Thesis (M.P.A.)--University of Hong Kong, 2001. / Includes bibliographical references. Also available in print.

Thesis (Ph. D.)--Texas Woman's University, 1990. / Includes bibliographical references (leaves 91-96).

Thesis (Ph. D.)--University of Hong Kong, 2010. / Includes bibliographical references (p. 312-325). Also available in print.

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / The dissertation explores relationships between social mobility and tribal identification, based on observations made among a sample of medical trainees at the University of Ibadan (formerly, the University College, Ibadan) in Western Nigeria. The thirteen-month study was carried out during 1962-63. Data were collected on 270 Southern Nigerians entering medical training in the years 1952-1960. Material was taken from university records, personal observations, unstructured interviews, and formal interviews with a sub-sample of 103 trainees drawn from among graduates or potential graduates in the years 1960-1965. Social background characteristics were compared with performance in training. Based on the ability to sit for and to pass all parts of the standard Second M. B. and Final M.B.-B.S. examinations and to graduate in the minimum five-year training period, representatives of large triues (Ibos, Yorubas) had a significantly higher pass rate than representatives of small tribes (Binis, Ijaws, Efiks, Ibibios, and several smaller groups). Corrections for caliber and location of secondary schools attended showed no variations in this pattern. Nor was it possible to account for these differential performances in terms of examination procedures, faculty bias, degree of exposure of various groups historically to foreign impact, or feelings of social isolation during training. [TRUNCATED] / 2031-01-01

<p>Loss of bone mass has long been recognized as a major factor which makes bones brittle and susceptible to fracture. Currently bone mass is measured using a dual energy photon transmission technique, and a fracture risk is derived from comparison with reference normal values. Although the risk of fracture increases as bone mass decreases, variations in trabecular bone architecture can also affect strength. Consequently, trabecular bone architecture is often cited as a factor which might contribute significantly to fracture risk. Currently, estimates of trabecular bone structure are derived from biopsy studies. Such studies are invasive, destructive, cannot be used routinely in patients ar volunteers, and certainly cannot be repeated at the same site to obtain longitudinal measurements. If routine clinical assessments of architecture are to be made, it is necessary to determine which imaging modality best reveals structure in a non-invasive manner. It is also necessary to determine how the competence of the structure can best be expressed quantitatively. This work has examined ways of assessing trabecular bone structure at the distal radius in-vivo to better understand the contribution of architecture to fracture risk. To this end, it proceeded on four major fronts. First, images of sufficient resolution were acquired using a commercial pQCT scanner and a clinical MR imager. Second, the image processing software necessary to segment the imaged trabecular structure was developed. Third, two indices were proposed to quantify the connectivity of the segmented structure. One index was derived from the application of trabecular strut analysis to a skeletonized representation of the bone network. The other quantified the marrow space by deriving a mean hole area and maximum hole area of the bone structure as it appears in two dimensions. The clinical value of these indices was tested by conducting pilot studies which examined the ability of the indices to discriminate a small group of Colles fracture patients from the normal population and to reflect normal age related changes in structure. The proposed structural parameters better discriminated Colles' fracture patients than did measures of bone mineral density. The fourth and last stage of this work examined the proportion of the variance in compressive strength of a group of radius bones that can be accounted for by bone mineral density and bone architecture. In seeking the features that were the most reliable indicators of bone strength, a combination of the mean hole area and maximum hole area had the highest correlation with peak load at fracture. This held true whether these two variables were derived from pQCT or MR images. Therefore, these structural indices may represent a potentially exciting and promising means of discriminating fracture outcomes and monitoring changes in trabecular bone structure.</p> / Thesis / Doctor of Philosophy (PhD)

