Doctor of Philosophy / The aim of this research was to describe the epidemiology of musculoskeletal (MS) injuries in two- and three-year-old Thoroughbred racehorses. A 27 month longitudinal study commencing in May 2000 was conducted. The study convenience sampled 14 trainers with facilities at metropolitan and provincial racetracks in New South Wales, Australia. In the 2000/01 and 2001/02 racing season, 323 and 128 two-year-olds, respectively, were enrolled in the study. The 451 Thoroughbred horses contributed, 1, 272 preparations and 78, 154 training days to the study. Of the 323 horses enrolled in the 2000/01 racing season, 219 contributed three-year-old data to the study. During the study period 8%, of training days had missing training data and 3% of the 1, 986 starts in the races or barrier trials were incorrectly recorded. The rate of incorrect entries varied with both study month and trainer. Similarly, the rate of training days with missing data varied between trainers and with study month. Four hundred and twenty-eight MS injuries were recorded in association with 395 preparations in 248 two- and three-year-old Thoroughbred racehorses. The IR for all categories of MS injuries, except for tendon and ligament injuries, were higher in twoyear- olds than three-year-olds, although the differences were only significant for shin soreness. Seventy-eight percent of horses enrolled in the study started, in a barrier trial or race, within one year on entering the study. After accounting for other confounders, horses that had sustained a MS injury were 0.50 times less likely to start, in a race or trial, race than those that did not sustain an injury. Seventy percent of horses returned to training after their first MS injury, and the cumulative percentage of these horses that had recovered within six months of the initial MS injury was 55%. After adjusting for clustering at the level of the trainer, the analysis showed that horses that exercised at a gallop pace ≥ 890 m/minute (but had not started in a race) prior to the onset of MS injury, were 2.14 times more likely to recover than horses whose maximum speed, prior to the onset of the first MS injury, was less than 890 m/minute. Similarly, horses that had started in a race or barrier trial were 4.01 times more likely to recover than horses whose maximum speed was less than 890 m/minute. 8 Training days were grouped into units referred to as preparations. A preparation began on the day that the horse was enrolled in the study, or when a horse returned to training after an absence of more than seven days from the stable. The preparation continued until the horse was lost to follow-up or left the stable for a period of more than seven consecutive days. Univariable and multivariable analytical methods were used to examine the association between a range of independent variables and four preparationlevel measures of performance: (i) the duration of preparations, (ii) length of time from the beginning of the preparation until the first start in a race or barrier trial, (iii) length of time from the first start until the end of the preparation and (iv) rate of starts in races or barrier trials. After adjusting for confounders, younger horses tended to have shorter preparations, took longer to start in a race or barrier trial, had a shorter interval from the first start to the end of the preparation and fewer starts per 100 training days. MS injury was not conditionally associated with any of the outcomes considered in this chapter. Multivariate statistical models were used to explore risk factors for MS injuries. The results suggest that MS injuries involving structures in the lower forelimb (carpus to fetlock inclusive) could be reduced by limiting exposure to high-speed exercise. This supports the proposition that training injuries are caused by the accumulation of micro damage. The results suggest there are a number of other factors that vary at the trainer level that may be risk factors for injuries, in particular joint injuries. These include unmeasured variables such as the rate of increase in distance galloped at high-speed, conformation of the horse, skill of the riders and farrier and veterinary involvement.

