Figure skating is considered to be a physically and psychologically demanding sport. It has been estimated that 50% 78% of figure skating injuries could be prevented. It is suggested that off-ice training may reduce injury risk. The primary aim of this project was to identify incidence and occurrence of injury in female competitive and recreational solo figure skaters. The secondary aim was to identify the role of off-ice training and its association with injury and level of skating. The third aim was to investigate associations between injury, age and maturity.<p> Competitive (n=14) and STARSkate (n=17) Saskatchewan female solo figure skaters, age range 10-18 reported their injury and training data in retrospective questionnaires for a period of 9 months. The injury rate per 100 hours of training was 0.26 for competitive figure skaters (CFSs) and 0.44 for StarSkate figure skaters (SSFSs). The injured skaters were significantly older, more mature and heavier than non-injured figure skaters (p<0.05) and had been involved in figure skating for 8 or more years. There were 21 figure skating-related injuries (57% overuse and 43% acute) reported by SSFSs (8 overuse and 4 acute) and CFSs (4 overuse and 5 acute).<p> There were no significant associations between the number of overuse injuries sustained and the level of skating, (÷2 = 0.003, p>0.05) and no significant associations between the number of acute injuries sustained by the CFS and SSFS groups (÷2 = 0.053, p>0.05). There were no significant associations found between the number of injuries sustained by the CFS and SSFS groups that followed or did not follow Skate Canada Long-term Athlete Development Model off-ice training recommendations (15 minutes off-ice training for every on-ice hour) (÷2 = 2.801, p>0.05).<p> SSFSs sustained more overuse injuries (8) than CFSs (4) and participated in significantly less hours of off-ice training and spent less time stretching. The overuse injury rates for 100 hours of off-ice training were 1.75 for SSFSs and 0.41 for CFSs. These findings suggest that more off-ice training in CFSs could have possibly served as an overuse injury prevention component in the cohort of this study.

Brain injuries (BI) are the leading cause of death and disability among people under the age of 45 (Ontario Brain Injury Association, 2004). With improved survival rates, more individuals each year return to the community with impairments and disabilities caused by their injury (Smith, Magill–Evans, and Brintnell, 1998). Adjusting to these impairments may affect the individual’s subjective well being; therefore, attention to community reintegration by researchers, policy developers, and health care providers is important. Using qualitative research methods and systems theory as the theoretical framework, the purpose of the study was to examine community reintegration from the perspectives of three key groups: individuals with BI, community based agencies, and primary care physicians regarding the meaning attributed to “successful reintegration”, as well as the key characteristics and barriers experienced during reintegration. “Successful” reintegration appears to be an individually derived concept. Participants consistently identified the need for information about the process of community reintegration, and resources available both during rehabilitation and after discharge from the hospital as being both a key aspect of community reintegration, as well as a barrier experienced during the return to community. / October 2006

Spinal cord injuries can cause the catastrophic loss of motor and sensory function. The neurological deficits that result are the consequence of not only the primary injury to the spinal cord, but also a complex milieu of secondary pathological processes that are now beginning to be understood. The major mechanisms that underlie this secondary pathology include vascular disruption, ischemia, oxidative stress, excitotoxicity, and inflammation. In light of this, the fact that this secondary pathology occurs after the initial impact makes it potentially amenable to therapeutic intervention. Pharmacotherapies may attenuate some of these processes and minimize secondary damage. Some of the promising treatments that are emerging for acute spinal cord injury are drugs that are already used by physicians for the treatment of unrelated diseases. These drugs, which have already been established to be safe for humans, offer the unique advantage over other novel therapeutic interventions that have yet to be tested in humans. This would save a tremendous amount of time and money needed for human safety studies, if considered as a treatment for spinal cord injury. Examples of such drugs include minocycline (an antibiotic), erythropoietin (a recombinant hormone used to treat anemia), and statins (a popular class of blood cholesterol reducers), all of which have demonstrated the ability to attenuate the various pathophysiological processes initiated after trauma to the central nervous system. In a series of studies, erythropoietin, darbepoetin, atorvastatin, simvastatin, and minocycline were all evaluated for their ability to improve neurologic recovery in a clinically relevant model of spinal cord injury. My experiments revealed that erythropoietin, darbepoetin, atorvastatin and minocycline did not significantly improve neurological recovery. These negative results were in stark contrast to the positive findings which had been published in the literature suggesting that differences in experimental models and methodology influence the neuroprotective efficacy of these drugs. Simvastatin, on the other hand, demonstrated significant improvements in locomotor and histological outcomes. Although this is indeed exciting, the results were modest at best. My results highlight the need for further preclinical work on the above treatments to refine and optimize them prior to proposing them for human testing.

