Rheumatoid Arthritis: Prospects for Therapeutic Intervention

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    Recent experimental and clinical studies have placed new emphasis on the role of angiogenesis in chronic inflammatory disease. Vascular endothelial growth factor (VEGF) and its receptors are the best characterized system in the regulation of rheumatoid arthritis (RA) by angiogenesis. Furthermore, in addition to its angiogenic role, VEGF can act as a direct proinflammatory mediator during the pathogenesis of RA, and protect rheumatoid synoviocytes from apoptosis, which contributes to synovial hyperplasia. Therefore, the developments of synovial inflammation, hyperplasia, and angiogenesis in the joints of RA patients seem to be regulated by a common cue, namely, VEGF. Agents that target VEGF, such as anti-VEGF antibody and aptamer, have yielded promising clinical data in patients with cancer or macular degeneration, and in RA patients, pharmacologic modulations targeting VEGF or its receptor may offer new therapeutic approaches. In this review, the authors integrate current knowledge of VEGF signaling and information on VEGF antagonists gleaned experimentally and place emphasis on the use of synthetic anti-VEGF hexapeptide to prevent VEGF interacting with its receptor
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