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Tuesday, April 11th
10:45 AM

Associations Between the Ankle-Brachial Index and Markers of Arterial Dysfunction and Non-Classical Monocytes in HIV-Infected Individuals

Sean Terada, Whitman College

Science 159

10:45 AM - 11:00 AM

Prevalence rates of peripheral arterial disease, a common vascular disease indicative of plaque buildup, have been reported in HIV-infected populations to be as high as 20.7 percent. Although the direct cause is still unknown, many factors have been attributed to this increased risk, including persistent inflammation and immune activation, as well as treatment side effects. Peripheral arterial disease is commonly diagnosed using the ankle-brachial index, which measures a ratio of blood pressures in the limbs. My presentation investigates potential associations between the ankle-brachial index and measurements of arterial dysfunction as well as non-classical monocytes. Results of our research showed that abnormal ankle-brachial index scores were significantly associated with lower levels of non-classical monocytes and increased carotid artery intima-media thickness. This research provides further understanding of the potential role that non-classical monocytes play in the progression of atherosclerosis in HIV-infected individuals.

11:00 AM

Analyzing Immune Cells in Chronic Graft-Versus-Host Disease

Cora Amundson, Whitman College

Science 159

11:00 AM - 11:15 AM

High-risk leukemias are very difficult to successfully treat in both children and adults. Stem cell transplants are one treatment method that can cure patients. However, transplantation can cause chronic graft-versus-host disease (cGVHD), a serious and potentially life-threatening side effect. In cGVHD, the transplanted donor immune cells attack the patient’s healthy tissue. Naive T cells are immune cells that have not been activated to target a specific antigen and are implicated in attacking healthy tissue in cGVHD. We analyzed immune cells from patients who received a naive T cell-depleted transplant as a strategy to prevent cGVHD. We sought to identify the proteins that were more highly expressed on immune cells in patients who later developed cGVHD. Our goal was to determine if it is possible to predict which patients are at high risk of cGVHD before its onset for the purpose of treating future transplant recipients prophylactically.

11:15 AM

Searching for the Cure: A Promising HIV Strategy Unlike Any Currently Being Pursued

Paal Nilssen, Whitman College

Science 159

11:15 AM - 11:30 AM

For more than three decades, Human Immunodeficiency Virus (HIV) has posed a challenge for retroviral drug discovery. Despite previous palliative measures to treat the chronic disease, the morbidity of HIV still prevails significantly and will likely continue to increase as the survivors age. Enormous progress has been made in recent decades to uncover how HIV attaches to blood cells, enters inside, replicates and then leaves the cell. However, large gaps remain when it comes to how the virus disassembles itself. Conventional drug discovery platforms approach antiviral therapeutics directly by preventing HIV particles to bind to the host cell. I used an alternative, more indirect approach, one that includes approaching HIV from multiple mechanistic angles, specifically through HIV disassembly. This approach allows one to determine the rippling effects after an initial inciting event has occurred and the following effects it has on all aspects of body regulation.

11:30 AM

Delineating the Path Through Which Fibroblast Growth Factors Produce Remission from Type 2 Diabetes

Danielle Wieck, Whitman College

Science 159

11:30 AM - 11:45 AM

Since the discovery of insulin in 1921, therapies for Diabetes mellitus focus on pancreatic islets in an attempt to normalize blood glucose levels and stall disease progression. However, in the 19th century, the central nervous system was implicated in the pathology and potential therapy of diabetes. This presentation focuses on a return to the CNS as a way of treating diabetes via the family of Fibroblast Growth Factors. FGFs, specifically FGF1, 19 and 21, have been implicated in the prolonged lowering of blood glucose levels in rodent models, offering a potential CNS-focused therapy. This study aims to delineate the FGF1 signaling cascade by looking at effects of a mutant FGF, R50. We found that by comparing the effects of FGF1 and R50 on rodent models of diabetes we could further delineate the mechanism by which FGF1 works to produce remission.