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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.
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Journal ArticleDOI
The transporter-mediated cellular uptake of pharmaceutical drugs is based on their metabolite-likeness and not on their bulk biophysical properties: Towards a systems pharmacology ☆
TL;DR: It is shown that lipophilicity is a very poor predictor of drug permeability, and that the knowledge of both pharmacology and systems biology modelling need to be brought together into a new systems pharmacology.
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KiPar, a tool for systematic information retrieval regarding parameters for kinetic modelling of yeast metabolic pathways
TL;DR: KiPar is a dedicated information retrieval system designed to facilitate access to the literature relevant for kinetic modelling of a given metabolic pathway in yeast, and develops an integrative approach, combining public data and software resources for the rapid development of large-scale text mining tools targeting complex biological information.
Journal ArticleDOI
Formulation and some biological uses of a buffer mixture whose buffering capacity is relatively independent of pH in the range pH 4–9
Douglas B. Kell,J.Gareth Morries +1 more
TL;DR: It is shown how this buffer mixture may be used to determine the force-flux relationship of proton transfer between two aqueous phases separated by a phospholipid bilayer in vesicular systems and it is demonstrated that this relationship is linear over a wide range of delta mu approximately H+.
Posted ContentDOI
Substoichiometric molecular control and amplification of the initiation and nature of amyloid fibril formation: lessons from and for blood clotting
TL;DR: The idea is developed that in many cases the anomalous fibrin fibre formation seen in such diseases actually amounts to amyloidogenesis, and the evidence is presented to develop the idea and summarise the evidence.