Penelope (Penny) Noble joined the then Oxford Cardiac Electrophysiology group, led by Professor Denis Noble in January 1996 as a Research Scientist. Having studied physiology and biochemistry in a joint honours degree as an undergraduate, she went on to study techniques in mathematics and computation and their application for science in one of the first post-graduate courses to combine the two disciplines. Once she had gained this MSc from York University, she initially went on to apply and develop her knowledge of database work with the European Collection of Animal Cell Cultures. Following this Penny spent some time working as a research assistant in molecular neuroscience then switching to the field of cardiac electrophysiology undertaking work in the maintenance of the simulation software package Oxsoft HEART, initially developed by Prof Denis Noble and others. She then applied her knowledge of physiology and mathematical modelling to assist in the development work of existing and new mathematical cell models of cardiac cell types from various species, including the initial development of a human ventricular cell model. More recently she has been a key worker in the curation effort to ensure that all published cell models are publicly available in the form of CellML files, which can be downloaded from the CellML website and run using in house software, COR, now being developed as OpenCOR.
Penny’s most recent studies, in collaboration with others in the Noble group, include looking at the ability of the models to produce EADs and DADs and the underlying mechanisms involved in both production and ‘cure’ of repolarisation failure and hence coming to an understanding of the necessary and sufficient conditions for EADs in silico and in vivo, and from this investigations into the abilities of multi-component, multi-action drugs as potential remedies for cardiac arrythmias.
How the Hodgkin-Huxley equations inspired the Cardiac Physiome Project.
Noble D. et al, (2012), J Physiol, 590, 2613 - 2628
Ca²⁺-induced delayed afterdepolarizations are triggered by dyadic subspace Ca2²⁺ affirming that increasing SERCA reduces aftercontractions.
Fink M. et al, (2011), Am J Physiol Heart Circ Physiol, 301, H921 - H935
Ca2+-induced delayed afterdepolarizations are triggered by dyadic subspace Ca2+ affirming that increasing SERCA reduces aftercontractions
Fink M. et al, (2011), American Journal of Physiology - Heart and Circulatory Physiology, 301
Competing oscillators in cardiac pacemaking: historical background.
Noble D. et al, (2010), Circ Res, 106, 1791 - 1797
Mathematical models of the electrical action potential of Purkinje fibre cells.
Stewart P. et al, (2009), Philos Trans A Math Phys Eng Sci, 367, 2225 - 2255