3 research outputs found
Autonomous stochastic resonance in fully frustrated Josephson-junction ladders
We investigate autonomous stochastic resonance in fully frustrated
Josephson-junction ladders, which are driven by uniform constant currents. At
zero temperature large currents induce oscillations between the two ground
states, while for small currents the lattice potential forces the system to
remain in one of the two states. At finite temperatures, on the other hand,
oscillations between the two states develop even below the critical current;
the signal-to-noise ratio is found to display array-enhanced stochastic
resonance. It is suggested that such behavior may be observed experimentally
through the measurement of the staggered voltage.Comment: 6 pages, 11 figures, to be published in Phys. Rev.
An Advanced Synthetic Image Generation Model and its Application to Multi/Hyperspectral Algorithm Development
Localization of post -golgi trafficking of tumor necrosis factor-a in macrophages.
Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine secreted by activated macrophages, In this study, we examined the intracellular distribution and trafficking of TNF-alpha, Immunofluorescence and immunogold localization demonstrated that in lipopolysaccharide (LPS)-stimulated RAW264 macrophages, the greatest concentration of TNF-alpha is found in the perinuclear Golgi complex, Staining of the Golgi complex appeared 20 min after activation of cells and persisted for 2-12 h, and TNF-cu appeared on the cell surface only transiently during this time. The rate of disappearance of Golgi staining correlated with the release of the cleaved, mature TNP-alpha into the medium, Pulse chase labeling and subcellular fractionation studies indicated that both 26-kDa and 17-kDa forms of TNF-alpha may be present at the level of the Golgi complex, Post-Golgi trafficking of TNF-alpha was modulated by agents that disrupt the cytoskeleton, Interferon-gamma (IFN-gamma), which primes macrophages for TNF-alpha-dependent cellular cytotoxicity, potentiated the effect of LPS by sustaining enhanced intracellular pools of TNF-alpha and also promoted redistribution of TNF-alpha into post-Golgi vesicular compartments. We propose that the primary pool of biologically active TNF-alpha in activated macrophages is held in the Golgi complex and that the cytokine is recruited directly from this intracellular pool for release in response to tumor cells or pathogens