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Douglas B. Kell
Researcher at University of Liverpool
Publications - 657
Citations - 55792
Douglas B. Kell is an academic researcher from University of Liverpool. The author has contributed to research in topics: Systems biology & Dielectric. The author has an hindex of 111, co-authored 634 publications receiving 50335 citations. Previous affiliations of Douglas B. Kell include Max Planck Society & University of Wales.
Papers
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Journal ArticleDOI
Immunological Tolerance, Pregnancy, and Preeclampsia: The Roles of Semen Microbes and the Father.
Louise C. Kenny,Douglas B. Kell +1 more
TL;DR: Overall, it is argued for a significant paternal role in the development of PE through microbial infection of the mother via insemination through microbes from the gut, oral and female urinary tract microbiomes as the main sources of the infection.
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The potential therapeutic effects of ergothioneine in pre-eclampsia.
TL;DR: This review discusses the use of ERG as a possibly mitochondrial‐targeted anti‐oxidant, focusing on its physical properties, potential mechanisms of action, safety profile and administration in relation to pregnancies complicated by pre‐eclampsia.
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The radio-frequency dielectric properties of yeast cells measured with a rapid, automated, frequency-domain dielectric spectrometer
TL;DR: In this paper, a computerized, rapid-scanning, frequency-domain dielectric spectrometer, capable of operating in the range 5 Hz-13 MHz, and based on commercially available components, is described.
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What would be the observable consequences if phospholipid bilayer diffusion of drugs into cells is negligible
TL;DR: The intellectual and observable consequences of assuming that, for drugs, phospholipid bilayer diffusion is negligible - 'PBIN' - (i.e., may be neglected, relative to transporter-mediated transmembrane fluxes).
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Substantial fibrin amyloidogenesis in type 2 diabetes assessed using amyloid-selective fluorescent stains.
Etheresia Pretorius,Martin J. Page,Lize Engelbrecht,Graham C. Ellis,Douglas B. Kell,Douglas B. Kell +5 more
TL;DR: It is shown that the clotting of plasma from type 2 diabetics is also amyloid in nature, and that this may be prevented by the addition of suitable concentrations of LPS-binding protein.