Ergonomics aims to improve worker health and enhance productivity and quality. Knowledge and practical evidence of this relationship would be instrumental for optimising organisational performance particularly in industrially developing countries where the discipline is still in its developmental stages. Therefore this thesis set out to analyse the relationship between ergonomics deficiencies and performance. A survey was first conducted to establish the severity of quality problems in the South African manufacturing industry and to determine if these were related to Ergonomic deficiencies. The results indicated that quality problems continue to plague industry, a challenge associated with huge cost implications. Furthermore organisations were not cognisant of the fact that ergonomics deficiencies such as poor workstation design and awkward or constrained working postures are a major contributing factor to poor quality and performance decrements. This demonstrates that much is yet to be done in raising awareness about the benefits of ergonomics in South Africa and other industrially developing countries. However, for this to be effective, tangible evidence of these purported benefits is required. In lieu of this, a laboratory study was then conducted to establish the relationship between awkward working postures and the performance of precision tasks. Acknowledging that the task and the worker are interrelated elements, the impact of precision task demands on the postural strain experienced by the human was also investigated. A high and low precision task quantified positional precision while a force task (combination of pushing and pulling) was utilised to assess the ability to maintain a precise force over time. These three tasks were performed in eight different postures; namely seated, standing, stooping 300 and 600, working overhead, lying supine, and twisting to either side. A combination of the tasks and postures resulted in 24 experimental conditions that were tested on forty eight healthy male and female participants. The performance related dependent variables were movement time, deviation from the centre of the target, and the trend/slope followed by the force exerted. Muscle activity of eight arm, shoulder and back muscles, iii supplemented with heart rate and local ratings of perceived exertion, were utilised to quantify the impact of the tasks and the postures on the individual. The results revealed that awkward working postures do in fact influence performance outcomes. In this regard, awkward working postures (such as overhead work and lying supine and stooping) were evidenced to significantly affect movement time, deviations from the target and the ability to maintain a constant force over time. These variables have a direct relationship with organisational priorities such as productivity and quality. Furthermore, the results indicated that high precision demands augment postural strain elicited through high muscle activity responses and may have negative implications for the precipitation of musculoskeletal disorders. Essentially, the work done on this thesis reflected the complex nature of ergonomics by drawing on both macro and micro-ergonomics approaches. In so doing, challenges perceived to be relevant to industry as reported by organisations formed the foundation for further laboratory studies. Therefore, more collaborative research and knowledge transfer between industry and ergonomics researchers is a necessity particularly in industrially developing countries where ergonomics is still in its developmental stages.