Census estimates in 2010 indicated that 6,3 percent South Africans aged 5 years and older are currently classified as disabled in five of the nine provinces in the country. The national figure for 2005 was 5 percent, with the figure for females (6,5 percent) slightly higher than that for males (6,1percent). Spinal cord injured persons and their significant others experience a range of emotions which affect their relationships with themselves, others and their environment. To deal with the life-changing consequences of the injury and regain control, these persons not only require a variety of coping strategies but rediscovery of resilience is inevitable if the experience of personal purpose and meaningful existence is ever to be regained. In the Nelson Mandela Bay Municipal area, Port Elizabeth, South Africa – the geographical area in which this research study was undertaken - persons with spinal cord injuries have many challenges to face due to the shortcomings the existing resource for health care delivery in the post-discharge phase. The research objectives identified for the study were, firstly, to explore and describe the lived experiences of persons with spinal cord injuries; secondly, to explore and describe the lived experiences of the significant others of persons with spinal cord injuries; and thirdly, to develop a strategy to guide the professional nurse and the health care team in facilitating the health care of persons with spinal cord injuries. The study was a qualitative, exploratory, descriptive, and contextual method of inquiry. The data obtained was used to formulate the strategy with its three sub-strategies to guide professional nurses and the health care team to facilitate renewed resilience and the re-establishment of meaning for persons with spinal cord injuries. Although the experiences of the significant others were explored in order to thicken the description of the experiences of persons with spinal cord injuries, the strategy developed was limited to the persons with spinal cord injuries. Although it is well documented that there are significant physical needs, the themes that emerged from the current research mostly related to psychological and social aspects. In acknowledging the human being as unitary multi-dimensional being, the researcher in his discussions and quest to address the issue of renewed resilience in spinal cord injured persons towards finding purpose and re-establishing meaning in their lives, focused on their psychological, spiritual and social health. The outcome of the study is a strategy constructed to facilitate renewed resilience, and three sub-strategies ‘addressing experienced emotions’, ‘facilitating meaningful relationships’ and ‘facilitating effective coping’. The strategy has as purpose the empowering of spinal injured persons in their efforts to re-establish meaning by serving as a tool to guide professional nurses and members of the health care team in their facilitating of renewed resilience in persons with spinal cord injury. It is envisaged that the co-ordination of the strategy will take place from the health care delivery facility nearest to the spinal cord injured individual concerned. In order for persons with spinal cord injuries to become accountable members of society, all levels and aspects of care aimed at physical, psychological, spiritual and social well-being need to be holistically addressed. The front-line role of the professional nurse is vital as the professional nurse acts as the co-ordinator for the health care team in ensuring that persons with spinal cord injuries receive quality and holistic care in order to deal meaningfully with the life-altering consequences of a spinal cord injury. Through this study, valuable insight was gained with regard to experiences of both persons with spinal cord injuries and that of their significant others. Recommendations were made for nursing practice, nursing education and nursing research.

Electrical injury is known to alter the normal physiological function of nerves. In most cases, the change in function is only minor, but in severe instances the physiological function may be lost entirely. The changes in function involve the ability of the nerve to transmit an impulse, which is a function of the nerve's ability to create and maintain an electrical gradient across its membrane. When the nerve is exposed to an electrical current, the ability to maintain an electrical gradient across the membrane is reduced or lost. This change may be transient or permanent. The changes in the gradient hinder the nerve from propagating the impulse, which is the means of information transfer to and from the CNS (central nervous system). Due to the manner in which human victims are typically exposed to an electric shock, the peripheral axons usually display the greatest change in physiological function.

Pathologic processes and surgical manipulations of the spinal column may result in alterations of the biomechanical properties of the spine through increases or decreases in the range of motion or stability of the spine. A decrease in range of motion between two adjacent vertebrae subsequent to arthrodesis or ankylosis appears, clinically, to be well tolerated without significant alterations to the functions of the spine; however, a decrease in spinal column stability as a result of pathologic changes or surgical alterations can result in catastrophic spinal cord injury. In order to determine the effect of various surgical procedures and trauma on the spinal column, in vitro biomechanical studies may be employed using a servohydraulic testing apparatus and cadaver vertebral motion units. The T₁₃ - L₁ vertebral motion units of 48 mix breed dogs were dissected free of surrounding musculature and prepared for biomechanical testing by mounting with cross pins and polymethylmethacrylate. Specimens were surgically altered by facetectomy, lateral fenestration, diskectomy, and combinations of these procedures. Specimens were subjected to lateral bending at a rate of 2.5 cm per minute to failure in a swing arm bending jig designed to simulate four point bending. The slopes of bending moment vs. angular displacement curves were compared and significance determined by the method of least squares. A statistical difference (p < 0.05) was found between the stiffness of all diskectomy groups when compared to any other group. Unilateral and bilateral facetectomies, and fenestration induced a non-significant decrease in stiffness in comparison to control specimens. This data may be combined with that of previous testing of the canine thoracolumbar spine in flexion-extension and rotation to determine the clinical effects of surgical manipulations and trauma on spinal stability. These results suggest that fenestrations and facetectomies do not appear to increase the risk of injury to the canine thoracolumbar spinal cord during lateral bending in the in vitro model; however, thoracolumbar spinal fractures involving the vertebral body as represented by the diskectomy in vitro model may significantly destabilize the spine in lateral bending. / Master of Science

