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        Anode power deposition in dry EDM

        Felipe T. B. Macedo,Moritz Wiessner,Christoph Hollenstein,Caroline P. Martendal,Friedrich Kuster,Konrad Wegener 한국정밀공학회 2019 International Journal of Precision Engineering and Vol.6 No.2

        Dry electrical discharge machining (DEDM) has been developed as an environmentally friendlier alternative to the traditional EDM in oil-based dielectric. Proper understanding of the physics of the DEDM discharges is necessary in order to improve this new manufacturing technology, since its workpiece material removal and tool electrode wear mechanisms are governed by plasma-material interactions. The present work proposes the application of theoretical models, numerical simulations, and advanced diagnostics from the field of plasma physics as effective tools to estimate the electric discharge power deposition onto the anode workpiece in DEDM. Collisional-radiative models are used here to calculate several plasma properties, from which the anode power deposition can be estimated. In addition, electrical circuit simulations, which use a modified Cassie-Mayr model, calculate the fraction of the total electric discharge power that is consumed by thermal conduction into the anode electrode material. The methods proposed in the present work provide fundamental information for further workpiece material erosion modelling and simulation under different DEDM processing conditions.

      • MST1-dependent vesicle trafficking regulates neutrophil transmigration through the vascular basement membrane

        Kurz, Angela R. M.,Pruenster, Monika,Rohwedder, Ina,Ramadass, Mahalakshmi,Schä,fer, Kerstin,Harrison, Ute,Gouveia, Gabriel,Nussbaum, Claudia,Immler, Roland,Wiessner, Johannes R. American Society for Clinical Investigation 2016 The Journal of clinical investigation Vol.126 No.11

        <P>Neutrophils need to penetrate the perivascular basement membrane for successful extravasation into inflamed tissue, but this process is incompletely understood. Recent findings have associated mammalian sterile 20-like Kinase 1 (MST1) loss of function with a human primary immunodeficiency disorder, suggesting that MST1 may be involved in immune cell migration. Here, we have shown that MST1 is a critical regulator of neutrophil extravasation during inflammation. Mst1-deficient (Mst1(-/-)) neutrophils were unable to migrate into inflamed murine cremaster muscle venules, instead persisting between the endothelium and the basement membrane. Mst1(-/-) neutrophils also failed to extravasate from gastric submucosal vessels in a murine model of Helicobacter pylori infection. Mechanistically, we observed defective translocation of VLA-3, VLA-6, and neutrophil elastase from intracellular vesicles to the surface of Mst1(-/-) neutrophils, indicating that MST1 is required for this crucial step in neutrophil transmigration. Furthermore, we found that MST1 associates with the Rab27 effector protein synaptotagmin-like protein 1 (JFC1, encoded by Sytl1 in mice), but not Munc13-4, thereby regulating the trafficking of Rab27-positive vesicles to the cellular membrane. Together, these findings highlight a role for MST1 in vesicle trafficking and extravasation in neutrophils, providing an additional mechanistic explanation for the severe immune defect observed in patients with MST1 deficiency.</P>

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