As soon as the building of the body is completed, the ageing process begins. In the natural course of events, the functioning of some organ systems finally ebbs below the threshold necessary to maintain the body, resulting in death. This occurrence is relatively rare, because diseases superimpose themselves upon the ageing process, bringing premature death resulting from pathological causes. This study focused on the cholinergic system of the rat forebrain. The cholinergic neurons in the brain are said to be involved in memory and learning, and a decrease in the activity of its enzymes has been reported in certain diseases, such as Alzheimer's disease. In the present study, the in vitro effects on the cholinergic system, of aluminium and mercury and tryptophan metabolites, kynurenic acid and quinolinic acid, are determined. Aluminium has been considered as a possible factor in Alzheimer's disease. Mercury in high concentrations is toxic, and its use in amalgam for dental treatment is under consideration with regard to its possible role in promoting neurological disease. The tryptophan metabolites increase in the brain with age and may have a role in pathological diseases. Quinolinic acid, when administered in toxic concentrations produces a possible model for Huntington's disease. This study investigated the effects of the above mentioned toxins on: (1) The synthesis of acetylcholine by choline acetyltransferase; (2) The specific binding of acetylcholine muscarinic receptors; (3) The degradation of acetylcholine by acetyl cholinesterase, Choline acetyltransferase activity did not change in the presence of aluminium chloride, kynurenic acid and quinolinic acid from 1 nM to 1 mM. Mercuric chloride had no significant effect on the enzymes activity from a concentration of 1 nM- 1 pM. At 10 pM there was a significant decrease in cholineacetyltransferase activity (P < 0.001). Enzyme activity continued to decrease at 100 pM (P < 0.0002). At 1 mM, enzyme activity was virtually non existent (P < 0.0001). Acetyl cholinesterase activity was not affected by aluminium chloride, kynurenic acid and quinolinic acid. Mercuric chloride from 1 pM - 1 mM significantly reduced the enzyme activity (P < 0.05). The binding of the antagonist, [³H] quinuclidinyl benzilate (QNB), to acetylcholine muscarinic receptors, revealed that aluminium chloride did not affect the binding of the antagonist, in the concentration range of 1 nM - 100 pM, to the receptors. At 1 mM, aluminium chloride appears to increase the sensitivity of the receptors for the ligand (P < 0.01). Mercuric chloride also does not appear to have any significant effect on receptor binding in this range. However, at 1 mM there appears to be a very significant decrease in receptor binding (P < 0.01). This decrease may be attributed to the interaction of mercury with the sulfhydryl groups in muscarinic receptors. Kynurenic acid had no effect on the receptor binding. Quinolinic acid, in the concentration range from 10 nM - 1 mM increased the binding ofthe receptor to [3Hi QNB significantly (P < 0.001). The study also investigated the effect of the tryptophan metabolites of the kynurenine pathway on pineal indole metabolism. The kynurenine pathway is a major route of tryptophan metabolism in the pineal gland, along with indole metabolism. Investigations showed that kynurenic acid produced a decrease in N-acetylserotonin concentrations ( P < 0.001) and melatonin concentrations (P < 0.003). Further experiments using quinolinic acid produced a similar decrease in N-acetylserotonin (P < 0.001) and melatonin (P < 0.015). A decrease was also noted in the level of 5-methoxytryptophol (P < 0.0005). These findings suggest that aluminium chloride, kynurenic acid and quinolinic acid have no possible role in the decrease of activity of cholinergic enzymes which is observered in diseases such as Alzheimer's disease. The results regarding the effect of mercury chloride on the cholinergic system suggest that low exposure to the toxin will not adversely effect the enzymes. The decrease in N-acetylserotonin and melatonin concentrations reported here, may be a result of kynurenic acid and quinolinic acid having an inhibitory effect on the enzyme, serotonin Nacetyltransferase, which is responsible for the conversion of serotonin to N-acety/serotonin.

Please read the abstract in the section 00front of this document / Dissertation (MA (HMS))--University of Pretoria, 2007. / Biokinetics, Sport and Leisure Sciences / unrestricted

The location of the available research literature and its relationship to the pedagogy of the female high voice is the subject of this thesis. The nature and pedagogy of the female high voice are described in the first four chapters. The next two chapters discuss maintenance of the voice in conventional and experimental repertoire. Chapter seven is a summary of all the pedagogy. The last chapter is a comparison of the nature and the pedagogy of the female high voice with recommended areas for further research. For instance, more information is needed to understand the acoustic factors of vibrato, singer's formant, and high energy levels in the female high voice.

The rising costs of prescription drugs in the maintenance of personal health and wellbeing have increased the interest in medicinal plants. The World Health Organization estimates that 65 percent-80 percent of the world’s population use traditional medicine as their primary form of health care. In this project the focus has been on the use of Leonotis leonurus extracts as a traditional medicine. The major chemical constituent of this plant is marrubiin, which is a diterpenoid labdane lactone formed from a precursor called premarrubiin. Aqueous and acetone extract (AL and OL extract, respectively) of this plant has been found to have an antithrombotic effect, with IC50 values of 3mg/ml and 6mg/ml, respectively. The extracts also have an effect on fibrinolysis, where the lysis time was decreased by more than 50 percent by the organic extract and standard marrubiin. In whole blood ADP-induced platelet aggregation, the organic extract inhibited aggregation by 68 percent at a final concentration of 138μg/ml (equivalent to 7.2μg/ml marrubiin). Marrubiin has also been screened for antithrombotic/anticoagulant activity; no antithrombotic activity has been observed but it increased the rate of fibrinolysis, by decreasing lysis time by 64 percent and also decreasing fibrin formation. From these findings it can be concluded that marrubiin has a fibrinolytic effect and antiplatelet aggregation effect. In the diabetic studies, in hyperglycemic condition, the OL (10μg/ml) extract and standard marrubiin significantly increased insulin secretion by 200 percent (2-fold) and 400 percent (4-fold), respectively, with respect to the control. The OL extract and standard marrubiin stimulated the release of insulin, the stimulatory index was significantly increased by 450 percent (4.5-fold) and 500 percent (5-fold), respectively, with respect to the control. In the apoptotic studies, in the normoglycemic and hyperglycemic conditions, the OL extract decreased the occurrence of apoptosis, in a dose-dependent manner, with the lower concentrations inducing apoptosis significantly higher than the relevant controls. Standard marrubiin did not have an effect on apoptosis in hyperglycemic condition, but it decreased the occurrence of apoptosis by 200 percent (2-fold) under normoglycemic conditions. The OL extract increased proliferation by 148 percent (1.48- fold) and 155 percent (1.55-fold) in normoglycemic and hyperglycemic conditions, respectively. The same effect was observed for standard marrubiin, where, proliferation was increased by 180 percent (1.8-fold) and 200 percent (2.0-fold) in normoglycemic and hyperglycemic conditions, respectively. RT-PCR displayed that standard marrubiin inhibited the expression of insulin by 50 percent under normoglycemic conditions.

