Analysis of adaptive algorithms for an integrated communication network

Techniques were examined that trade communication bandwidth for decreased transmission delays. When the network is lightly used, these schemes attempt to use additional network resources to decrease communication delays. As the network utilization rises, the schemes degrade gracefully, still providing service but with minimal use of the network. Because the schemes use a combination of circuit and packet switching, they should respond to variations in the types and amounts of network traffic. Also, a combination of circuit and packet switching to support the widely varying traffic demands imposed on an integrated network was investigated. The packet switched component is best suited to bursty traffic where some delays in delivery are acceptable. The circuit switched component is reserved for traffic that must meet real time constraints. Selected packet routing algorithms that might be used in an integrated network were simulated. An integrated traffic places widely varying workload demands on a network. Adaptive algorithms were identified, ones that respond to both the transient and evolutionary changes that arise in integrated networks. A new algorithm was developed, hybrid weighted routing, that adapts to workload changes

Evolution of Tachyon Kink with Electric Field

We investigate the decay of an inhomogeneous D1-brane wrapped on a $S^1$ with an electric field. The model that we consider consists of an array of tachyon kink and anti-kink with a constant electric flux. Beginning with an initially static configuration, we numerically evolve the tachyon field with some perturbations under a fixed boundary condition at diametrically opposite points on the circle $S^1$. When the electric flux is smaller than the critical value, the tachyon kink becomes unstable; the tachyon field rolls down the potential, and the lower dimensional D0- and $\bar {\rm D}0$-brane become thin, which resembles the caustic formation known for this type of the system in the literature. For the supercritical values of the electric flux, the tachyon kink remains stable.Comment: 27 pages, 8 figures, some changes, one reference added, version to appear in JHE

S100a9 Knockdown Decreases the Memory Impairment and the Neuropathology in Tg2576 Mice, AD Animal Model

Inflammation, insoluble protein deposition and neuronal cell loss are important features in the Alzheimer's disease (AD) brain. To investigate the regulatory genes responsible for the neuropathology in AD, we performed microarray analysis with APPV717I-CT100 transgenic mice, an animal model of AD, and isolated the S100a9 gene, which encodes an inflammation-associated calcium binding protein. In another AD animal model, Tg2576 mouse brain, and in human AD brain, induction of S100a9 was confirmed. The endogenous expression of S100a9 was induced by treatment with Aβ or CT peptides in a microglia cell line, BV2 cells. In these cells, silencing study of S100a9 showed that the induction of S100a9 increased the intracellular calcium level and up-regulated the inflammatory cytokines (IL-1β and TNFα) and iNOS. S100a9 lentiviral short hairpin RNA (sh-S100a9) was injected into the hippocampus region of the brains of 13-month-old Tg2576 mice. At two months after injection, we found that knockdown of S100a9 expression had improved the cognition decline of Tg2576 mice in the water maze task, and had reduced amyloid plaque burden. These results suggest that S100a9 induced by Aβ or CT contributes to cause inflammation, which then affects the neuropathology including amyloid plaques burden and impairs cognitive function. Thus, the inhibition of S100a9 is a possible target for AD therapy

Mechanisms of airfoil noise near stall conditions

The focus of this paper is on investigating the noise produced by an airfoil at high angles of attack over a range of Reynolds number Re≈2×10⁵–4×10⁵. The objective is not modeling this source of noise but rather understanding the mechanisms of generation for surface pressure fluctuations, due to a separated boundary layer, that are then scattered by the trailing edge. To this aim, we use simultaneous noise and surface pressure measurement in addition to velocimetric measurements by means of hot wire anemometry and time-resolved particle image velocimetry. Three possible mechanisms for the so-called “separation-stall noise” have been identified in addition to a clear link between far-field noise, surface pressure, and velocity fields in the noise generation

Amyloid Precursor Protein Binding Protein-1 Modulates Cell Cycle Progression in Fetal Neural Stem Cells

Amyloid precursor protein binding protein-1 (APP-BP1) binds to the carboxyl terminus of the amyloid precursor protein (APP) and serves as the bipartite activation enzyme for the ubiquitin-like protein, NEDD8. In the present study, we explored the physiological role of APP-BP1 in the cell cycle progression of fetal neural stem cells. Our results show that cell cycle progression of the cells is arrested at the G1 phase by depletion of APP-BP1, which results in a marked decrease in the proliferation of the cells. This action of APP-BP1 is antagonistically regulated by the interaction with APP. Consistent with the evidence that APP-BP1 function is critical for cell cycle progression, the amount of APP-BP1 varies depending upon cell cycle phase, with culminating expression at S-phase. Furthermore, our FRET experiment revealed that phosphorylation of APP at threonine 668, known to occur during the G2/M phase, is required for the interaction between APP and APP-BP1. We also found a moderate ubiquitous level of APP-BP1 mRNA in developing embryonic and early postnatal brains; however, APP-BP1 expression is reduced by P12, and only low levels of APP-BP1 were found in the adult brain. In the cerebral cortex of E16 rats, substantial expression of both APP-BP1 and APP mRNAs was observed in the ventricular zone. Collectively, these results indicate that APP-BP1 plays an important role in the cell cycle progression of fetal neural stem cells, through the interaction with APP, which is fostered by phopshorylation of threonine 668