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Thomas R. Shannon, DVM, PhD |
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| Last Name: | Shannon | |
| First Name: | Thomas | |
| M. I.: | R. | |
| Degree & Certifications: | DVM, PhD | |
| Endowed Professorship: | ||
| Rank & Title: | Associate Professor | |
| Department: | Molecular Biophysics and Physiology | |
| College: | Graduate College, Rush Medical College | |
| Office Location: | 1750 W. Harrison St.
Jelke Building Ste. 1213 Chicago, IL 60612 | |
| Laboratory Location: | 1750 W. Harrison St. Jelke Building Ste. 1237 Chicago, IL 60612 | |
| Phone: | (312) 942-675 | |
| Fax: | (312) 942-6711 | |
| E-mail: | tshannon@rush.edu | |
| Education: | PhD, University of Missouri, 1994
DVM, University of Missouri, 1989 | |
| Research Areas: | Cardiovascular Diseases, Circulatory and Respiratory Physiology, Physiological Processes | |
| Laboratory Techniques: | Electrophysiology Cell/in vivo, Imaging Techonology, Microscopy (Electron Transmission Fluorescence Confocal), Patch Clamp/Individual Channel Recording, Spectrophotometry | |
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| Faculty/Staff Description: | Thomas Shannon, DVM, PhD, is a member of the Section of Cellular Signaling. He is interested in ionic channels, voltage gated ionic channels, fluorescence signal detection and electrophysiology, particularly as they relate to excitation-contraction coupling in striated muscle. Shannon uses multiple biochemical and biophysical approaches to study the control of the load of calcium in the storage organelle (the sarcoplasmic reticulum) of normal and abnormal cells of the heart. He has demonstrated on beating heart cells that the load in the normal sarcoplasmic reticulum is released partially to the cytosol in the process of a heart beat. Quantitative determination of these released fractions will allow him to understand the mutual interactions of Ca load and Ca release, and thus the control of contractile force, an important determinant of cardiac ejection (blood flow) in health and disease. For instance, Shannon has also demonstrated that the SR Ca load is reduced during heart failure and his research suggests that this reduction may be a critical factor in causing reduced cardiac contraction in this condition. Ongoing experiments are aimed at determining what causes this reduced SR Ca load. |
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MBP Shannon Link| View Short Profile |
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