The purposes of this study were to quantify, in three dimensions (3D), kinematic parameters of the free throw shot with both the women's small ball and the large ball, and to compare the parameters of the small ball to the large ball. Nine female varsity college basketball players were filmed and the 3D data were computed with the Nonlinear Transformation method. Statistical analysis of parameters including ball trajectory and body position failed to show an effect for ball condition. Since the velocity of release was not statistically different between the two balls and the ball mass was different, the results suggest that impulse is the differing factor.

Force dived animals undergo cardiovascular changes characterized by bradycardia, increased total peripheral resistance, and changes in blood flow distribution. Since these changes occur in decerebrated animals, the dive response must be a brainstem reflex. However, in voluntary dives, animals may show anticipatory bradycardia and may also adjust their cardiovascular responses according to anticipated dive duration, indicating suprabulbar influences upon dive responses. Studies of heart rate using telemetry have shown that there can be substantial differences in the dive response of voluntarily and force dived animals. Furthermore, some animals show a "fear bradycardia" when trapped in a stressful situation, leading some researchers to suggest that bradycardia during forced submersion is an artifact of the stress of the situation. Muskrats (Ondatra zibethica) were observed freely diving for food in an indoor tank using a video camera and VCR unit. EKG was telemetered from the animals and recorded on the audio channel of the VCR tape. Heart rate responses to voluntary dives were analyzed and compared with those from escape and forced dives. Heart rate responses were also recorded from decorticate and sham operated muskrats to elucidate the role that the cerebral cortex plays in the dive response. In all types of dives, muskrats exhibited a rapid and large bradycardia upon submergence (heart rate declined by greater than 55% of the predive heart rate). Obviously diving bradycardia in the muskrat was not due to fear or stress, but occurred as a response to submersion per se. There was no evidence of post-dive tachycardia or anticipatory immersion bradycardia. Disturbing the animal in a non-diving situation resulted in only a 13% decrease in heart rate. In intact animals voluntary, escape, and forced submergence resulted in progressively greater decreases in heart rate. Heart rate fell by 56% in voluntary dives, 65% in escape dives, and 73% in forced dives. Intensification of the bradycardia to a lower heart rate than that seen in voluntary dives was mediated by the cerebral cortex, as heart rate in decorticate muskrats in escape and forced dives did not fall below that seen in voluntary dives. This indicates that the final adjustment of dive heart rate is dependent upon an intact cerebral cortex. However, in decorticate muskrats there appeared to be a recovery of cortical function, as intensification of bradycardia in forced dives was dependent upon the time that had elapsed after surgery. This study shows that there is a cortical influence upon the cardiovascular system during diving. It also indicates that in experiments with unanesthetized animals, the degree of stress of the situation must be taken into account, as this may affect physiological responses. / Science, Faculty of / Zoology, Department of / Graduate