The anterior cruciate ligament (ACL) stabilizes the knee during various sporting activities and has great importance as the knee relies entirely on the ligaments and muscles for stabilization. The ACL commonly gets injured during sports activities such as basketball, soccer, and football. In the United States over 80,000 ACL injuries occur every year. There has been decades of research performed on ACL injuries regarding the injury mechanisms of non-contact ACL injuries, but yet they are still not well understood. This is mainly because trials and tests cannot be conducted on live subjects to understand the injury mechanisms. Existing in-vivo and in-vitro studies in the literature do not relate the effects of dynamic knee muscle forces and kinematics of sports activities with the strain in the ACL. In this thesis, in-vivo and in-vitro approaches are combined to quantify the effects of muscle group forces on ACL strain during jump landing. This is done by first obtaining muscle force profiles of the knee by performing motion capture and inputting the ground reaction forces and kinematics into a musculoskeletal model. Using the muscle forces and a six axis sagittal plane dynamic knee injury simulator the jump landing simulation can be performed. Six electromechanical actuators controlled by a multi-axis control system apply dynamic muscle forces at the insertion sites of the hamstrings, quadriceps, gastrocnemius, and a hip moment to simulate the hip flexors. The ACL strain is measured using a differential variable reluctance transducer mounted on the ACL. Our results show that the simulator is able to successfully perform jump landing. The muscle force-time profiles tracked the input very well. The ACL strain from our studies fell within a reasonable level compared to data from other studies of jump landing. This simulator has proven to be successful in simulating high-risk motions.

Figure skating is considered to be a physically and psychologically demanding sport. It has been estimated that 50% 78% of figure skating injuries could be prevented. It is suggested that off-ice training may reduce injury risk. The primary aim of this project was to identify incidence and occurrence of injury in female competitive and recreational solo figure skaters. The secondary aim was to identify the role of off-ice training and its association with injury and level of skating. The third aim was to investigate associations between injury, age and maturity.<p> Competitive (n=14) and STARSkate (n=17) Saskatchewan female solo figure skaters, age range 10-18 reported their injury and training data in retrospective questionnaires for a period of 9 months. The injury rate per 100 hours of training was 0.26 for competitive figure skaters (CFSs) and 0.44 for StarSkate figure skaters (SSFSs). The injured skaters were significantly older, more mature and heavier than non-injured figure skaters (p<0.05) and had been involved in figure skating for 8 or more years. There were 21 figure skating-related injuries (57% overuse and 43% acute) reported by SSFSs (8 overuse and 4 acute) and CFSs (4 overuse and 5 acute).<p> There were no significant associations between the number of overuse injuries sustained and the level of skating, (÷2 = 0.003, p>0.05) and no significant associations between the number of acute injuries sustained by the CFS and SSFS groups (÷2 = 0.053, p>0.05). There were no significant associations found between the number of injuries sustained by the CFS and SSFS groups that followed or did not follow Skate Canada Long-term Athlete Development Model off-ice training recommendations (15 minutes off-ice training for every on-ice hour) (÷2 = 2.801, p>0.05).<p> SSFSs sustained more overuse injuries (8) than CFSs (4) and participated in significantly less hours of off-ice training and spent less time stretching. The overuse injury rates for 100 hours of off-ice training were 1.75 for SSFSs and 0.41 for CFSs. These findings suggest that more off-ice training in CFSs could have possibly served as an overuse injury prevention component in the cohort of this study.

Research has shown that exposure to just 6 minutes of uncontrollable shock 24 hours following contusion injury impairs locomotor recovery and leads to greater tissue loss at the injury epicenter. Uncontrollable shock is known to elevate corticosterone levels in intact rats and corticosterone exacerbates cell death in the hippocampus following injury, suggesting the effects may be related to a stress-induced release of corticosterone. Uncontrollable shock also affects other indices of stress including, spleen weight and norepinephrine, and has been shown to elevate pro-inflammatory cytokines. The present experiments were designed to assess whether uncontrollable shock has similar effects after contusion injury. Experiment 1 examined whether injury itself produced a stress response. Subjects received anesthesia alone, a laminectomy, or a contusion injury. Twenty-four hours later, they were restrained for 6 minutes and blood was collected from the leg. They were sacrificed 24 hours later and spleens were weighed, and plasma corticosterone and norepinephrine were assessed using ELISAs. IL-1! and IL-6 levels at the injury site were also measured using an ELISA. Contusion injury had no impact on any of the biological outcomes. For Experiment 2, subjects received 6 minutes of uncontrollable tailshock or an equivalent amount of restraint. Subjects were sacrificed 6, 24, 72, or 168 hours later. Uncontrollable shock caused a decrease in spleen weight and increased plasma corticosterone within 24 hours. Increases in IL-1! and IL-6 were also seen. Morphine was used in Experiment 3 to block the “psychological” component of uncontrollable shock. Subjects received morphine (20 mg/kg; i.p.) or saline 30 minutes prior to uncontrollable shock and were sacrificed 24 hours later. Morphine did not prevent the consequences of uncontrollable shock and, in some cases, potentiated its effects. The effect of controllability was examined in Experiment 4. After receiving a contusion injury, subjects received either controllable (master) or uncontrollable (yoked) legshock over the course of 2 days. A third group served as unshocked controls. Master subjects did not differ from yoked subjects on any of the biological outcomes measured. Unshocked subjects, however, exhibited an increase in corticosterone, IL-6, and blood monocytes.

