2007 Appalachian Student Research Forum
Abstracts
(Names are listed alphabetically by first author in each Division and Category)
Division 1 – Undergraduates
Biomedical Sciences
RELATIONSHIP BETWEEN COLLEGIATE THROWERS’ ABILITY TO PRODUCE MAXIMUM FORCE AND THEIR ABILITY TO POTENTIATE
J.G. Calloway, J.M. Kraska , M.A. Kinser, M.E. Stone and M.W. Ramsey. Department of Kinesiology, Leisure and Sport Sciences, East Tennessee State University, Johnson City, TN 37614
PURPOSE: This investigation examined the relationship between a collegiate thrower’s ability to produce maximum force and post-activation (or post-exercise) potentiation.
METHODS: 5 male and 3 female collegiate throwers (mean + SD; age = 19.8 + 0.9 y; weight = 111.7 + 18.9 kg) participated in a specifically designed 4-week strength and conditioning program. At the end of the 4-week training cycle maximal force and explosive power were measured with and without a potentiation protocol. The ability to produce maximum force was determined by measuring the isometric peak force (IPF). On the first day athletes performed isometric pulls from the power position (mid-thigh) in a custom designed force rack over a force plate (1000 Hz). Along with the isometric pulls the athletes were instructed to perform an overhead ball throw. On day two the athletes performed a 1 RM snatch test and a potentiation protocol consisting of two trials of mid-thigh clean pulls at 60 kg, 100 kg, 120 kg, 140 kg, 160 kg, and 100 kg. Each trial was separated by approximately one to two minutes of rest in order to ensure that full recovery occurred between each trial. All trials were performed on a custom rack placed over a force plate (1000 Hz), two linear position transducers were attached to the ends of the barbell. Individual force time curve analyses were used to determine the peak force, peak velocity, peak power, and peak rate of force development for each trial. Peak rates of force development (RFD) and peak force were determined from the ground reaction forces, while the velocity data were derived from the vertical barbell displacements collected by the linear transducers. Power was then calculated from the force values and the velocity data. A
t-Test was used to determine if significant difference existed between pre- and post-potentiation values that were tested. Correlations were calculated using a pearson-r to determine the strength of the relationship between peak isometric force (N), RFD (0-250 ms), and the potentiation of dynamic peak force, peak velocity, and peak power, as well as ball throw (m), and maximum snatch (kg).
RESULTS: Potentiation values for peak force, peak velocity, peak power, and RFD showed significant statistical improvement (p 0.05). When correlating these potentiation values to IPF the correlations ranged from moderate to strong for peak force (r=0.47), peak velocity (r=0.34), and peak power (r=0.76). Isometric peak force also correlated strongly with ball throw (r=0.76) and maximum snatch (r=0.79).
CONCLUSION: These data indicate that the relationship between the ability to produce force (IPF) and the potentiation ability in athletes are related. Not only will stronger athletes perform better, but also their performance can be enhanced to an even greater extent, versus a weaker athlete, through potentiation.
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THE RELATIONSHIP BETWEEN POSTMENOPAUSAL HORMONE THERAPY AND THE EXERCISE ELECTROCARDIOGRAM: A RETROSPECTIVE STUDY
Lindsey Perry and Dr. Melessia Webb. Department of Professional Roles and Mental Health Nursing, East Tennessee State University, CON, Johnson City, TN 37614
Postmenopausal Hormone Therapy (PHT) is a hormone regimen consisting of estrogen or estrogen-plus-progestin which is administered to females in order to relieve symptoms of menopause and to prevent osteoporosis. Estrogen has been found to be molecularly similar to the drug digitalis, a positive inotrope. Consequently, PHT may be associated with significant ST-segment changes on the electrocardiogram. A retrospective chart review was conducted with the sample’s inclusion criteria of females, 50 years of age or older who had experienced a stress test followed by a cardiac catheterization in order to investigate a possible relationship between PHT and cardiac-stress testing. The patient’s cardiac catheterization results were used as the reference standard to identify true positive stress test from false positives. The researchers reviewed 128 medical records and collected the following data: demographics, laboratory values, medical history, current list of medications, stress test date and results, cardiac catheterization date and results, and interventions after cardiac catheterization. Results of this study did not identify a higher rate of false-positive results for stress tests in females taking PHT than females who were not taking PHT in the study group. However, females with a lower percentage of coronary artery occlusion of specific arteries, the right coronary artery (RCA), the left anterior descending artery (LAD), and the left circumflex artery (LCx), were associated with a false-positive stress test. In addition, the following medical histories were significant in relation to having a higher rate of false-positive stress tests: (1) no previous myocardial infarction (MI); (2) no invasive cardiac intervention; (3) peripheral vascular disease (PVD); (4) no significant vessel disease; (5) not taking a lipid-lowering agent; (6) not taking an antiplatelet medication; and (7) taking an antiarrythmic medication. It is also noteworthy that 40% (n = 51) of the study population had a false-positive stress test, while only 23% (n = 30) had a true-positive stress test result. Females, who had a higher rate of true-positive stress tests, were those with lower HDL cholesterol levels and a higher percentage of occlusion in the RCA, the LAD, and the LCx. Medical histories associated with a higher percentage of true-positive stress tests were positive history of MI, history of invasive cardiac intervention, having significant vessel disease, females taking a H2-Blocker, females taking an antiplatelet medication, and not taking a Proton Pump Inhibitor. Due to the small number of participants, the effect size was small with a power of 0.169; the researcher recommends that this study be conducted again with a larger sample size in order to increase the power of the study. The results may prove useful in future referral for noninvasive diagnostic testing for heart disease in females.