Blood flow distribution during forced and voluntary diving in ducks, and the energetic cost of diving was investigated. It has been suggested that in order for the leg muscles to generate enough power for ducks to dive, blood flow to those tissues must be maintained. A technique to determine blood flow distribution which could be used during voluntary diving was first developed and tested during forced laboratory dives of ducks. This technique was then used to determine the blood flow distribution during voluntary diving. Regional blood flow distribution was visualized by utilizing a radioactive tracer technique (macro aggregated albumin labelled with ⁹⁹ⅿ technetium). The tracer when injected into an animal is trapped and held by capillaries. During forced dives in dabbling (Anas platyrhynchos) and diving (Aythya affinis) ducks the blood flow distribution was found to be restricted to the thoracic and head areas. Whereas during a voluntary dive in A. affinis blood flow distribution was shown to be preferentially directed towards three tissue areas, the heart, brain, and active leg muscles. The work required to dive was determined from the measurement of subsurface drag forces and buoyancy in A. affinis. Subsurface drag increased as a nonlinear function of swimming velocity. At a velocity of 1 m•s⁻¹, the drag force was approximately 1.067 N. The average measured buoyant force of 11 ducks was 0.953 N. The calculated mechanical work done by ducks during a 14.4 s unrestrained dive was 9.34 J. The power output during voluntary was estimated to be 0.751 W (0.0374 ml 0₂•s⁻¹). During diving buoyancy is clearly the dominant force (8.8 J) against which ducks have to work while drag (0.54 J) adds little (~6%) to the energetic cost of diving. / Science, Faculty of / Zoology, Department of / Graduate

When dabbling ducks are involuntarily submerged, arterial vasoconstriction produces a large increase in the peripheral resistance to blood flow which is balanced by a decrease in output of the heart, and arterial blood pressure is maintained. Arterial baroreceptors sense systemic blood pressure, and provide the afferent information to the baroreflex for pressure regulation. The effector limbs of the baroreflex are the same as those involved in the diving responses, and the baroreceptors are likely to be important in the integration of the cardiovascular responses to diving. The purpose of this study was to investigate the role of the arterial baroreceptors in maintaining blood pressure during diving, and in the initiation and maintenance of the diving responses. Baroreceptor function was studied by diving ducks at various times after barodenervation, and by electrically stimulating the central end of one baroreceptor nerve in baroreceptor-denervated animals to simulate a controlled baroreceptor input before and during submersion. Intact baroreceptor innervation was not necessary for the development of peripheral vasoconstriction, but loss of the baroreceptors modified the cardiac response to submersion by impairing the vagally mediated bradycardia. There was no effect of baroreceptor nerve stimulation on peripheral resistance during diving, and the baroreflex operated via the heart rate in modulating blood pressure early in the dive. Later in the dive, stimulation was ineffective in altering either heart rate or blood pressue. Strong chemoreceptor drive results from decreased blood oxygen and increased carbon dioxide levels in the dive, and the results of experiments to determine the mechanism of baroreflex attenuation showed that an interaction between chemoreceptor and baroreceptor inputs may be at least partly responsible for reducing baroreflex effectiveness. The main conclusion from this work is that the arterial baroreceptors contribute to the diving responses through modulation of heart rate, to help balance the fall in cardiac output against the baroreceptor-independent peripheral vasoconstriction in the first minute of forced dives. / Science, Faculty of / Zoology, Department of / Graduate

This purpose of this study was to evaluate the contribution of post-dive peripheral tissue warming to the production of venous gas emboli (VGE) in divers. Inert gas elimination from the tissues is limited by both perfusion and diffusion. If changes in diffusion are matched by corresponding perfusion (vasoactive) changes, decompression should be asymptomatic (within allowable exposure limits). Under conditions when the diffusion of inert gas from the tissues is not matched by blood perfusion, VGE will ensue. Increasing tissue temperature will decrease inert gas solubility and thus diffusion into the blood. It has been demonstrated that problems may arise during rapid changes in peripheral temperature, as often occurs post-dive, when divers previously exposed to cold water actively rewarm themselves in showers or baths. The effect of moderate rewarming, however, may be to increase the rate of inert gas elimination without the formation of VGE since increased perfusion is encouraged. The effect of mild post-dive warming was investigated. Ten male subjects, between the ages of 21 and 29 years completed two dry chamber dives to 70 feet for 35 minutes (no decompression limit of the Canadian Forces Air Diving tables). Each dive was followed by a 30 minute head-out immersion in either a thermoneutral (28°C) or warm (38°C) bath. Non-invasive Doppler ultrasonic monitoring was then carried out at 30 minute intervals for the next 150 minutes to assess measurable VGE. Subjects did not display VGE formation in either the control or experimental conditions. Our findings suggest that: 1) the Canadian Forces table limits (for the profile employed) provide safe no-decompression limits not compromised by mild post-dive warming, and 2) mild peripheral warming, since not bubble generating, may be a useful adjunctive therapy in the management of decompression sickness by increasing the rate of inert gas elimination. / Education, Faculty of / Curriculum and Pedagogy (EDCP), Department of / Graduate