<p>Regulation of the flux-generating enzyme complex pyruvate dehydrogenase (PDHc) was examined in the context of its physiological function in human skeletal muscle. In the first two studies, the role of PDHc in intramuscular fuel selection and the mechanisms regulating PDHc transformation from its inactive form (PDHb) to its active form (PDHa) and PDHa activity were examined. In a third study, the role of PDHc in muscle lactate production during exercise and recovery was assessed and the factors controlling transformation to PDHa were also examined.</p> <p>In the first study, 5 subjects were examined during rest and cycling exercise at 75% of VO₂max after 3 days of consuming a low-carbohydrate (LCD) or high-carbohydrate (RCD) diet In the second study, 8 subjects were examined at rest and during cycling exercise at 40% and 80% VO₂max while they were infused with sodium acetate (ACE) or sodium bicarbonate (BIC). At rest, consumption of a LCD and ACE infusion increased the intramuscular acetylCoA-to-CoASH ratio and citrate, as a result of increased oxidation of available fat fuels and acetate, respectively. Elevation of the acetylCoA-to-CoASH ratio and citrate inhibited PDHa and phosphofructokinase activity, respectively. Consequently, the rates of pyruvate oxidation by PDHa and pyruvate production by glycolysis were reduced preventing the oxidation of intramuscular glucose. The resting results of these two studies were consistent with the operation of a reciprocal cycle of glucose and fat oxidation for intramuscular energy production. The events leading to glucose restriction were initiated by changes in acetylCoA accumulation which caused an increase in the acetylCoA-to-CoASH ratio and citrate concentration which induced the transformation of PDHa to PDHb and inhibition of glycolytic flux, respectively.</p> <p>In contrast, during exercise at 40%, 75% and 80% VO₂max, transformation from PDHb to PDHa was determined by Ca²⁺ and was not restricted in any of the conditions except the LCD condition. Lower PDHa activity and incomplete transformation to PDHa occurred in this condition, placing a restriction on intramuscular glucose utilization. However, the acetylCoA-to-CoASH ratio actually decreased in this condition, suggesting that the lower rate of transformation was independent of alterations in the acetylCoA-to-CoASH ratio. In contrast, when transformation to PDHa was not limited in any other condition there was an increase in the acetylCoA-to-CoASH ratio which should have limited transformation. Thus, during exercise, the restriction on muscle glucose oxidation occurred only after a LCD indicating that this reciprocal cycle of fuel selection and utilization was also operating during exercise and that PDHc transformation was an integral part of its operation. However, during exercise, the regulatory factors controlling PDHa differed from those that determined the activity of this enzyme at rest. Lower PDHa during exercise in the LCD condition was consistent with an increase in the PDH-kinase/PDH-phosphatase activity ratio, in the 3 day period before exercise, increasing the occupancy of monophosphate esters on both the transformation site and the inhibitory sites of the Elα components. Incomplete removal of these additional phosphate esters by PDH-phosphatase during exercise may have then resulted in lower PDHa and glucose conservation later on during exercise.</p> <p>In a third study, the role of PDHa in muscle lactate production during exercise and recovery was examined and the factors controlling PDHc transformation were determined in 7 subjects. During repeated 30 second bouts of maximal isokinetic cycling exercise, complete transformation to PDHa occurred concurrently with muscle lactate accumulation and increased mitochondrial oxidation, indicating that lactate production was not dependent on the development of tissue hypoxia. Instead, during exercise muscle lactate production resulted from a rate of glycolytic pyruvate production that was greater than PDHa activity. Conversely, during recovery, net lactate oxidation occurred as the lactate dehydrogenase equilibrium shifted more toward pyruvate production and PDHa remained partially active due to attenuation of the acetylCoA-to-CoASH ratio, reductions in the ratios of NADH-to-NAD and ATP-to-ADP and elevated concentrations of hydrogen ion and pyruvate.</p> <p>The present studies extend the analysis of PDHc regulation from in vitro and in situ studies to human skeletal muscle in vivo. The findings of the present studies suggest that the during muscle contraction the most important factor regulating PDHc transformation in human muscle is probably Ca⁺, while the other regulatory factors perform secondary roles. In contrast, during rest and recovery from maximal exercise, PDHc transformation to PDHa and PDHa activity are determined by the intramuscular ratios of acetyICoA-to-CoASH, NADH-to-NAD, ATP-to-ADP and the concentrations of hydrogen ion and pyruvate.</p> / Doctor of Philosophy (PhD)

