Browsing by Subject "effect"
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Item HIPAA's Effect on Patient Enrollment in Clinical Trials(2002-08-01) Ommani, Sophia J.; Kaman, Robert; Arredondo, LaChelle; Bens, Annita V.Ommani, Sophia J., HIPAA’s Effect on Patient Enrollment in Clinical Trials. Master of Medical Science, August, 2002, pp. 88, 10 tables, 11 figures, references, 34 titles. The new regulation disseminated under the Health Insurance Portability and Accountability Act may impose serious restrictions as to how medical information can be used and disclosed. The law’s basic provisions began to take effect in 1997 with three principles: 1) to make it possible for people to get coverage even when they have past or present medical conditions/health factors, 2) to help people maintain the coverage needed when changing insurance or jobs, and 3) to make insurance more accessible for those who work in small businesses. A separate provision in the law imposes strict regulations on the privacy and security or patient health information. This provision has created the need to conduct research on the impact that this will have on a variety of health care issues. While some clinical practice research may be conducted without information linked to medical records, other research relies on personal identifiers to track treatment of an individual over time or link multiple sources of patient information. A randomized study was conducted to test the hypothesis that HIPAA would effect patient enrollment in clinical trials, and results supported the hypothesis. A lack of 1) willingness to authorize release of medical information and 2) a lack of understanding of the informed consent with the HIPAA language were the two predominant reasons given for refusing to sign.Item In Vitro Effect of CNTF, FGF-9, IL-1α on Human Optic Nerve Head Astrocytes(2004-08-01) Tovar-Vidales, Tara; Wordinger, Robert J.; Alvarez-Gonzales, Rafael; Agarwal, NeerajTovar, Tara., In Vitro Effect of CNTF, FGF-9, and IL-1α on Human Optic Nerve Head Astrocytes. Master of Science (Biomedical Sciences), August 2004, 100 pp., 4 tables, 35 illustrations, bibliography, 163 titles. Glaucoma is a leading cause of blindness worldwide. A major risk factor for glaucoma is increased intraocular pressure that leads to pathological changes in the optic nerve head (ONH). Astrocytes within the ONH become activated in glaucoma and may create an environment detrimental to retinal ganglion cell axons. The factors that cause activation of the ONH astrocytes (ONA) are unknown, although there is evidence that CNTF, FGF-9, and IL-1α activate glial cells within the CNS. The purpose of this research was to determine if exogenous CNTF, FGF-9, and/or IL-1α activate human ONH astrocytes.Item The Effect of Exercise Training on Behavior and Oxidative Stress in Aging Mice(2005-08-01) Taylor, Sara A.; Michael Forster; Joan F. Carroll; Susan FranksTaylor, Sara A., The effect of exercise training on behavior and oxidative stress in aging mice. Doctor of Philosophy (Biomedical Sciences), August 2005, 136 pp., 17 figures, bibliography, 97 titles. Purpose: Accrued oxidative damage to brain tissue is a proposed mechanism of cognitive deficits observed in aging. In mammalian tissue, it is hypothesized that a balance normally exists between pro-oxidants (reactive oxygen/nitrogen species) and endogenous antioxidant enzymes that are able to inhibit the activity of reactive oxygen/nitrogen species. As long as this balance is maintained, oxidative damage is moderated, but if the production of pro-oxidants becomes excessive or if the activity of antioxidants lags, oxidative stress and ultimately oxidative damage to tissues may result. It is the hypothesis of this project that exercise training is able to prevent decreased antioxidant activity in brain tissue, produce a favorable shift in the pro-oxidant/antioxidant balance, and thus moderate oxidative damage in the aging mice brain. Methods: 3 and 20 month old C57BL/6 mice were either subjected to 8 weeks of treadmill exercise followed by 3 weeks of concurrent exercise and behavior testing, or else they were age-matched, non-exercised controls. Mice were tested on multiple behavioral tasks that tested sensorimotor learning as well as tasks that required utilization of various component of cognitive learning. After exercise and behavior testing regimens were completed, biochemistry assays for protein oxidative damage as well as for antioxidant enzyme activity were performed on several brain regions. Results: It is a finding of the study that moderate, short-term exercise initiated in aged C57BL/6 mice resulted in increased fitness in the aged mice to the same degree as observed in young mice, improved some psychomotor skills, including bridge-walking and reaction time, and improved age-impaired spatial memory performance. Moreover, exercise training showed a lack of effect on oxidative damage in all brain regions, increased activity of glutathione peroxidase in the cerebellum and striatum of young, but not aged mice, and it increased the activity of catalase in the cortex of aged mice. Conclusions: The data presented in this project shows that exercise does moderate some age associated cognitive deficits, and the findings do not preclude the possibility that exercise produces this effect by reducing accrued oxidative damage that occurs with aging.