Digitized by Kansas Correctional Industries

Call number: LD2668 .T4 1952 S6 / Master of Science

The liver is a target tissue for Vitamin A toxicity. High doses of Vitamin A have been shown to produce hepatomegaly, portal hypertension, fatty liver, and hepatic degeneration and fibrosis. Of concern to us was the potential interactions of Vitamin A with other known or potential hepatotoxicants. Male SD rats (18o-200 gm) were given Vitamin A (retinol, 250,000 IU/Kg) daily for 7 days by oral gavage. 24 hr after the last dose of Vitamin A, they were then challenged with CCl₄ (0.15 ml/Kg, ip). Ethane, as a marker of lipid peroxidation, was measured during the first 2 hr and hepatic injury was assessed at 24 hr after CCl₄. There was approximately 5-fold increase in ethane exhalation and 17-fold increase in Plasma GPT activity in Vitamin A/CCl₄ group. There was also increase in the incidence of hepatocellular necrosis. Vitamin A pretreatment did not increase the metabolism of 14CCl₄ as examined by the amount of exhaled ¹⁴CO₂, and the covalent binding of ¹⁴C-equivalents to liver lipids and proteins. In addition, liver levels of Vitamin E or GSH were not changed by Vitamin A. Electron microscopic analysis of livers from Vitamin A treated rats revealed activated Kupffer cells. To determine if the Kupffer cells were functionally more active, the clearance of intravenously administered colloidal carbon from the blood of Vitamin A treated rats was compared to that of control rats. It was found that Vitamin A treated rats cleared carbon particles three times faster than that of controls. Therefore, we hypothesized that Vitamin A activation of Kupffer cells may be the mechanism of potentiation of liver injury. When stimulated, these activated cells could release active oxygen species which could promote peroxidation of hepatocyte membranes and potentiate CCl₄-induced liver injury. To test this hypothesis animals were treated with superoxide dismutase or catalase to catalyze the degradation of active oxygen species; or with methyl palmitate to deactivate Kupffer cells. Superoxide dismutase, catalase or methyl palmitate completely inhibited the Vitamin A potentiation of CCl₄ induced liver injury, but did not alter the toxicity of CCl₄ in non-Vitamin A treated rats. In addition, these agents inhibited the enhanced lipid peroxidation observed in Vitamin A treated rats administered CCl₄. Therefore, we conclude that the Vitamin A potentiation of CCl₄ induced liver injury results from Vitamin A's ability to activate Kupffer cells. Upon minimal hepatocellular injury produced by CCl₄, these activated Kupffer cells are stimulated to release activated oxygen species. It is these reactive intermediates that induce the enhanced lipid peroxidation that results in the potentiated response.

