Participate in our research study to learn about your Body’s Lipid Metabolism.
WHAT WILL PARTICIPANTS BE ASKED TO DO?
* Provide a fasting blood sample
* Provide information such as Height, Weight, Medications and existing Medical conditions
* Consume a High Calorie Meal provided by us
* Provide a second blood sample approximately 3 hours later
ARE THERE BENEFITS TO PARTICIPATING?
* You will be compensated $20 dollars for the day you participate.
* You may be informed of your Lipid, Cholesterol and Glucose profiles; and will contribute to the medical diagnosis of cardiovascular disease.
Click on the link below to sign up.
Atherosclerosis, the leading cause of heart disease in developed nations, is an inflammatory disease marked by accumulation of monocytes and macrophages within the walls of arteries. Patients with severe cases of atheroscelosis exhibit elevated levels of blood lipids such as triglyceride-rich lipoproteins (TGRL). There is evidence that TGRL can induce blood vessel endothelial cells to upregulate inflammatory genes and express adhesion molecules that recruit monocytes.
Lipoproteins derived from human blood (green) bind to the surface of arterial endothelial cells
Our lab investigates how unhealthy dietary fats influence vascular inflammation and recruitment of monocytes to the arterial wall. We mimic the influence of a high-fat diet on arterial endothelium by repetitively exposing aortic endothelium in culture to TGRL that is freshly-isolated from human plasma. We have found that TGRL does not directly cause inflammation of the endothelium, but greatly enhances the inflammatory response to injury. We seek to address unanswered questions regarding the early stages of atherosclerosis by:
- Developing vascular-mimetic microfluidic channels (VMMC) to function as a diagnostic tool for assessing the affects of TGRL on recruitment of blood monocytes.
- Determining how blood lipoproteins such as TRGL interact with the endothelium, and through which signaling pathways they enhance inflammation.
- Elucidating the adhesion molecules and chemokines that support monocyte arrest and thereby establishing therapeutic targets to antagonize atherogenesis.