[LCSB] Presentation day on Wednesday (Valla), M.Sc. defense on Thursday (HU)

Gunnar Cedersund gunnar.cedersund at liu.se
Mon May 16 09:43:34 CEST 2011


Dear all,

in a few days, there are two interesting events on the systems biology calender, presenting works where mathematical modelling has been integrated as a tool in ordinary experimental biology

* The first is a big presentation day for students in systems biology. The students have taken the course TSRT17, which is a modelling project course. All projects contain real experimental data and previously unanswered biological questions, which throughout the projects have been answered using mathematical modelling. Apart from the student presentations, the systems biology company MathCore will also do a presentation. Wednesday May 18, 10-15, in E324 at Valla. Schedule below. 

* The second presentation is the M.Sc. defense by Robert Palmér. Robert has been in the group by Cedersund and Strålfors in parallel to the last two years of his undergraduate studies, and this has resulted in two systems biology papers in J Biol Chem, which are summarized and extended in his thesis. Robert now works as a modelling consultant for e.g. AstraZeneca, through the systems biology company MathCore. Thursday May 19, at 9.15 in "Karl-Johan salen", the Oncology house, Campus US. Abstract below. 

Welcome, 
Gunnar Cedersund, 0702-51 2323

P.S. Note that we have moved the next core facility meeting to May 30, 15.30-17, to not divert the attention from the other two events. 

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Schedule for the presentation day

10.15-10.20: Welcome

10.20-10.40: Group 1 Insulin signalling downstream of IRS1
10.40-11.00: Group 2 Non-intuitive peak order explained by modelling
11.00-11.15: Coffee break
11.15-11.35: Group 3 Insulin signalling and mechanisms for glucose uptake
11.35-11.55: MathCore Engineering AB - modelling consultancy for technical and systems biology applications
11.55-12.00: Summing up the morning

12-13.15: Poster session and lunch

13.15-13.30: Group 4 Explanation of decline in dose-response curves for high insulin concentrations
13.30-13.45: Group 5 Understanding the desensitization of heart adrenoreceptor signalling 
13.45-14.00: Group 6 Using contrast agents to non-invasively examine liver function
14.00-14.15: Group 7 Understanding and quantifying water transport in the brain
14.15-15.00: Poster session

Time and place: Wednesday May 18, in E324, which is in the Physics house at Valla


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Title: Multi-level modeling of insulin signaling and glucose homeostasis
Student: Robert Palmér, Diabetes and Integrative Systems Biology (isbgroup.eu), IKE
Opponent: Mikael Forsgren, CMIV
Time and place: Thursday May 19, at 9.15 in "Karl-Johan salen", the Oncology house, Campus US.

As a part of the emergence of systems biology, mathematical modeling has appeared as an increasingly important tool in the understanding of complex biological processes. One process that, in particular, has been investigated using modeling is that of glucose homeostasis, the main biological process associated with type 2 diabetes. Up until recently, most mathematical models of glucose homeostasis have been developed to describe various sub-systems, or physiological levels, of the process. Lately, however, attempts have been made to create more comprehensive models, so called multi-level models, linking characteristics of the different sub-systems and levels.
We recently performed two studies leading to the development of a multi-level model of glucose homeostasis, connecting phosphorylation and glucose uptake dynamics of the insulin signaling pathway in adipocytes, to whole-body glucose and insulin fluxes. In this thesis, this multi-level model is extended to include more detailed mechanisms on the process of insulin binding. Specifically, a previously developed model of how insulin interacts with the insulin receptor is connected to the multi-level model. The resulting model is shown capable of describing detailed characteristics of insulin binding in adipocytes, something that could not be achieved without the added mechanisms. Moreover, as the detailed mechanisms of insulin binding now have been included in our multi-level modeling framework, it is possible to study how they affect, and are affected by, the rest of the insulin signaling pathway and whole-body dynamics of glucose homeostasis. 
The results of this thesis provide a successful example of how models describing different sub-systems and levels can be merged into a more complete model. Furthermore, the results constitute an important step towards a more comprehensive understanding of glucose homeostasis. Such a comprehensive understanding may, for instance, be essential for the finding the underlying cause and future treatments of type 2 diabetes.

 


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