Predation accounts for the majority of ruffed grouse mortality beyond the brooding period throughout grouse range. Most studies of ruffed grouse ecology have taken place in the central portion of the species range including the Great Lakes states and southern Canada where aspen (Populus tremuloides) is dominant. Populations in the central range of grouse distribution exhibit 10-year cyclic patterns of decline that have been associated with the invasions of boreal predators such as great horned owls and northern goshawks during crashes in small mammal populations. I completed an accuracy assessment of field sign to determine the role of scavenging as it related to diagnosing causes of proximate mortality. Potentially large numbers of grouse are scavenged after death, which can alter or completely falsify the reported cause of death.. My results indicated that stand-level and micro-site habitat variables did not influence scavenger detection of ruffed grouse carcasses (P > 0.05). Scavenging was limited to 24 of 64 carcasses and was entirely attributed to mammalian species. Scavenging behavior was related to the condition of the carcass following death (P = 0.003) and the ambient temperature (P = 0.01). As the temperature increased and as a carcasses entrails and muscle became more exposed, the probability of being scavenged increased. Nineteen percent of whole carcasses placed in the field were scavenged and would have been attributed to mammal predation based on the field sign; 56% of 32 mock avian kills were scavenged would have been attributed to mammal predation. I related indices of predators and weather patterns to trends in ruffed grouse predation. Using data collected at 10 study sites between February, 1997 and December, 2000, I compared predation rates, and animal and weather indices to predation rates, across sites, years, regions, seasons and month combinations pooled across years. Avian predators were the primary predators of ruffed grouse in the Appalachian region (50% of all predation). Predation rates on ruffed grouse were highest in fall (8.3%), due to high predation on juveniles, and spring (7.4%) in association with raptor migration and pre-breeding activity of grouse. Predation patterns and predator abundance did not indicate the occurrence of predator invasions during the years of this study. Predation rates on ruffed grouse were positively related to the presence of rain and negatively related to the average low temperature and number of rabbits and squirrels observed per hour. Observations of owls and Cooper's hawks per hour were correlated with predation rates on grouse while those of red-tailed, red-shouldered and broad-winged hawks were not. / Master of Science

This thesis explores physiological changes occurring after acute brain injury. The first two chapters focus on traumatic brain injury (TBI), a significant cause of disability and death worldwide. I discuss the evidence behind current management of secondary brain injury with emphasis on partial brain oxygen tension (PbtO2) and intracranial pressure (ICP). The second chapter describes a subgroup analysis of the effect of hypothermia on ICP and PbtO2 in 17 patients enrolled to the Eurotherm3235 trial. There was a mean decrease in ICP of 4.1 mmHg (n=9, p < 0.02) and a mean decrease in PbtO2 (7.8 ± 3.1 mmHg (p < 0.05)) in the hypothermia group that was not present in controls. The findings support previous studies in demonstrating a decrease in ICP with hypothermia. Decreased PbtO2 could partially explain worse outcomes seen in the hypothermia group in the Eurotherm3235 trial. Further analysis of PbtO2 and ICP guided treatment is needed. The third chapter focuses on delayed cerebral ischaemia (DCI) after aneurysmal subarachnoid haemorrhage (aSAH), another form of acute brain injury that causes significant morbidity and mortality. I include a background of alpha-calcitonin gene-related peptide (αCGRP), a potential treatment of DCI, along with results from a systematic review and meta-analysis of nine experimental models investigating αCGRP. The meta-analysis demonstrates a 40.8 ± 8.2% increase in cerebral vessel diameter in those animals treated with αCGRP compared with controls (p < 0.0005, 95% CI 23.7 to 57.9). Neurobehavioural scores were reported in four publications and showed a Physiological responses to brain tissue hypoxia and blood flow after acute brain injury standardised mean difference of 1.31 in favour of αCGRP (CI -0.49 to 3.12). I conclude that αCGRP reduces cerebral vessel narrowing seen after SAH in animal studies but note that there is insufficient evidence to determine its effect on functional outcomes. A review of previous trials of αCGRP administration in humans is included, in addition to an original retrospective analysis of CSF concentrations of αCGRP in humans. Enzyme-linked immunosorbent assay of CSF (n = 22) was unable to detect αCGRP in any sample, which contrasts with previous studies and was likely secondary to study methodology. Finally, I summarise by discussing a protocol I designed for a dose-toxicity study involving the intraventricular administration of αCGRP to patients with aSAH and provide some recommendations for future research. This protocol was based upon the systematic review and was submitted to the Medical Research Council's DPFS funding stream during the PhD.