published_or_final_version / Diagnostic Radiology / Master / Master of Philosophy

Digitized by Kansas Correctional Industries

Bibliography: leaves 267-287.

Graduation date: 1995

Ultraviolet (UV) radiation damages both eukaryotic and prokaryotic cells by causing the formation of free radicals which damage cell membranes and DNA. Antioxidant vitamins have been shown to protect cells from UV-induced damage by scavenging free radicals. The protection of skin and its normal flora is necessary for the health of individuals in resisting diseases caused by microorganisms and delaying the long-term damage caused by UV radiation.This research investigated the effects of the antioxidants vitamin A and ascorbic acid, as well as UV-irradiation on both prokaryotic (Staphylococcus epidermidis) cells and eukaryotic (human fibroblast skin) cells. This information is important in determining the effects of vitamin treatment on skin and its normal flora.Results indicate that ascorbic acid is rapidly (within six hours) degraded after being dissolved in water or medium. Treatment of cells with ascorbic acid must take into account this rapid degradation. S.epidermidis cells were protected from UV-induced damage by treatment with ascorbic acid but were more sensitive to UV-irradiation when treated with vitamin A. Human fibroblast cells treated with ascorbic acid did not exhibit morphological changes when compared to untreated cells. / Department of Biology

No description available.

Thesis submitted in fulfilment of the requirements for the award of the degree of Master of Technology Radiography (Diagnostic) in the Faculty of Health and Wellness Sciences at the Cape Peninsula University of Technology 2009 / Since their discovery in 1895, the use of x-rays is continuously evolving in medicine making the diagnosis of injuries and diseases more practicable. It is therefore not surprising that x-rays contribute 90% of the radiation dose to the population from manmade sources (DWP, 1992). Moreover, these radiation doses are associated with both fatal and non-fatal cancer risk that is detrimental to adults between 20 to 60 years (Wall, 1996). Radiation dose to individuals therefore needs to be actively monitored in order to minimise such risk. Barium contrast examinations were characterised as one of the radiological examinations that contributed enormously to the collective dose to the patients in the radiology department (DWP, 1992). Determining the diagnostic reference levels of such examinations would reduce the over-exposure of individuals to ionising radiation. Currently in South Africa (SA), there are no diagnostic dose reference levels for barium meal (BaM) and barium enema (BaE) examinations. This study therefore investigated the radiation doses delivered to patients referred for BaM and BaE, obtained potential regional reference doses for these examinations, compared the radiation doses obtained with those from similar dosimetry studies and investigated sources of dose variation among the study sites. A total of 25 BaM and 30 BaE patients in the age range 18 to 85 years, weighing 50 kg to 90 kg, at 3 hospitals in the Western Cape, SA were investigated. The radiation dose to the patients was measured using Dose Area Product (DAP) meters that were permanently fitted onto fixed fluoroscopy units at these 3 hospitals. The third quartile DAP values were 20.1 Gycm2 and 36.5 Gycm2 for BaM and BaE respectively. The median DAP values were 13.6 Gycm2 and 27.8 Gycm2 for BaM and BaE respectively. The median values were recommended as the potential Diagnostic Reference Levels for BaM and BaE as they are less affected by outlying values of under or over- weight (Yakoumakis, Tsalafoutas, Sandilos, Koulentianos et al, 1999). The weights of the patients, fluoroscopy time, the number of images obtained, the use of digital or conventional fluoroscopy equipment and the level of training of the radiologists were the factors considered for dose variation among the 3 hospitals.

Background: Exposure of skin to UVB radiation (290-320 nm) modulates the immune system, with most studies showing a suppression of Th1-driven immune responses. Investigations into the effects of UVB exposure on allergic respiratory responses have been limited. This study investigated the systemic effects of UVB on Th2-associated immune responses using two different murine models of allergic respiratory inflammation. The mechanism of immune regulation was also examined. Methods and Results: Two murine models of asthma were used: the papain model and the ovalbumin (OVA) model using papain and OVA, respectively, as the allergens. In the papain model, C57BL/6, histamine receptor-1 knockout (H1RKO) and histamine receptor-2 knockout (H2RKO) mice were exposed to a single 4 kJ/m2 dose of UVB (twice a minimal oedemal dose) on shaved dorsal skin three days prior to intranasal sensitisation with papain, a cysteine protease homologue of the house dust mite (Dermatophagoides pteronyssinus) allergen Der p 1. Sensitisation and boost each consisted of five daily intranasal doses of 1 µg papain whilst the challenge consisted of three daily intranasal doses of 100 µg papain. Asthmatic symptoms were assessed 24 h after the final challenge dose. H1RKO mice demonstrated enhanced papain-specific inflammatory responses in the lung-draining lymph nodes (LDLNs) whilst the responses of H2RKO mice closely mimicked those of C57BL/6 mice. UVB irradiation three days before sensitisation reduced in vitro papain-specific proliferation of LDLN cells from C57BL/6 and H1RKO mice but not H2RKO mice 24 h after challenge. The regulatory effect of UVB was transferred by adoptive transfer of 5 x 106 unfractionated LDLN cells from UVB-irradiated, papain-sensitised and -challenged C57BL/6 and H1RKO donor mice into naïve recipients of the corresponding strain that were ii subsequently sensitised and challenged with papain. Additionally, UVB exposure suppressed papain-induced IL-5 and IL-10 production in vitro by LDLN cells from H1RKO mice but not from C57BL/6 mice or H2RKO mice. The results of this study demonstrate systemic immunomodulation of responses to intranasally delivered antigen by UVB irradiation and the induction of regulatory cells in the LDLN following UVB exposure. Furthermore, these results implicate a role for the H2R in UVB-induced suppression of antigen-specific responses in the draining lymph nodes.

Most breast cancer patients undergo radiation diagnostics and are also treated with radiotherapy. In addition to being an important treatment modality, ionizing radiation (IR) is a potent tumour-causing agent that has been linked to breast cancer development. However, the exact molecular etiology of IR-induced mammary gland carcinogenesis remains unknown. We set out to analyze the role of DNA methylation in mammary gland responses to low dose IR using a well-established rat model. We also studied low dose IR effects on global gene expression and microRNAome. We found that exposure to low, mammography-like dose of IR led to a significant loss of global DNA methylation in rat mammary gland tissue. Furthermore, low dose IR significantly affected rat mammary gland transcriptome and microRNAome. The datasets generated within the scope of this thesis may be used to identify novel predictive biomarkers for assessment of the magnitude of IR effects on mammary gland tissue. / xi, 120 leaves ; 29 cm

Bibliography: leaves 267-287 / xviii, 287, [ca. 40] leaves, [10] leaves of plates : ill ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1985