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  <title><![CDATA[ChBE Spring2007 Seminar Series]]></title>
  <body><![CDATA[<p>Gregory T. Reeves, a Post-doc in the Department of Chemical Engineering and the Lewis-Sigler Institute of Integrative Genomics at Princeton University, presents <em>Modeling Chemical Kinetics: Applications from Atomic to Continuum Scale</em> as part of ChBE's spring seminar series.
</p>
<p>* Refreshments will be served at 3:30 PM in the Lower Level 1 Gossage Atrium<br />
* Lecture commences at 4:00 PM in L1255 in the Ford ES&amp;T Building
</p>
<p>Seminar Abstract<br />
In a developing organism, what begins as a single cell must give rise to diverse tissues and body<br />
structures. The pattern formation that underlies these crucial developmental processes must be<br />
regulated at a variety of levels, from gene sequence to anatomy. With the growing body of<br />
experimental data, and the realization of the high degree of complexity in development,<br />
mechanistic models of development have become essential for integrating data, guiding future<br />
experiments, and predicting the effects of genetic and physical experiments. However, the<br />
formulation and analysis of quantitative models of development are limited by high levels of<br />
uncertainty in experimental measurements, along with a large number of both known and<br />
unknown system components. At the same time, an expanding arsenal of experimental tools can<br />
constrain models and directly test their predictions, making the modeling efforts not only<br />
necessary, but feasible [1].
</p>
<p>As an example, we have formulated a mechanistic model to describe the pattern formation<br />
controlled by the epidermal growth factor receptor (EGFR) network in the fruit fly, Drosophila<br />
melanogaster. This receptor network, which is used dozens of times throughout the<br />
development of all animal species, has also been found to be active in multiple types of tumors,<br />
and thus, pharmacological studies of EGFR inhibition are common [2]. In our system, the EGFR<br />
ligand, Spitz, is controlled by a negative feedback loop through a diffusible inhibitor, Argos,<br />
which acts as a ligand sink [3]. We have shown that the model is consistent with previous<br />
experimental data, and that the negative feedback loop serves to impart robustness to the pattern<br />
[4]. We have discovered that neither correct patterning, nor robustness, requires a finely-tuned<br />
dynamic length scale of Argos action [5]. Therefore, we are currently conducting experiments,<br />
to be used in conjunction with the model, to estimate values of biophysical parameters, such as<br />
the dynamic length scale of Argos. We expect further analysis of this</p>]]></body>
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      <value><![CDATA[<strong>Josie Giles</strong><br />School of Chemical &amp; Biomolecular Engineering<br /><a href="http://www.gatech.edu/contact/index.html?id=jg234">Contact Josie Giles</a><br /><strong>404-385-2299</strong>]]></value>
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      <email><![CDATA[josie.giles@chbe,gatech,edu]]></email>
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