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Iain Gardner
Researcher at Imperial College London
Publications - 15
Citations - 796
Iain Gardner is an academic researcher from Imperial College London. The author has contributed to research in topics: Nicotinic acetylcholine receptor & Furafylline. The author has an hindex of 11, co-authored 15 publications receiving 594 citations.
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Adverse outcome pathways: opportunities, limitations and open questions.
Marcel Leist,Ahmed Ghallab,Ahmed Ghallab,Rabea Graepel,Rosemarie Marchan,Reham Hassan,Reham Hassan,Susanne Hougaard Bennekou,Alice Limonciel,Mathieu Vinken,Stefan Schildknecht,Tanja Waldmann,Erik H.J. Danen,Ben van Ravenzwaay,Hennicke Kamp,Iain Gardner,Patricio Godoy,Frédéric Y. Bois,Albert Braeuning,Raymond Reif,Franz Oesch,Dirk Drasdo,Dirk Drasdo,Stefan Höhme,Michael Schwarz,Thomas Hartung,Thomas Braunbeck,Joost B. Beltman,Harry Vrieling,Ferran Sanz,Anna Forsby,Anna Forsby,Domenico Gadaleta,Ciarán Fisher,Jens M. Kelm,David A. Fluri,Gerhard F. Ecker,Barbara Zdrazil,Andrea Terron,Paul Jennings,Bart van der Burg,Steven Dooley,Annemarie H. Meijer,Egon Willighagen,Egon Willighagen,Marvin Martens,Chris T. Evelo,Chris T. Evelo,Enrico Mombelli,Olivier Taboureau,Olivier Taboureau,Alberto Mantovani,Barry Hardy,Bjørn E. V. Koch,Sylvia Escher,Christoph van Thriel,Cristina Cadenas,Dinant Kroese,Bob van de Water,Jan G. Hengstler +59 more
TL;DR: The history of the AOP concept and its most prominent strengths are discussed, including the advantages of a formalized approach, the systematic collection of weight of evidence, the linkage of mechanisms to apical end points, the examination of the plausibility of epidemiological data, the identification of critical knowledge gaps and the design of mechanistic test methods.
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An Introduction to Drug Disposition: The Basic Principles of Absorption, Distribution, Metabolism, and Excretion
TL;DR: This presentation is intended to provide an introductory overview of the life cycle of a drug in the animal body and indicates the significance of such information for a full understanding of mechanisms of action and toxicity.
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Prediction of human drug-induced liver injury (DILI) in relation to oral doses and blood concentrations
Wiebke Albrecht,Franziska Kappenberg,Tim Brecklinghaus,Regina Stoeber,Rosemarie Marchan,Mian Zhang,Kristina E Ebbert,Hendrik Kirschner,Marianna Grinberg,Marianna Grinberg,Marcel Leist,Wolfgang Moritz,Cristina Cadenas,Ahmed Ghallab,Ahmed Ghallab,Jörg Reinders,Nachiket Vartak,Christoph van Thriel,Klaus Golka,Laia Tolosa,José V. Castell,Georg Damm,Georg Damm,Daniel Seehofer,Daniel Seehofer,Alfonso Lampen,Albert Braeuning,Thorsten Buhrke,Anne Cathrin Behr,Axel Oberemm,Xiaolong Gu,Naim Kittana,Bob van de Water,Reinhard Kreiling,Susann Fayyaz,Leon van Aerts,Bård Smedsrød,Heidrun Ellinger-Ziegelbauer,Thomas Steger-Hartmann,Ursula Gundert-Remy,Anja Zeigerer,Anett Ullrich,Dieter Runge,Serene M. L. Lee,Tobias S. Schiergens,Lars Kuepfer,Alejandro Aguayo-Orozco,Agapios Sachinidis,Karolina Edlund,Iain Gardner,Jörg Rahnenführer,Jan G. Hengstler +51 more
TL;DR: An in vitro/in silico method was established that predicts the risk of human DILI in relation to oral doses and blood concentrations of test compounds to the probability of hepatotoxicity and application to the rat hepatotoxicant pulegone resulted in an ADI similar to values previously established based on animal experiments.
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Cytochrome P450 mediated bioactivation of methyleugenol to 1'-hydroxymethyleugenol in Fischer 344 rat and human liver microsomes.
TL;DR: The rate of 1'-hydroxylation of methyleugenol in vitro in 13 human liver samples varied markedly (by 37-fold), with the highest activities being similar to the activity evident in control rat liver microsomes, which suggests that the risk posed by dietary ingestion of methylesugenol could vary markedly in the human population.
Journal ArticleDOI
Interindividual variability in P450-dependent generation of neoantigens in halothane hepatitis.
Erik Eliasson,Iain Gardner,Helen Hume-Smith,Isabelle de Waziers,Philippe Beaune,J. Gerald Kenna +5 more
TL;DR: The results suggest that the balance between metabolic bioactivation by CYP2E1 and detoxication of reactive metabolites by cellular nucleophiles could be an important metabolic risk factor in halothane hepatitis.