ABSTRACT Peripheral nerves are most commonly affected by pressure, traction, friction, anoxia or cutting and these injuries can easily cause allodynia of the limbs. Beta-endorphin is an endogenous pain inhibitor. It can produce profound and long-lasting analgesia for patients with intractable pain. Prominent endogenous opioid peptides are modulated by the hypothalamic-pituitary-adrenal axis. The expression of pro-opiomelanocortin (POMC) produces opioid peptides, including the beta-endorphins, other shorter endorphins, adrenocorticotropic hormones (ACTH), and melanocyte-stimulating hormones (MSH). The aim of this study is to evaluate the efficacy of POMC gene therapy for neuropathic pain that is caused by chronic constriction injury (CCI) in a rat model. Experimental painful peripheral neuropathy is induced by CCI of the sciatic nerve which results in allodynia of the hind limb. We used the method of conventional electrical stimulation to quantitatively analyze the efficacy of gene therapy. In addition, two nociceptive tests, including thermal-withdrawal latency and mechanical withdrawal threshold, were also conducted to evaluate the effect of treatment. Adult male Sprague Dawley rats (250-300 g, n = 24) were divided into three groups: (1) the control group (n = 8); (2) the sciatic nerve ligation group that received an injection of adenoviral vectors with green fluorescent protein (Ad-GFP) (n = 8); and (3) the sciatic nerve ligation group that received an injection of adenoviral vectors with POMC gene (Ad-POMC) (n = 8). The electrophysiological studies and nociceptive tests were carried out on day 3 before ligation and days 3, 7 and 14 after ligation. The POMC injection was performed on day 3 after ligation. We measured the amplitude and onset latency of maximal compound muscle action potential (CMAP) in braches of the sciatic nerve (nerves to the gastrocnemius, tibialis anterior), motor nerve conduction velocity, H-reflex and F-wave by electrical stimulation and denervation sign by electromyography (gastrocnemius, tibialis anterior). In addition, the latency of the thermal-withdrawal and threshold of mechanical withdrawal were also recorded. The results showed that prominent thermal-withdrawal latencies and mechanical withdrawal thresholds were elevated in the sciatic nerve ligation group with POMC gene therapy on days 14 and 21 after ligation. It also demonstrated that administrations of POMC gene therapy which produced the beta-endorphins to elevate the pain threshold and reduced the allodynia of the injured limbs. In conventional electrophysiological studies, no significant differences were noted between the Ad-GFP and Ad-POMC groups. The reduction of CMAP amplitude was recorded in rats of the sciatic nerve ligation groups. There was no significant difference in the mean onset latency of CMAP and nerve conduction velocity (NCV) within these three groups, except for the fact that the NCV of the tibial nerve was slowing in the Ad-GFP group on day 14. Electrophysiological analysis was revealed prolonged or absent H-reflex and F-wave in animals of the neuropathy groups by electrical stimulation. Electromyography showed prominent denervation potentials over the sampling muscles in the sciatic nerve ligation groups. In conclusion, POMC gene therapy for neuropathic pain is very efficacious. However, the influence of POMC gene therapy for nerve protection or minimizing the progress of nerve injury will require further investigations.

The objective of this study was to examine the relationship between two types of locus of control among a sample of Texas A&M varsity athletes and their frequency of selfreported injury in athletic competition and practice in a 12 month period. Using a webbased survey, 640 varsity athletes were asked to respond to a questionnaire which evaluated Locus of Control type using an adapted version of the Health Locus of Control Scale. Respondents were also asked to self-report their frequency of injury within the past 12 months. Locus of Control was not found to be a significant predictor of athletic injury.