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NATURAL VITAMIN E ISOFORMS, GAMMA AND DELTA MODULATE TGFβ 2 IN PC-3 PROSTATE CANCER CELL LINES
Regina Phillips, Chuan Xing Ho, Sarah Whaley, Koyamangalath Krishnan, William Stone and Sharon Campbell. Department of Internal Medicine, East Tennessee State University, COM, Johnson City, TN 37614
In early stages of cancer, TGFβ (primarily TGFβ1) inhibits tumor development, but at later stages of tumor progression, cancer cells evade the growth inhibition by TGFβ. TGFβ is switched from a tumor suppressor to a tumor promoter. Lu et al. has demonstrated that the PC-3 cancer cell line exhibits constitutive expression of NF-ĸB, an anti-apoptotic transcription factor. The constitutive expression of NF-ĸB conveys resistance to Tumor Necrosis Factor alpha (TNF-α), a natural apoptotic stimuli. Transforming Growth Factor β2 (TGFβ2) has been identified as a factor mediating the constitutive activation of NF-ĸB. The Alpha-Tocopherol, Beta Carotene study found that substantially fewer participants taking alpha-tocopherol developed prostate cancer. Helzlsouer et al. furthered these findings by showing that high plasma concentrations of gamma-tocopherol enhanced the effects previously seen with alpha-tocopherol. Further research has shown that vitamin E is able to induce cell death in PC-3 cells with the effect being greatly increased when cells are treated with both TNFα and vitamin E, suggesting a possible mechanism of action for TGFβ induced cell death. In this study, the gamma and delta isoforms of vitamin E were tested for their ability to halt cell proliferation in PC-3 prostate cancer cell lines in comparison with alpha-tocopherol at 20, 40 and 60 µM. By western blotting and ELISA assays, it was found that the gamma and delta isoforms are more potent inhibitors of cell proliferation than alpha-tocopherol. These natural vitamin E isoforms are able to allow PC-3 cells to overcome the resistance to TNFα-mediated cell death. We further demonstrate that these isoforms down regulate the expression of TGFβ2, NF-ĸB, and TGFβ Receptor 1.
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CELL CYCLE REGULATORY PROTEINS IN TASTE CELL TURNOVER IN MICE
Colin Spaulding, Dr. Theresa Harrison and Lorraine Adams. Department of Biology and Department of Anatomy and Cell Biology, East Tennessee State University, COM, Johnson City, TN 37614
The cells in mammalian taste buds are known to regenerate throughout life every 10 – 14 days, but this process of taste receptor cellular turnover, particularly details concerning the regulation of progenitor cell division and differentiation, is still poorly understood. In all cells, cellular division and cell cycle exit prior to differentiation is regulated primarily by cell cycle regulatory proteins (CCRPs) such as cyclin dependent kinases (Cdks), Cdk inhibitors (CKIs), and the cyclin family of proteins. Studies have shown that normal taste buds express the CKI, p27(Kip1) (Hirota et al, 2001). Previous experiments in this laboratory (Adams et al, 2006) demonstrated that animals with null mutations for the p27(Kip1) gene (“knockouts”) have normal taste bud morphology, but an increased rate of cell turnover, and cyclin D2 is the major D cyclin expressed in taste tissues. In the present experiments, we wanted to examine in more detail the expression of p27(Kip1) and cyclin D2 in normal taste buds, and to determine if the absence of p27(Kip1) in mutants results in changes in the expression of D cyclins and/or other CKIs which may act to maintain the generally normal phenotype observed in taste buds of p27(Kip1)
knockout mice. We used single and double-label immunohistochemical techniques to evaluate the expression of D cyclin isoforms and proteins of the Cip/Kip family of CKIs in circumvallate
