Atherosclerosis is the buildup of plaque in artery walls due to injuries to the endothelial lining. Endothelial cells regulate blood flow through signal transduction and are sensitive to physical forces like shear stress from fluid movement. We developed a systems biology model with over 700 molecular reactions to investigate and predict how endothelial cells respond to shear stress at the molecular level. While our model matched some experimental data, it failed to capture other dynamics, suggesting there are still unknown interactions and responses that need to be incorporated.
This document provides a summary of Konstantinos Lykostratis's professional experience and qualifications. It outlines his experience as a project manager and systems biology researcher, including his roles developing software solutions and mathematical models. It also lists his educational background, obtaining a PhD in computational systems biology and bioinformatics from University College London, and a BSc in human genetics from the University of Leicester.
1. The document discusses systems biology approaches to modeling the endothelial cell response to fluid shear stress. It describes experimental techniques to apply controlled fluid shear stress and measure downstream cellular responses.
2. Mathematical models are formulated to represent molecular interactions and pathways involved in the shear stress response. Model predictions are compared to experimental data to validate and refine the models.
3. The models can provide insights into critical components, feedback loops, and how external perturbations may influence the cellular response to shear stress. Further experimental validation of model predictions is needed.
The document outlines the complex network of molecular interactions involved in the cellular response to shear stress. It shows calcium channels activating phospholipase C which generates diacylglycerol and IP3, mobilizing calcium and activating protein kinase C. Protein kinase C phosphorylates targets and is inhibited by other kinases and phosphatases. Calcium activates calpain protease which degrades talin and paxillin, affecting focal adhesion complexes and mechanotransduction.
This thesis examines how endothelial cells respond and polarize in response to fluid flow through three-dimensional modelling and simulations. It first reviews prior models of cytoskeleton dynamics and mechanics. It then presents a Brownian dynamics model of actin polymerization during lamellipodium formation. A boundary integral representation is used to model fluid flow over a single cell. A Kelvin-body model couples this flow to a PDE model of Rho GTPase activity to understand mechanotransduction and signal transduction dynamics during endothelial cell polarization and elongation in response to fluid flow. Validation against experimental data on Rho GTPase activation time courses is also discussed.
This PhD thesis presents a mathematical model of the signalling pathways regulating endothelial cell responses to fluid shear stress. The model consists of 8 interconnected modules describing processes such as calcium dynamics, calpain activity, integrin activation, and the phosphorylation of proteins like FAK and Src. Differential equations are used to simulate the dynamic behaviour of molecular species over time under varying shear stress conditions. The model aims to improve understanding of how fluid flow stimulation is converted into biochemical signals in endothelial cells and how this relates to the development of atherosclerosis.
Atherosclerosis is the buildup of plaque in artery walls due to injuries to the endothelial lining. Endothelial cells regulate blood flow through signal transduction and are sensitive to physical forces like shear stress from fluid movement. We developed a systems biology model with over 700 molecular reactions to investigate and predict how endothelial cells respond to shear stress at the molecular level. While our model matched some experimental data, it failed to capture other dynamics, suggesting there are still unknown interactions and responses that need to be incorporated.
This document provides a summary of Konstantinos Lykostratis's professional experience and qualifications. It outlines his experience as a project manager and systems biology researcher, including his roles developing software solutions and mathematical models. It also lists his educational background, obtaining a PhD in computational systems biology and bioinformatics from University College London, and a BSc in human genetics from the University of Leicester.
1. The document discusses systems biology approaches to modeling the endothelial cell response to fluid shear stress. It describes experimental techniques to apply controlled fluid shear stress and measure downstream cellular responses.
2. Mathematical models are formulated to represent molecular interactions and pathways involved in the shear stress response. Model predictions are compared to experimental data to validate and refine the models.
3. The models can provide insights into critical components, feedback loops, and how external perturbations may influence the cellular response to shear stress. Further experimental validation of model predictions is needed.
The document outlines the complex network of molecular interactions involved in the cellular response to shear stress. It shows calcium channels activating phospholipase C which generates diacylglycerol and IP3, mobilizing calcium and activating protein kinase C. Protein kinase C phosphorylates targets and is inhibited by other kinases and phosphatases. Calcium activates calpain protease which degrades talin and paxillin, affecting focal adhesion complexes and mechanotransduction.
This thesis examines how endothelial cells respond and polarize in response to fluid flow through three-dimensional modelling and simulations. It first reviews prior models of cytoskeleton dynamics and mechanics. It then presents a Brownian dynamics model of actin polymerization during lamellipodium formation. A boundary integral representation is used to model fluid flow over a single cell. A Kelvin-body model couples this flow to a PDE model of Rho GTPase activity to understand mechanotransduction and signal transduction dynamics during endothelial cell polarization and elongation in response to fluid flow. Validation against experimental data on Rho GTPase activation time courses is also discussed.
This PhD thesis presents a mathematical model of the signalling pathways regulating endothelial cell responses to fluid shear stress. The model consists of 8 interconnected modules describing processes such as calcium dynamics, calpain activity, integrin activation, and the phosphorylation of proteins like FAK and Src. Differential equations are used to simulate the dynamic behaviour of molecular species over time under varying shear stress conditions. The model aims to improve understanding of how fluid flow stimulation is converted into biochemical signals in endothelial cells and how this relates to the development of atherosclerosis.
Tools for government intervention in the economy (Greek)Dimitris Ktenidis
In this presentation there is a general description of the tools that the government uses in order to intervene in the economy. It is targeted for newly hired Greek public servants
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Την Δευτέρα 30 Μαΐου 2016 πραγματοποιήθηκε εκδήλωση – ομιλία με θέμα «Φορολογικό και Ασφαλιστικό Νομοσχέδιο», στη Δημοτική Τοπική Οργάνωση Πετρούπολης της Νέας Δημοκρατίας. Βασικοί ομιλητές ήταν ο Αντιπρόεδρος της Νέας Δημοκρατίας & Βουλευτής Β΄ Αθηνών, Χατζηδάκης Κωστής, ο Υπεύθυνος του Τομέα Εργασίας, Κοινωνικής Ασφάλισης και Πρόνοιας της Νέας Δημοκρατίας Βουλευτής Επικρατείας Βασίλης Οικονόμου και ο Συντονιστής Οικονομικών Υποθέσεων της Νέας Δημοκρατίας, Βουλευτής Φθιώτιδος κ. Χρήστος Σταϊκούρας
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