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Institut für Physiologie und Pathophysiologie

Mathematical Modelling

Computational Methods are particularly useful in close combination with experimental techniques. This allows the direct input of latest experimental results into the model and vice versa. Therefore, we are developing models for calcium regulation or actin-myosin interaction in parallel to our fluorescence microscopy experiments.

 

Calcium regulation

Calcium ions inside the cell are present in various different "states". In addition to the free ions, calcium is also bound to several intrinsic and extrinsic calcium-binding sites (of which the fluorescence indicator is very often the most important one). Calcium ions can also be sequestered in intracellular membrane-bound organelles, for example, mitochondria, the endoplasmic reticulum (ER), or the sarcoplasmic reticulum (SR) of muscle fibers.

 

All these parameters have to be taken into account for the development of suitable models for the complex process of intracellular calcium regulation. As only calcium ions bound to the fluorescence indicator can be experimentally measured, all other quantities have to be derived from these model calculations.

 

The mathematical treatment requires an intelligent simplification of the associated differential equations using inherent symmetries, like cylindrical symmetry in skeletal muscle. Numerical solutions can finally be obtained with the help of a suitable discrete grid for time and space.

 

 

 

 

Modeling molecular motors

Muscle contraction is based on the interaction of only two proteins: actin and myosin. However, there are a number of associated proteins that are responsible for the regulation and tuning of this molecular motor. We are interested in developing a “motility model” that integrates various factors influencing the speed of shortening and force generation.

 


Neue Publikationen

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Improving electrical properties of iPSC-cardiomyocytes by enhancing Cx43 expression. J Mol Cell Cardiol. 2018 Jul;120:31-41. doi: 10.1016/j.yjmcc.2018.05.010. Epub 2018 May 16.

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Role of CD40 and ADAMTS13 in von Willebrand factor-mediated endothelial cell-platelet-monocyte interaction. Proc Natl Acad Sci U S A. 2018 Jun 12;115(24):E5556-E5565. doi: 10.1073/pnas.1801366115. Epub 2018 May 23.

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The VAMP-associated protein VAPB is required for cardiac and neuronal pacemaker channel function. FASEB J. 2018 Jun 7:fj201800246R. doi: 10.1096/fj.201800246R. [Epub ahead of print]

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Persistent sodium current modulates axonal excitability in CA1 pyramidal neurons. J Neurochem. 2018 Jun 4. doi: 10.1111/jnc.14479. [Epub ahead of print]

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Metabolic modulation of neuronal gamma-band oscillations. Pflugers Arch. 2018 May 28. doi: 10.1007/s00424-018-2156-6. [Epub ahead of print]

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The lncRNA CASC9 and RNA binding protein HNRNPL form a complex and co-regulate genes linked to AKT signaling. Hepatology. 2018 May 23. doi: 10.1002/hep.30102. [Epub ahead of print]

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Early Blood-Brain Barrier Disruption in Ischemic Stroke Initiates Multifocally Around Capillaries/Venules. Stroke. 2018 Jun;49(6):1479-1487. doi: 10.1161/STROKEAHA.118.020927. Epub 2018 May 14.

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Impact of carbonylation on glutathione peroxidase-1 activity in human hyperglycemic endothelial cells. Redox Biol. 2018 Jun;16:113-122. doi: 10.1016/j.redox.2018.02.018. Epub 2018 Mar 1.

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CXCR-4 expression by circulating endothelial progenitor cells and SDF-1 serum levels are elevated in septic patients. J Inflamm (Lond). 2018 May 16;15:10. doi: 10.1186/s12950-018-0186-7. eCollection 2018.

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In silico assessment of the conduction mechanism of the Ryanodine Receptor 1 reveals previously unknown exit pathways. Sci Rep. 2018 May 2;8(1):6886. doi: 10.1038/s41598-018-25061-z.

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Astrocytic glutamine synthetase is expressed in the neuronal somatic layers and down-regulated proportionally to neuronal loss in the human epileptic hippocampus. Glia. 2018 May;66(5):920-933. doi: 10.1002/glia.23292. Epub 2018 Jan 19.

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Parallel detection of theta and respiration-coupled oscillations throughout the mouse brain. Sci Rep. 2018 Apr 24;8(1):6432. doi: 10.1038/s41598-018-24629-z.

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Endothelial progenitor cells accelerate endothelial regeneration in an in vitro model of Shigatoxin-2a-induced injury via soluble growth factors. Am J Physiol Renal Physiol. 2018 Mar 7. doi: 10.1152/ajprenal.00633.2017. [Epub ahead of print]


Institut für
Physiologie und Pathophysiologie

Universität Heidelberg

Im Neuenheimer Feld 326

69120 Heidelberg

Telefon:+49 6221 54-4035
Telefax:+49 6221 54-4038
E-Mail:sekretariat.hecker@
physiologie.uni-heidelberg.de