papillae of adult wild type and p27(Kip1) knockout mice. Light and confocal microscopy techniques were used to analyze the investigated proteins in fluorescent-labeled sections of tissue. Mature taste buds in wild type animals showed between 10 – 15% of their total cells to be labeled for p27(Kip1). Experiments to quantify the occurrence of p27(Kip1) and cyclin D2 labeled cells in the taste buds of wild type mice revealed averages of 5 – 6 cells per taste bud labeled for p27(Kip1) and cyclin D2. Extensive overlap was found between labeled cell groups, such that 55% of p27(Kip1) labeled cells also express cyclin D2, and 78% of cyclin D2 labeled cells were double-labeled for p27(Kip1). When investigating the possibility of upregulation of other CCRPs in the p27 (Kip1) null mutants, the results were negative for other members of the cyclin family (i.e. D1, D3) and, in initial experiments, for other members of the Cip/Kip family of CKIs (p21, p57). Experiments to date indicate that the hypothesis that normal taste bud morphology in knockout animals is maintained due to compensatory increases in expression of other Cip/Kip family CKIs and/or D cyclin proteins is not correct. Other CKIs (i.e. the INK family) may be more important in regulating taste bud cell numbers. Surprisingly, cyclin D2 continues to be expressed by some cells in the taste bud despite the fact that they have apparently withdrawn from the cell cycle. This suggests that, in addition to its role in facilitating transit through the cell cycle, cyclin D2 may play a different role in maturing and/or mature cells within the taste bud.
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FANCONI PROTEINS IN DOUBLE STRANDED DNA REPAIR
Robin Woodard, Ph.D. and Henning Kuich. Department of Natural Sciences, University of Virginia's College at Wise, Wise, VA 24293
Fanconi Anemia is a hereditary form of Aplastic Anemia. Aplastic Anemia is a disorder in which destruction of bone marrow leads to a deficiency of circulating erythrocytes, leukocytes, and platelets. As a result, patients exhibit symptoms such as easy bruising, fatigue, and a decreased ability to fight off infections. In Fanconi Anemia, known mutations lead to a decrease in chromosomal repair in bone marrow cells and their consequent inefficiency in blood cell production. The Fanconi complex necessary to repair these chromosomal breaks is composed of the proteins FancA, FancC, FancG, and FancF. Upon chromosome breakage, FancE accumulates in the nucleus via an interaction with FancC, which in turn leads to the binding of these two proteins to the remainder of the Fanconi Complex. Once the components are assembled, the complex localizes to the chromosome break and initiates a repair pathway. DNA-PK is a kinase known to be vital to repair of double stranded (ds) DNA breaks as well as the joining of ds breaks induced during non-homologous recombination. It is composed of 3 subunits. The subunits Ku-70 and Ku-87 are responsible for binding the DNA and form a dimer upon exposure to ds breaks. This dimer recruits the catalytic subunit (360 kDa), which in turn activates a ds break repair pathway. This study investigated the relationship between the DNA-PK and the Fanconi repair pathway by looking for interactions between proteins of the different pathways in the presence of double stranded breaks. Upon verification of the binding of Ku-70 and Ku-87 to the simulated double stranded breaks, it was shown that FancC in fact does interact with the same ds breaks. This interaction could be attributed to interactions with ds breaks, Ku-70, Ku-87, or any combination of the three. This study was also able to show that FancA does not seem to directly interact with ds breaks or either of the Ku proteins.
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Natural Sciences & Mathematics
FERMAT’S LAST THEOREM, A COMBINATORIAL APPROACH
Connie Blalock. Depart of Mathematics, East Tennessee State University, Johnson City, TN 37614. Dr. Debra Knisley, advisor.
Fermat’s Last Theorem is perhaps one of the most famous theorems in all of mathematics. The theorem states that the equation xn + yn = zn does not have positive integer solutions if n > 2. Of course, there are many solutions if n = 2, such as 32 + 42 = 52. The case when n = 2 has a well known geometric interpretation, namely x, y and z are lengths of sides of a right triangle. Fermat claimed to have proof that no solution exists if n > 2, but he simply did not have room in the margin to write the proof down. For more than 300 years, mathematicians tried to prove Fermat’s claim, or find a counter example. Finally, the theorem was proved by Andrew Wiles, a mathematics professor at Princeton, in 1995. His proof, however, was clearly not the proof that Fermat claimed to have since it requires mathematics not yet invented at the time of Fermat.