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Brianne Guilford Project Title: The role of oxidative stress in diabetic neuropathy Research Mentor: Douglas Wright |
| Description: Diabetic neuropathy is one of the principle chronic complications of both type 1 and type 2 diabetes mellitus and currently affects more than half of diabetic patients. Sensory loss, including both chronic numbness and sensitivity to pain or touch, develops in the majority of affected patients. The mechanisms that lead to painful or insensate symptoms in diabetic neuropathy are poorly understood. Oxidative stress is one of many variables that have been implicated as a critical feature in diabetic neuropathy. The goal of my current project is to characterize oxidative stress in painful and insensate neuropathy and determine if antioxidants have differential effects in mouse models that vary in their oxidative stress levels. | |
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William Messamore Project Title: Cortical Control of Hindlimb Muscles Research Mentor: Paul Cheney |
| Description: Cortical organization relates directly to aspects of movement disorders, making understanding normal cortical organization and control of movement a topic of clinical and rehabilitative importance. The cortical control of the arm and hand in primates has been studied extensively; however, there have been only a handful of studies focusing on the control of the lower limb. Recent research in our lab has elucidated the basic features of the M1 cortical hindlimb map along with the strength and nature of the synaptic linkages. I plan to determine the characteristics of M1 cortical output effects on ipsilateral hindlimb muscles, in comparison to effects on the contralateral side. In addition I plan on using electrophysiological recording techniques to determine the organization of output effects from single M1 cortical neurons to hindlimb muscles including fast and slow ankle extensor muscles. The data collected from these experiments will form the foundation for interpreting data from future experiments designed to investigate recovery of lower extremity function following brain injury. | |
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Kristin Russell Project Title: Functional and biochemical effects of brain fatty acid content on recovery from juvenile TBI Research Mentor: Beth Levant |
Description: Children under 5 years of age are at high risk for sustaining traumatic brain injuries (TBI) and tend to have poorer outcomes despite the greater neuroplasticity in children. Omega-3 polyunsaturated fatty acids (PUFA), a major component of neural membranes, accumulate in the brain during late gestation and early childhood. Low dietary content of these essential fatty acids results in decreased omega-3 PUFA accumulation in the developing brain. Omega-3 PUFAs have multiple neuroprotective and anti-inflammatory activities, thus low dietary omega-3 PUFA content may put children at risk for poorer outcomes after TBI. Therefore, my research focuses on how the functional and biochemical outcomes of juvenile TBI are influenced by the fatty acid composition of the brain. Additionally, I am researching the possibility of using omega-3 fatty acids as a therapeutic after TBI to decrease inflammation and apoptosis and improve outcomes. Knowing the full relationship between omega-3 PUFAs and brain injuries could lead to novel therapeutic strategies to improve the outcomes of TBI. |
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Jessica Witherspoon Project Title: Glenohumeral Joint Laxity: A Neural Contribution Research Mentor: Terence McIff |
| Description: The purpose of this study is to assess neural density and collagen composition of the glenoid labrum and capsule as they relate to anterior and posterior shoulder laxity. When reduced glenohumeral joint (GHJ) stiffness occurs, GHJ laxity increases resulting in shoulder instability, which can progress to subluxation and dislocation. According to research, the occurrence and reoccurrence of subluxations and dislocations become career ending for the workforce as well as for athletes. Rehabilitation and surgery protocols have been established to address instability related to GHJ dynamic stabilizers (musculature); however, there is a 14-94% reoccurrence post rehabilitation and/or surgery. This study will investigate the properties of the glenoid labrum and capsule, which are static stabilizers, as they relate to GHJ laxity and stiffness. It is hypothesized that the shoulders with a larger laxity zone and less tissue stiffness will present with lower neural densities as well as lower type I (providing tensile strength) to type III (sustaining elasticity) collagen ratios. The specific aims of this study are: 1) to define anterior and posterior GHJ instability based on the analysis of stiffness and zone of laxity in cadaveric models without muscular involvement; 2) to identify neural density in the labrum and capsule and determine whether it correlates with GHJ laxity; and 3) to determine whether the ratio of type I to type III collagen in the glenoid labrum and capsule correlates with GHJ stiffness. The clinical load and shift stability test will be performed on fifteen cadaveric shoulder pairs in the sagittal plane by a physical therapist and the Instron material testing machine to establish the zone of laxity and stiffness. Samples will then be collected from the anterior, anteroinferior, posterior and posteroinferior aspects of the labrum and capsule to evaluate the neural density of pacini and ruffini corpuscles as well as golgi tendon organs. In addition, the type I to type III collagen ratio will be determined. From these data, labral and capsular proprioceptive properties and stiffness will be correlated with available anterior and posterior joint movement for each shoulder. Determining the neural density, using immunofluorescence, will allow recognition of proprioceptive contribution to GHJ stability. Evaluating type I to type III collagen protein ratio, using enzyme-linked immunoassay (ELISA) will implicate the extent of tensile strength available to limit joint movement. We expect the shoulders with larger laxity zones and less stiffness will exhibit reduced neural density and type I to type III collagen ratio. Due to the high reoccurrence rate and career ending consequences of shoulder instability, it is vital to understand all the components that maintain shoulder stability, especially neural signaling that may be affected by changes in neural density . This study will aide in the development of specific treatment approaches for preventing or treating shoulder instability. | |
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