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John Owen

Researcher at University of Southampton

Publications -  245
Citations -  9331

John Owen is an academic researcher from University of Southampton. The author has contributed to research in topics: Lithium & Electrolyte. The author has an hindex of 44, co-authored 208 publications receiving 8614 citations. Previous affiliations of John Owen include Imperial College London & Columbia University.

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Mesoporous Platinum Films from Lyotropic Liquid Crystalline Phases

TL;DR: In this paper, the use of liquid crystalline plating solutions could be a versatile way to create mesoporous electrodes for batteries, fuel cells, electrochemical capacitors, and sensors.
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Plasma levels of beta-thromboglobulin and platelet factor 4 as indices of platelet activation in vivo

TL;DR: Measurement of plasma levels of two secreted platelet proteins has been suggested as a means for detecting increased platelet activation in vivo and it appears that when there is increased release of beta- thromboglobulin and platelet factor 4 in vivo, there is an increase in the ratio of plasma beta-thrombglobulin to plasma plateletFactor 4 compared to that found in normal individuals.
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Macrophage ABCA1 reduces MyD88-dependent Toll-like receptor trafficking to lipid rafts by reduction of lipid raft cholesterol.

TL;DR: The data suggest that macrophage ABCA1 dampens inflammation by reducing MyD88-dependent TLRs trafficking to lipid rafts by selective reduction of FC content in lipid rafting.
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3D lithium ion batteries{from fundamentals to fabrication

TL;DR: In this article, the design principles for 3D microbatteries and estimates the geometrical and physical requirements of the materials are discussed and selected examples of recent progress in the techniques available for fabrication of 3D battery structures.
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Thrombolytic therapy with tissue plasminogen activator or streptokinase induces transient thrombin activity

TL;DR: It is concluded that activation of coagulation occurs in response to thrombolytic therapy despite heparin administration and this thrombin action, though transient, would be sufficient to cause rethrombosis if localized and incompletely opposed by fibrinolytic activity.