Cyclosporin A (CsA) was incubated at concentrations of 5.0 x 10⁻⁶ M for 72 hours, and at concentrations of 1.0 and 0.5 x 10⁻⁶ M for 30 days with kangaroo rat proximal tubular epithelial cells (PtK₂) in order to evaluate its effects on the cytoskeleton. Alterations in the cytoskeleton were assessed by indirect immunofluorescence of viable cells, and by two dimensional electrophoresis of a high salt extract from the cells. There is a selective alteration of the cytokeratin intermediate filament organization in both the short term (5 x 10⁻⁶ M, 72 hr) and long term (1 and 0.5 x 10⁻⁶ M, 30 days) exposures. There are either peri-nuclear rings formed or the formation of a single aggregate clump of the cytokeratins within the cytoplasm. Other components of the cytoskeleton, the microtubules and the microfilaments remain unaffected at both short term and long term exposures. Along with this cytokeratin alteration in CsA exposed cells is the decrease or elimination of an acidic triplet of cytokeratin protein monomers, human equivalent K15 (50 kd), K16 (48 kd), K17 (46 kd). This may be related to CsA-associated nephrotoxicity.

This work used <i>Pax6</i>^+/- mice as a model for Pax6-realted corneal diseases and assessed the roles of oxidative stress and epithelial injury in the aetiology of ARK. Histological investigation revealed epithelial lesions in <i>Pax</i>6^+/- corneas. Proteomic analysis demonstrated reduced levels of protective enzymes, transketolase, aldehyde dehydrogenase 3A1 and glutathione S-transferase α4, and cytoskeletal proteins. Keratin 5 and 12 in <i>Pax</i>6^+/- adult mouse corneas. These physical/structural and chemical defects imply that <i>Pax</i>6^+/- corneas may be in a chronic ‘stressed and wounded’ state. Using a DNPH/protein oxidation assay, <i>Pax</i>6^+/- corneal protein oxidation was found to be consistently higher than that in <i>wild-type</i> (WT), and to get worse with age, in parallel with the development of corneal opacity. H₂O₂ was used to induce oxidative stress in mouse corneas and this was found to activate the Ca²⁺ (protein kinase C/ phospholipase C) → p38/p42/p44 mitogen activated kinase signalling pathway. Oxidative stress-induced Pax6 exclusion form cell nucleus led to abnormal expression of non-corneal epithelial markers, indicating a metaplasia process that may cause normally transparent epithelial cells to become opaque. This report for the first time describes cytoskeleton architectures <i>in vivo</i> using flat-mount mouse corneal epithelial by fluorescent staining and confocal microscopy, which is potentially applicable to studies interested in cytoskeleton <i>in vivo</i>. Keratin, desmoplakin and actin cytoskeletal structures were found to be heterogeneous and defective in <i>Pax</i>6^+/- cells. Twenty-one hours after wounding WT corneal epithelia <i>in vivo</i>, healing cells developed desmoplakin and actin structural features, intercellular gaps, interdigitated filopodia-like processes and vesicles similar to the unscratched <i>Pax</i>6^+/- corneal epithelia. These data support the hypothesis of a ‘chronic wounded’ state in apparently uninjured <i>Pax</i>6^+/- corneal epithelia and reveal the cytoskeletal origins of poor adhesion and cellular structure.

This thesis examines the administrative separation process and attrition documentation as well as the characteristics of recruits who attrite from the U.S. Navy's Recruit Training Command (RTC). A random sample of 754 "retained files" from Customer Service Desk RTC was examined for attrition documentation and the information obtained was compared with attrition documentation contained in the Corporate Enterprise Training Activity Resource System (CETARS). The comparison is used to determine the accuracy of CETARS in documenting the reasons for medical and psychiatric attrition and its relationship to Separation Program Codes (SPD) listed on the DD 214 discharge form. The results indicate that CETARS is 95.2 percent accurate in documenting medical reasons for attrition and 94.2 percent accurate for psychiatric reasons. It was unclear whether a relationship existed between SPD codes and CETARS in documenting attrition. The specific reasons for psychiatric attrition include the following: Personality Disorder, Adjustment Disorder, Borderline Personality Disorder, and Attention Deficit Hyperactivity Disorder. In addition to the analysis of attrition documentation, we analyzed data on 216,028 recruits entering RTC between fiscal year 2000 and 2004 to determine the predictors of non-psychiatric attrites versus psychiatric attrites. Logit regression found that the predictors of both types of attrition were similar.