Thesis (Ph. D.)--Illinois State University, 1991. / Title from title page screen, viewed December 9, 2005. Dissertation Committee: Patricia H. Klass (chair), Cheryl L. Cohn, John F. Chizmar, Ronald S. Halinski, Edward R. Hines. Includes bibliographical references (leaves 108-117) and abstract. Also available in print.

Thesis ( Ph.D.) -- McMaster University, 2001. / Includes bibliographical references (leaves 90-94). Also available via World Wide Web.

Thesis (M.S.)--University of Florida, 2002. / Title from title page of source document. Includes vita. Includes bibliographical references.

Thesis (M.S.)--Georgia State University, 2007. / Title from title page. Yu-sheng Hsu, committee chair; Xu Zhang, Jia-wei Liu, committee members. Electronic text (44 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Oct. 10, 2007. Includes bibliographical references (p. 35-36).

The treatment of menopausal symptoms by combined hormone replacement therapy (HRT) utilises drug formulations whereby a progestii1 is added to the oestrogen component to decrease the risk of endometrial carcinoma prnduced by the oestrogen. However, administration of large doses of progestins can increase low density lipid cholesterol, as well as reduce some of the beneficial effects of oestrogens. Local administration of progestins to the uterus may allow a much smaller dose to be used reducing the antagonism produced by progestins on desired oestrogenic effects. The simplest way to administer drugs to the uterus is by inserting a device through the cervix, however, this procedure may be associated with bacterial contamination of the uterus leading to pelvic infection. This study has therefore set out to develop a device for the delivery of antimicrobial agents to the uterus to reduce microbial contamination associated with transcervical insertion, and also the delivery of progestins which could be used as an adjunct to oestrogen HRT by targeting the progestin locally to the endometrium.

The original description of the ischaemic penumbra asserted that both cerebral blood flow and metabolism would be required to monitor therapeutic intervention in acute ischaemic stroke. However, imaging in stroke trials has predominantly used biomarkers of infarction or perfusion-weighted signal to identify the pathophysiological processes that occur. This approach has neither identified novel treatment targets, nor been shown to consistently select patients who might benefit from intervention. The aim of this thesis was to use magnetic resonance imaging (MRI) biomarkers to identify and describe the pathophysiology of acute ischaemic stroke in patients. Patients admitted to the John Radcliffe Hospital in Oxford were recruited into a clinical imaging study. Serial imaging data were acquired, predominantly in the first hours after symptom onset, to capture the early dynamics of brain pathophysiology. Tissue status was meticulously defined over time to ensure robust interpretation of the novel imaging biomarkers: multiple post labeling delay arterial spin labeling to measure cerebral blood flow (CBF), and amide proton transfer to generate an intracellular pH-weighted signal. At a group level, the regions with the most severe injury had the lowest mean CBF and the greatest acidosis at presentation. There was a gradient of mean CBF and pH-weighted signal from the most ischaemic tissue to healthy tissue, but at the level of the individual there was considerable overlap in both parameters. The dynamics of perfusion were not sufficient to explain tissue outcome. Both acidosis and alkalosis were observed up to 24 hours in tissue that infarcted, and the nature of the pH change correlated with the timing of infarction. These data show that single imaging biomarkers cannot explain the pathophysiology of stroke and tissue fate. There is heterogeneity of pathophysiology both within and between patients, and the dynamics of these processes vary. Insight from pH-weighted imaging highlights the limitations of using perfusion imaging alone to assess tissue status, and supports the use of complementary metabolic imaging in the investigation of ischaemic stroke.

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