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Stephen J. Beebe
Researcher at Old Dominion University
Publications - 183
Citations - 12440
Stephen J. Beebe is an academic researcher from Old Dominion University. The author has contributed to research in topics: Electric field & Pulse duration. The author has an hindex of 55, co-authored 181 publications receiving 11804 citations. Previous affiliations of Stephen J. Beebe include University of Texas Medical Branch & Eastern Virginia Medical School.
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Journal ArticleDOI
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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Progesterone and 17 alpha-hydroxyprogesterone. Novel stimulators of calcium influx in human sperm.
TL;DR: The effects of these progestins to increase [Ca2+]i, by activating a receptor-operated calcium channel, is the first report of such an activity in sperm.
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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.