K
Karl H. Schoenbach
Researcher at Old Dominion University
Publications - 494
Citations - 20999
Karl H. Schoenbach is an academic researcher from Old Dominion University. The author has contributed to research in topics: Electric field & Cathode. The author has an hindex of 75, co-authored 494 publications receiving 19923 citations. Previous affiliations of Karl H. Schoenbach include Eastern Virginia Medical School & Darmstadt University of Applied Sciences.
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Microplasmas and applications
TL;DR: The microplasmas are generated under conditions that promote the efficient production of transient molecular species such as the rare gas excimers, which generally are formed by three-body collisions as mentioned in this paper.
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Intracellular effect of ultrashort electrical pulses.
TL;DR: The intracellular effect extends conventional electroporation to cellular substructures and opens the potential for new applications in apoptosis induction, gene delivery to the nucleus, or altered cell functions, depending on the electrical pulse conditions.
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Nanosecond pulsed electric field (nsPEF) effects on cells and tissues: apoptosis induction and tumor growth inhibition
TL;DR: The studies show that nsPEF effects are distinctly different than electroporation pulses and provide the first evidence for the potential application of nsPEf to induce apoptosis and inhibit tumor growth.
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Nanosecond pulsed electric fields cause melanomas to self-destruct
Richard Nuccitelli,Uwe Pliquett,Xinhua Chen,Wentia Ford,R. James Swanson,Stephen J. Beebe,Stephen J. Beebe,Juergen F. Kolb,Karl H. Schoenbach +8 more
TL;DR: It is shown that 40 kV/cm electric field pulses 300 nanoseconds in duration can rapidly stimulate pyknosis, reduce blood flow and fragment DNA in murine melanoma tumors in vivo with a total field exposure time of 1.8 microseconds.
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Nanosecond, high-intensity pulsed electric fields induce apoptosis in human cells
TL;DR: NSPEF technology provides a unique, high‐power, energy‐independent tool to recruit plasma membrane and/or intracellular signaling mechanisms that can delete aberrant cells by apoptosis.