Tid og sted for prøveforelesning
Bedømmelseskomité
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Dr. Martin Falcke, Mathematical Cell Physiology, Max-Delbrück-Centrum für Molekulare Medizin
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Professor Nic Smith, Oxford University Computing Laboratory
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Professor Hans Petter Langtangen, Department of Informatics, University of Oslo
Leder av disputas
Dag Langmyhr
Veileder
- Glenn T. Lines
- Joakim Sundnes
- Ole M. Sejersted
For mer informasjon
I denne oppgaven bruker Hake matematiske modeller for å undersøke funksjonen til friske hjerteceller og i celler fra et sviktende hjerte. Han bidrar til forståelsen av støy i kalsium signalering og for hvilke fysiologiske vilkår under hjertesvikt som kan forringe sammentrekningen til en hjertecelle.
In this thesis Hake uses computational models to investigate the function of healthy and failing heart cells. He contributes to the understanding of noise in calcium signaling and to what physiological conditions during heart failure that can impair contraction of a heart cell. The work has been performed at Simula Research Laboratory.
Heart failure (HF) is a progressive and chronic disease, characterized by an impaired ability of the heart to fill and pump blood. Experimental models of HF is commonly used to study the physiological conditions behind HF, and medical treatments can be tested using such models. In recent years, computational studies have emerged as a complement to the experimental ones. Using laws from physics and chemistry, modelers have been able to describe physiological phenomena using mathematical and statistical equations. The computational models can be used to test hypotheses about the function of heart cell and possible treatments, which cannot be done using experimental models.
The thesis focuses on a computational model of calcium dynamics in an intracellular sub-domain of a heart cell that is inaccessible for direct experimental measurements: The dyadic cleft. Calcium signaling in the dyadic cleft controls the contraction strength of a heart cell and during heart failure it is believed that this signaling is impaired. Signaling in micro domain such as the dyadic cleft is fundamentally random and stochastically. Hake first addresses the issue on what scale stochastic processes needs to be model. Based on this theoretical study, he then investigate possible causes for impaired calcium signaling during heart failure. He shows that physiological conditions during heart failure, such as altered action potential shape and altered structure of the dyadic cleft can impair calcium signaling and hence contraction of a heart cell.
Kontaktperson
For mer informasjon, kontakt Lena Korsnes.