Undergraduate Research Program

2008-09 Levinson Scholars

Levinson 10-year Quote 3

Lauren Hanson in lab

Lauren Hanson
2008-09 Levinson Scholar









Kate Buckley - Bioengineering

Kate Buckley in labKate Buckley’s strong interest in cardiac repair began when she was introduced to the field by her mentor, Dr. Mike Regnier. Kate has been passionate about research since she arrived in the lab in the fall of her freshman year, and is motivated by a continuing interest in the therapies she investigates and the constant need for translational research that aims to address current health problems. Kate is particularly interested in creating genetic and cellular therapies in cardiac muscle that could be applied to different types of heart disease. The Levinson Scholarship has given her the opportunity to explore a novel research question that will allow her to delve deeper into the exciting opportunities that research offers.

In addition to research, Kate enjoys traveling and being actively involved in the Bioengineering program and the Honors Program. Kate is an avid learner and is constantly seeking new applications for her training as a bioengineer and research scientist.

After graduating, Kate plans to attend graduate school to continue her work with cardiac repair. She aims to one day perform clinically applicable research and teach students in the field of bioengineering and physiology.

Mentor: Mike Regnier, Bioengineering

Project Title: Gene therapy and the adrenergic response: L48Q cTnC virally transduced adult cardiomyocytes.

Abstract: Heart disease is the leading cause of death in the United States. After a heart attack (one of the most common results of heart disease), the heart undergoes an extensive remodeling process when normal cardiovascular function is disrupted. At the University of Washington exciting new therapeutic strategies are being developed to that improve and repair heart function. Gene based therapies that target cardiac myofilaments offer a way to halt or even reverse this process by altering contractile properties of the heart. Genetic transfer of the mutant L48Q troponin C offers potential as a therapeutic tool to improve function of surviving myocardium by enhancing Ca 2+ triggering of contraction. However, if this therapy is to be useful following an infarct, it must allow the ability for the heart to respond to adrenergic stimulation under stress. This project will investigate the adrenergic response of infarcted and non-infarcted myocardium with L48Q cTnC transfection into the myofilaments. Using cultured adult rat heart cells, the levels of adrenergic stimulation will be varied and the response characterized by measuring the changes in contraction and relaxation parameters. Contraction measurements will be made on individual cardiomyocytes using video microscopy coupled to computer software that measures cell and sarcomere length changes. After completing studies in cultured cardiomyocytes, this study will extend to an animal model of gene transfection to study the effect of L48Q cTnC and the adrenergic response at the in vivo and whole organ level. These studies are essential to determine if this gene therapy has the potential to be clinically relevant and reduce changes leading to heart failure. If so, L48Q cTnC has great potential as a therapeutic tool for several forms of cardiac disease.

Lauren Hanson - Neurobiology & Public Health

Lauren Hanson in labGrowing up the daughter of two physical therapists instilled a passion for health and a curiosity about the human nervous system in me early on. When I began my first quarter at the University of Washington I had my sights set on pursuing a career in medicine but felt completely lost in how to successfully achieve that end. My intense desire to understand the intricacies of the correctly and incorrectly functioning human body inspired me to apply for entrance into the neurobiology program in my sophomore year. Early admittance into this program has allowed my neurobiology courses to serve as a foundation for my academic experience as an undergraduate. Through my neurobiology studies I found my true passion and have since forged what I know is the right path for me as an undergraduate. Following the first year of this program I actively sought a place in Dr. Moody’s lab knowing that his developmental neurobiology based research was something I wanted to pursue. My passion for the research I have been conducting over the past year and a half is driven both by my inquisitive nature and by the possible clinical applications my work may have for disorders in humans . An understanding of correct brain development has the potential to facilitate an understanding of later development when the mechanisms I study may contribute to pathological forms of brain activity such as seizures.

Mentor: Dr William Moody, Neurobiology

Project Title: Initiation Mechanisms of Spontaneous Synchronous Activity in Neonatal Mouse Cortex

Abstract: Spontaneous Synchronous Activity (SSA) plays a central role in mammalian nervous system development. In mouse cortex, SSA is vital for the development of neuronal characteristics necessary for normal information processing. For SSA to carry out its developmental functions and mature firing properties to emerge, it must begin and end within a critical temporal window. As such, how the timing and generation of SSA are controlled is a major question in neurobiology. The Moody lab has determined that a discrete pacemaker region in mouse cortex controls SSA. The question about pacemaker function has been approached from three different directions: multi-cell calcium imaging of neuronal activity, molecular studies of ion channel types, and direct electrophysiological recording from single neurons in living brain slices. My work thus far has used the technique of single-cell electrical recording, patch clamp, because it provides access to the most direct information about pacemaker mechanisms via single cell behaviors and responses. A likely candidate for a pacemaker current is the low-threshold inactivating (T-type) Ca2+ current so we have investigated the role this current plays in SSA using the three previously mentioned experimental approaches. Molecular studies of ion channels have shown that the T-type Ca2+ channel protein is highly concentrated in the ventro-lateral pacemaker region which matches the point of origin of SSA waves detected in our multi-cell calcium imaging experiments. Additionally, imaging experiments have shown that Mibefradil, a T-type Ca2+ blocker, blocks SSA. My previous patch clamp recording analysis comparing pacemaker and follower neurons shows significantly longer burst durations in pacemaker neurons, which is consistent with the presence of T-type Ca2+ currents. From these findings my future experiments will attempt to further elucidate the mechanisms of pacemaker initiation of SSA in mouse cortex using single-cell electrical recording to isolate the T-type Ca2+ current in voltage clamp recordings. I will also investigate the effects of Mibefradil on SSA in single cells in the pacemaker and follower regions and determine if the pacemaker quality of the initiation zone is a function of a network property or individual pacemaker qualities of the discrete component cells.

