7 research outputs found

    A Modified Boost Converter with Reduced Input Current Ripple

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    Battery-powered trends in consumer electronics, transportation, and renewable energy sectors increase demands on DC/DC converter technology. Higher switching frequency and efficiency reduces solution size and cost, while increasing power capabilities. Still, switching noise remains the primary drawback associated with any DC/DC converter. Reducing a converter’s input ripple helps prevent switching noise from spreading to other systems on a shared DC power bus. This thesis covers the analysis, simulation, and implementation of a recently-proposed boost converter topology, alongside an equivalent standard boost converter, operating in steady-state, continuous conduction mode. A Matlab-based simulation predicts each converter’s input ripple performance using a state-space model. The converters’ hardware implementation minimizes component and layout differences to create an equivalent comparison. The simulation and hardware measurements demonstrate a 40% input current ripple reduction using the modified topology. Replacing standard boost converters with the modified topology minimizes the switching noise conducted through a system’s DC power network

    Interaction of endothelial cells and neutrophils in vitro: kinetics of thrombomodulin, intercellular adhesion molecule-1 (ICAM-1), E-selectin, and vascular cell adhesion molecule-1 (VCAM-1): implications for the relevance as serological disease activity markers in vasculitides

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    Recently markers of endothelial cell activation or injury gained increasing interest as serological parameters of disease activation in vasculitides. Among these, soluble serum thrombomodulin, ICAM-1, VCAM-1 and E-selectin are of particular interest. However, only thrombomodulin showed the expected close correlation. The objective of this study was to investigate in vitro the kinetics of these endothelial cell receptors after interaction of unstimulated or cytokine-activated polymorphonuclear neutrophils (PMN) and endothelial cells in order to find evidence explaining these different clinical findings. Over the time period of up to 48 h of incubation the kinetics of thrombomodulin, ICAM-1, E-selectin, and VCAM-1 levels in the supernatant of endothelial cells in co-culture with neutrophils were determined in vitro by ELISA under basal and partially cytokine-activated (tumour necrosis factor-alpha) conditions. Increased levels of ICAM-1, E-selectin and VCAM-1 were already found due to cytokine activation of endothelial cells alone. This increase was augmented after coincubation with neutrophils. In contrast, a significant increase of thrombomodulin in the supernatant was only found due to cell injury after cell–cell interaction of cytokine-activated endothelial cells with neutrophils. In conclusion, this in vitro model of the kinetics of soluble endothelial cell receptors after cell–cell interaction of cytokine-activated PMN and endothelial cells underlines the advantage of thrombomodulin in contrast to the adhesion molecules as a marker of endothelial damage. Therefore, soluble thrombomodulin seems to be a promising, valuable serological disease activity marker in vasculitides

    The Absence of the African-American Owned Business: An Analysis of the Dynamics of Self-Employment

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    Estimates from the Panel Study of Income Dynamics (PSID) indicate that African-American men are one-third as likely to be self-employed as white men.  The large discrepancy is due to a black transition rate into self-employment that is approximately one half the white rate and a black transition rate out of self-employment that is twice the white rate.  Using a new variation of the Blinder-Oaxaca decomposition technique, I find that racial differences in asset levels and probabilities of having self-employed fathers explain a large part of the black/white gap in the entry rate, but almost none of the gap in the exit rate

    Kupffer cells modulate iron homeostasis in mice via regulation of hepcidin expression

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    Hepcidin, a small cationic liver derived peptide, is a master regulator of body iron homeostasis. Cytokines and iron availability have so far been identified as regulators of hepcidin expression. Herein, we investigated the functional role of Kupffer cells for hepcidin expression because of their vicinity to the hepatocytes and their importance for iron recycling via erythrophagocytosis. We investigated C57Bl6 mice and littermates, in which Kupffer cells were eliminated in vivo upon intravenous injection of liposome-encapsulated clodronate. Primary cultures of hepatocytes and Kupffer cells were used to study direct regulatory effects ex vivo. The in vivo depletion of Kupffer cells resulted in a significant increase in liver hepcidin expression, which was paralleled by a significant reduction in serum iron levels. The same pattern of regulation by Kupffer cell depletion was observed upon injection of bacterial lipopolysaccharide into mice and in primary (Hfe −/−) and in secondary iron-overloaded mice. Accordingly, the messenger ribonucleic acid (mRNA) concentrations of the hepcidin iron-sensing molecule hemojuvelin were not significantly changed upon Kupffer cell depletion. When primary hepatocytes were cocultivated with Kupffer cells or stimulated with a Kupffer cell-conditioned medium ex vivo, a significant reduction in hepatocyte hepcidin mRNA expression was observed. Our data suggest that Kupffer cells control body iron homeostasis by exerting negative regulatory signals toward hepcidin expression, which may be primarily referred to the secretion of yet unidentified hepcidin-suppressing molecules by Kupffer cells

    Allgemeine Radiologie und Morphologie der Knochenkrankheiten

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