Thesis (Ph. D.)--University of Washington, 1989. / Vita. Includes bibliographical references (leaves [94]-105.).

It is widely accepted that the occurrence of myocardial infarction (MI) among Black South Africans is much lower than that of South Africans of European or Asian ancestry. Over the past decade, this disease among Black Africans in urban areas appears tc be increasing. The prevalence of MI among Black Africans admitted fo Baragwanath Hospital (BGH) over a four year period (1984-1987) was determined by computer identification of all patients demonstrating elevated creatine kinase isoenzymes. Diagnosis of MI was confirmed by reviewing the hospital bedletters.

Thesis (M.A.)--Boston University / Rat heart muscle was subjected to quantitated conditions of anoxia achieved by extracting oxygen from Ringer's solution under vacuum and heat. Special Van Slyke analyses measured the amount of oxygen remaining in solution after the extraction procedures had been carried out. Myocardial response to anoxia was studied in terms of survival, or the ability of the heart tissue to remain alive during anoxia with resumption of function when placed in an oxygenated environment, and in terms of function, or the ability of heart muscle to contract during anoxia [TRUNCATED]

A research report submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in partial fulfilment of the requirements for the degree of Master of Science in Occupational Therapy Johannesburg / Visual perceptual impairment is a common consequence of stroke which may affect all areas of occupational performance. The evidence for the management of these deficits in occupational therapy is not clear. The purpose of this qualitative study was therefore to determine the expert opinion for best practice in the management of visual perceptual deficits in adults post stroke in the South African context. Interviews with eight expert occupational therapists indicated that a lack of clarity exists in this area of clinical practice. Findings indicate this is a complex area of practice where management needs to be focussed on occupation based therapy for the individual patient in their context. The use of standardised and non-standardised assessments and compensation verses remediation in intervention must be individually determined, and the use of a “top down” approach was considered preferable. This study presents the first step in the development of clinical guidelines for management of this deficit in occupational therapy in South Africa.

Thesis (Ph. D.)--University of Louisville, 2003. / Department of Physiology and Biophysics. Vita. "December 2003." Includes bibliographical references (leaves 102-115).

The original publication is available at http://www.samj.org.za / The clinical presentation of a young hypertensive White man with acute high lateral non-transmural myocardial infarction (MI) is documented. This diagnosis was established on the grounds of a history of chest pain, elevated serial serum enzyme levels, technetium-99m pyrophosphate ('hot-spot') scintigraphy, exercise thallium-201 ('cold-spot') scanning, left ventricular cine angiography and selective coronary arteriography. Daily resting 12-lead ECGs failed to demonstrate unequivocal features of acute non-transmural subendocardial MI. The diagnostic difficulties facing the clinician in a case of acute MI associated with a non-diagnostic ECG are stressed, and the ECG features of acute subendocardial MI are reviewed. / Publishers' version

ABSTRACT The Sarcolemmal Membrane Associated Protein 3 (SLMAP3) is a tail-anchored membrane protein, which is ubiquitously expressed in tissues including myocardium. It is a component of subcellular membranes and the centrosome, and it appears to serve distinct roles in cell growth and membrane biology. In addition, mutations in SLMAP have been linked to Brugada syndrome, which leads to cardiac dysfunction and death. Here, we have examined the effects of different levels of SLMAP3 on postnatal heart function, pre and post myocardial infarction (MI).Transgenic (TG) mice with a cardiac specific expression of SLMAP3 isoform were generated and assessed with echocardiography to measure function, immunohistochemistry for histology, TUNEL assay for apoptosis, Masson’s trichrome staining for fibrosis, and Western blots for protein expression. Baseline echocardiography of 8 weeks old TG mice showed a normal cardiac function that was expressed in ejection fraction percent (%EF=66%±7.42), which was similar to those of wild type mice (%EF=67%±9.36), p<0.05, n=20-25 (in each group). MI was induced by permanent ligation of left anterior descending (LAD) artery in 9 week old WT & TG mice, while sham was the control. No death was recorded in SLMAP3 TG mice up to one year post MI, whereas 70% of WT mice had deceased, p<0.01, n=17-18 (in each group). Cardiac function was assessed by echocardiography (at 4 week post MI) showed a partially restored ejection fraction percent (%EF~49.2%±17.02) in SLMAP3 TG mice post MI compared to (%EF~36.4%±15.25) in WT mice post MI, p<0.05, n=15-16 (in each group). Furthermore, infarct size (IS) as well as collagen area (CA) post MI were significantly attenuated (IS~43%±8.82, CA~35%±5.15) in SLMAP3 TG myocardium in comparison to WT (IS~53%±9.30, CA~47%±7.36), p<0.05, n=20- 22 (each group). Moreover, expression of the heart failure biomarker galectin3 was markedly ii attenuated (1.8±0.20) in SLMAP3 TG hearts post MI compared to (3.2±0.35) in WT, p<0.01, n=4-5 (in each group). The apoptotic index in SLMAP3 TG myocardium assessed by TUNEL was markedly decreased (77±11.48) in comparison to WT (112±15.32), p<0.05, (n=20-22 in each group). Further, expression of proapoptotic proteins (Caspase3 and Bax) was significantly attenuated in SLMAP3 TG (p<0.05, n=4-5 in each group) while the expression of the prosurvival proteins (Bcl2 and caveolin3) was significantly upregulated (p<0.05, n=4-5 (in each group) in post MI. These data indicate that increased SLMAP3 levels serve to protect myocardium post MI through mechanisms which promote cell survival and limit cardiac fibrosis. Strategies to increase SLMAP3 level in myocardium may provide new therapeutic options in the treatment of heart failure.

No description available.

Thesis (M.A.(Sielk)--University of Pretoria, 2001. / Includes bibliographical references (p. 279-306).

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 4 uppsatser.