Thesis (D.Tech) - Central University of Technology, Free State, 2006 / Since 2002 all medical technologists and technicians have been obliged to participate in the compulsory continuing professional development (CPD) programme implemented by the Health Professions Council of South Africa (HPCSA). It was foreseen that CPD would not be equally accessible to medical technologists and technicians in urban and rural areas. The reason for this survey was to identify obstacles that might prevent medical technologists and technicians, especially those in rural areas from participating in CPD activities and to identify ways to overcome these obstacles. The survey was conducted in three phases. During the first phase quantitative information, concerning the profession of medical technology in South Africa, and CPD in general was obtained from registered medical technologists and technicians by means of a questionnaire. Information obtained from the questionnaire as well as that obtained from the literature led to the second phase in which an interview questionnaire was compiled. Structured interviews were conducted with medical technologists and technicians employed throughout South Africa, gathering mainly qualitative information regarding medical technology and CPD. Lack of time and financial constraints and to a lesser extent travelling were identified as the major obstacles to participating in CPD activities. The obstacles were an even bigger problem to those employed in rural areas. It was also confirmed that everybody involved in medical technology should be positively motivated to create and participate in CPD activities. A method suggested was to practise CPD activities during working hours which is cost effective but restricted, because of the workload. In addition medical technologists and technicians should participate in activities offered by the Society of Medical Laboratory Technologists of South Africa (SMLTSA) and attempt formal further qualifications. Being involved in research projects and identifying case studies could result in publishing in accredited journals. During the third phase of the survey a concept CPD framework was compiled. According to the framework all role players involved in the profession of medical technology must collaborate and contribute to making CPD activities accessible to all registered medical technologists and technicians and create a positive attitude to CPD. The role players include the HPCSA, employers and top management, the SMLTSA, medical companies, other health professionals, higher education institutions and the individual. It must be emphasised that the task of collecting CPD credits remains the responsibility of the medical technologist or medical technician. The framework offered suggestions for CPD activities whereby medical technologists and technicians could accumulate CPD credits. One major concern indicated in the framework, was that CPD should not only be measured by CPD credits but the outcomes of CPD should be reflected in the profession and the workplace and a system must be implemented to measure CPD outcomes. The CPD framework was evaluated by a panel of experts familiar with the profession of medical technology and the CPD programme, using the Delphi technique. This final CPD framework will be referred to the HPCSA for implementation in all South African pathology laboratories and the blood transfusion services. The aim of the framework is to assist the CPD guidelines currently under revision in establishing a usable CPD programme.

The major focus of this project was cloning and sequencing the α-1 sub-unit of Na+/K+-ATase gene in bovine corneal endothelium. The Na+/K+-ATase, also called the Na+ pump, is a crucial transmembrane protein. By transporting water and ions from and through the cornea into the aqueous humor, it is responsible for maintenance of structural integrity, corneal hydration and thereby transparency of the cornea. The Na+ pump is characterized by a complex molecular heterogeneity that results from differential association of multiple isoforms of both a (the catalytic) and [3 (glycoprotein) sub-units. In the corneal endothelium, α-1 α-2, β-l and β-2 sub-units are expressed. Pathological and mechanical causes can disrupt the endothelial morphology and deregulate the pump function leading to corneal swelling and opacity. Recent works have focused on the study of pump expression, and the influence of different factors on the upregulation of its expression. For example, hypersaline and hyperosmotic treatment significantly increases pump expression.

Hypertension is a disease characterized by increased activity of the Renin Angiotensin System (RAAS) and immune related vascular dysfunction. Angiotensin II (Ang II) is the final effector molecule of the RAAS and has numerous biologic activities that perpetuates vascular remodeling and inflammation. Ang II signaling of inflammatory cells may be due the presence of RAAS components on T lymphocytes. Many studies have shown the importance of pro-inflammatory T cell phenotypes, through cytokine analysis, in hypertensive models. However, the specific characterization of the RAAS on these phenotypes has yet to be determined. We sought to establish the expression of RAAS components on naïve T cell subsets and compare that to changes in expression that may be seen with AngII treatment and anti-CD3/28 stimulation. Here we find that AngII and anti-CD3/28 treatments significantly increase the expression of RAAS components on T cell populations.

Lysyl oxidase (LOX) is the enzyme that mediates cross-linking between collagen and elastin molecules during cardiac remodeling, LOX expression and activity is upregulated in response to the mechanical stresses that occur during hypertension. The aim of this study was to investigate the role of lysl oxidase (LOX) changes in cardiac structure and mechanical function during angiotensin II (AngII) induced hypertension. C57 male mice were given the LOX suicide substrate: β-aminoproprionitrile (BAPN) in their drinking water (300mg/kg/d). On day 14 of BAPN treatment an osmotic pump of AngII (490ng/kg/hr) was implanted. Weekly echo measurements were gathered. 28 days after pump implantation cardiac tissue was harvested for various assays including, LOX enzymatic activity, hydroxyproline quantification, and histological analysis. AngII treated groups showed an increase LOX protein expression, LOX activity, collagen cross-linking, and total collagen content while ECHO results showed an up-regulation aortic velocity time integral (AoVTI) and LV mass and down regulation of E/E-A VTI. When BAPN was co administered with AngII there was an attenuation seen in all these areas. While AngII+BAPN treated mice showed a return of these parameters to normal control levels. These results provide evidence that Angiotensin II-Induced hypertension causes the overexpression of LOX. LOX's overstimulation has a major influence in the cardiac structure and function. Conversely both the structural and mechanical changes can be extenuated with administration of the LOX suicide substrate BAPN.