P. Ellner (Cornell University)
Modeling coral disease: within-host dynamics, individual demography, and population consequences
Outbreaks of infectious disease, often newly emerged pathogens, have been a major factor in coral reef degradation and loss. I will describe some recent and ongoing work on modeling coral-pathogen interactions, ranging from hypothesis-driven (modeling how the mucus layer surrounding the coral regulates the initial establishment of pathogens) to largely data-driven (using individual-level demographic data to predict the population consequences of a fungal disease in sea fan corals).
Levy (University of Maryland, College Park)
Can mathematics cure leukemia? (and what that can tell us about mathematical biology)
Leukemia is a cancer of the blood that is characterized by an abnormal production of white blood cells. The treatment of Chronic Myelogenous Leukemia (CML) was revolutionized over the past decade with the introduction of new molecular-targeted drugs such as Imatinib. While these drugs keep leukemia in most patients in remission, they do not cure the disease. In this talk we will show how mathematical modeling combined with new experimental data, suggests the feasibility of a low-risk, clinical approach to enhancing the effect of the drug therapy, possibly leading to a durable cure of the disease. We will use this scientific problem to demonstrate challenges that face the dialogue between mathematics and biology.
Other Guest Speakers:
Mark Kramer (Boston University)
Experiences of a mathematical neuroscientist: on the market & in the lab
I will discuss briefly my recent faculty job search as an interdisciplinary math biologist and attempt to offer practical (and mostly inept) advice. I will also discuss applications of mathematical techniques to problems in neuroscience, with particular focus on brain rhythms, and an example of how the study of biological systems can motivate new mathematics.
Jon Seger (University of Utah)
The paradox of variation, revisited
Genetic variation is wildly abundant, but the neutral theory says it should be even more wildly abundant than it is in most species, and roughly proportional to population size. In fact levels of nucleotide diversity are disturbingly similar among species, in addition to being absolutely too low. The explanations offered most often are either (1) that species often pass through population "bottlenecks" that reduce their effective population sizes to similarly low numbers, or (2) that episodes of adaptive evolution "sweep" all parts of the genome at fairly regular intervals. Both of these explanations assume that populations are chronically far from equilibrium under the combined forces of mutation, selection and drift. A third possibility is that mildly deleterious mutations sweep the genome everywhere and constantly at a very slow rate. I will present some models showing that this process can actually do the job, at least for the mitochondrial genomes of species with very large populations, such as the cyamids (whale lice) that live on right whales.
See the Schedule for times and location.