Rita Sodt - Computer Science

Rita SodtRita Sodt began her research during her first year at the University of Washington. She thinks getting involved with research early on in her undergraduate studies was one of the best decisions she made because it has really enriched her undergraduate experience and helped her discover where her interests lie. Rita came to work in the Swanson lab because she was excited by its unique approach to cancer research. Using a mathematical model to simulate brain tumor growth it is possible to make predictions about how a tumor would spread; predictions that can lead to improved tumor treatments. Early on in her research, Rita gravitated towards the programming problems in the lab, including image analysis and simulations of tumor growth, and decided to major in computer science. She loves working in an interdisciplinary research setting, especially because as she is working on a computer science related project she gets to learn new things all the time about applied math and biology, and understand the big picture behind the research. She plans to pursue graduate studies in computer science and continue research related to computer science and health care.

Mentor: Dr. Kristin Swanson, Pathology

Project Title: Simulation of Anisotropic Growth of Gliomas Using Diffusion Tensor Imaging

Abstract: Gliomas are highly invasive brain tumors that account for nearly half of all primary brain tumors. Since current medical imaging techniques only detect a portion of these cancerous cells, a computational model was developed by Dr. Kristin Swanson to give more information about the extent of the tumor invasion below the threshold of imaging and to give a prediction of glioma growth that can be tailored to individual patient’s tumor. This computational model is currently based on two elements: cell proliferation and isotropic cell diffusion. Isotropic diffusion assumes that cell migration is random, however it is commonly accepted that glioma cells migrate preferentially along the direction of white matter tracts. In order to account for this observed diffusion, I will write a program that calculates the growth of gliomas that includes anisotropic diffusion. To do this I will use a published technique utilizing diffusion tensor imaging (DTI) to show the directional orientation of brain matter throughout the brain, which indicates the direction that glioma cells tend to migrate. My project will result in an improved mathematical model that can be used to simulate 3D virtual tumors. Hopefully after modifying the model to include anisotropic cell diffusion, the simulated tumors will more closely predict the growth of tumors that we observe in vivo. I will compare the results of our simulations to observed tumor growth to determine how well the model predicts the growth of gliomas.

Kathryn Winglee - Computer Science, Microbiology

Kathryn Winglee in labKathryn Winglee is interested in infectious diseases, but she is also intrigued by technology and its applications to biological research. As a double major in computer science and microbiology, she hopes to use her skills in both fields to study pathogens and how they cause disease. She began doing research the summer after her high school graduation, building a microfluidic device to perform PCR then studying hepatitis C before joining the Ramakrishnan lab. Her research on tuberculosis in the Ramakrishnan lab, where she has written a program capable of tracking fluorescent objects in 3D, has allowed her to both create and apply new technology to the study of a major global disease. She also has experience as a TA for the general microbiology lab. Her plan is to continue with similar research in graduate school.

Mentor: Lalita Ramakrishnan, Microbiology

Project Title: Changes in Infected Macrophages During Tuberculosis Pathogenesis and Granuloma Formation

Abstract: Tuberculosis (TB) is a bacterial disease that causes nearly two million worldwide deaths every year. One important characteristic of this disease is the formation of granulomas, aggregations of infected macrophages and other immune system cells, in the infected host. Understanding how granuloma formation in TB infections occurs is vital to understanding this disease. One animal model of TB makes use of zebrafish embryos infected by Mycobacterium marinum, a close relative of Mycobacterium tuberculosis, the causative agent of human TB. Zebrafish embryos are transparent, allowing real-time observation of the course of infection. In previous quarters, software has been created to track fluorescent M. marinum as it is carried inside macrophages during infection. This program will be used to study the movements and characteristics of macrophages during infection. By combining the use of fluorescent M. marinum and host immune cells with this program, the effects of carrying intracellular bacteria on macrophage motility, as well as the characteristics of macrophages that form and maintain granulomas, will be investigated. Finally, these studies will be extended to the effects of different bacterial mutations on macrophages during pathogenesis. The results will provide a better understanding of how pathogenic mycobacteria interact with their host to cause one of the world’s major diseases.