Clomazone is an effective herbicide widely used for preemergence grass control in rice. However, use of clomazone on sandy textured soils of the western Texas rice belt may cause serious rice injury. When labeled for rice in 2001, sandy textured soils were excluded. Laboratory experiments were conducted to determine the effect of soil characteristics and water potential on plant-available clomazone and rice injury. A centrifugal double-tube technique was used to determine plant-available concentration in soil solution (ACSS), total amount available in soil solution (TASS), and Kd values for clomazone on four soils at four water potentials. A rice bioassay was conducted parallel to the plant-available study to correlate biological availability to ACSS, TASS, and Kd. TASS was significantly different in all soils at the 1% level of significance. The order of increasing TASS for the soils studied was Morey Edna Nada Crowley which correlated well with soil characteristics. Two field experiments at three locations were conducted in 2002 and 2003 to determine the optimum rate range that maximizes weed control and minimizes crop injury across a wide variety of soil textures and planting dates. At Beaumont, Eagle Lake, and Ganado, TX, preemergence application of 0.41 to 0.56, 0.38 to 0.43, and 0.36 to 0.42 kg ha-1 clomazone, respectively, provided optimum weed control with minimal rice injury. Data suggests that clomazone is safe to use on rice on sandy textured soils. Injury may occur, but, rates suggested from this research will minimize injury and achieve excellent weed control. As a result, amendments to the herbicide label will allow clomazone use on sandy textured soils giving rice producers more flexibility and access to another effective herbicide.

Coronary artery disease limits myocardial blood flow and results in myocardial infarction. Reperfusion therapies restore coronary flow, but may also cause myocardial ischemia reperfusion injury (MIRI). Multiple critical factors contribute to MIRI and among them, oxidative stress plays an important role. This burst of oxidative stress during reperfusion is caused by a variety of sources which collectively are called reactive oxygen species (ROS). Peroxynitrite is more cytotoxic than other ROSs, which at high concentration serves as a detrimental molecule with a variety of target. Peroxynitrite is largely produced during the early reperfusion due to the dramatically increased concentrations of superoxide (O2●-) and nitric oxide (NO). Current cardioprotective therapies against MIRI include exogenous antioxidant treatment and conditioning treatment that induced endogenous antioxidant signaling which upregulates heme oxygenase1 (HO-1), which confers its antioxidant effect in cells and tissues by degrading the latent oxidant heme and generating downstream antioxidant molecules. More importantly, peroxynitrite is closely related to HO-1 in pathogenesis of MIRI and pharmacological or genetic methods that induce over-expression of HO-1 in turn decrease the peroxynitrite generation. In this thesis we report the results of three studies designed to explore the interaction of peroxynitrite and HO-1 in cardioprotection against MIRI. In the first study we demonstrated that HO-1 plays an essential role in chronic antioxidant treatment against MIRI in 4-week diabetic rats. Chronic antioxidant treatment with two kinds of antioxidants that target different sources of ROSs was administrated in an in vivo study with streptozotocin (STZ)-induced type 1 diabetic rats. Antioxidant treatments synergistically attenuate MIRI and cardiac dysfunction in type 1 diabetic rats by enhancing HO-1 expression, and inhibition of HO-1 expression cancelled antioxidant cardioprotection. This finding was supported by in vitro experiments in a cardiomyocyte hypoxia-reoxygenation model. The second study explored the peroxynitrite/HO-1 interaction in propofol post-conditioning (PPC) in acute MIRI with both ex vivo and in vivo animal models. We showed that PPC conferred similar cardioprotection as an established intervention˗ischemic post-conditioning (I-PostC). PPC cardioprotection was achieved through down-regulating peroxynitrite formation and activation of HO-1 and its related signaling molecules. This finding indicates that anaesthetic post-conditioning treatment (such as PPC) can achieve similar cardioprotection as ischemic post-conditioning and can avoid potential mechanical injury that may be caused by I-PostC. Inhibition of peroxynitrite reduction and subsequent enhanced HO-1 expression may be the fundamental mechanism of PPC cardioprotection. Lastly, we further explored PPC cardioprotection against MIRI in diabetic rats. We found that the diabetic heart lost its sensitivity to PPC and the diminished effect of PPC in inducing HO-1 over-expression may be a key mechanism. Exogenous supplementation of adiponectin, an adipocyte-derived plasma protein with anti-diabetic and anti-inflammatory properties, restored diabetic heart sensitivity to PPC that is associated with restoration of HO-1 expression. This finding may provide a potential therapy rescuing diabetic patient challenged by myocardial infarction. The studies described in this thesis have enhanced our knowledge concerning the role of peroxynitrite in the pathogenesis of MIRI and the critical role of HO-1 in different cardioprotective therapies, in particular anaesthetic postconditioning cardioprotection. / published_or_final_version / Anaesthesiology / Doctoral / Doctor of Philosophy