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Using math to understand muscle physiology from molecule to cellMathematical Biology
|Speaker: ||Sam Walcott, Dept. of Mathematics, UC Davis|
|Location: ||2112 MSB|
|Start time: ||Mon, Apr 14 2014, 3:10PM|
Muscle contraction is the basis for voluntary movement, cardiac contraction and gastric motility. From an engineering perspective, we might expect to be able to model muscle as an active material and write a relatively simple constitutive law relating, say, stress and strain. The impact of this constitutive law on biology and medicine would be tremendous, allowing (for example) accurate prediction of surgical outcomes. However, due to the complexity of muscle at the molecular scale no such law exists.
The motivating idea behind my work is to use molecular-scale measurements to build up this constitutive law. The advantage of this "bottom-up" approach is that molecular-scale experiments are more tightly controlled than macro-scale measurements: the investigator controls molecular components, the surrounding environment and the geometry of the system. As a result, there is a great opportunity to precisely model these experiments and then predict measurements at larger scales. As an additional benefit, such a modeling framework is of great use to biologists, allowing quantitative analysis of new experiments.
I will talk about three stories in pursuit of this overarching goal of a constitutive law for muscle. In the first story, I will describe how our modeling work has connected a wide set of simplified experiments, and allowed us to weigh in on two questions of biological importance: 1. why do muscle molecules contract faster when working together than when working alone; and 2. how does elevated phosphate (important in muscle fatigue) affect muscle chemistry. In the second story, I will describe how the body turns muscles "on" and "off," and how this regulation machinery affects theories of muscle contraction. Finally, I will describe how we can use these theories to understand the effect of myosin binding protein c, a molecule known to underlie the majority of genetic heart defects.