3,713 research outputs found
Faster is More Different: Mean-Field Dynamics of Innovation Diffusion
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
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
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
It is well-known that the -state clock model can exhibit a
Kosterlitz-Thouless (KT) transition if 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 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
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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