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TAILORING EXERCISE FOR ADVANCED PANCREATIC CANCER CARE: UNDERSTANDING AND INTEGRATING THE PATIENT PERSPECTIVE
(2025-07-02) Cyr, Chloe; No; Master of Science; School of Health & Human Performance; Received; Robin Urquhart; Yes; Ravi Ramjeesingh; Chris Blanchard; Melanie Keats
Pancreatic cancer is associated with poor prognosis and high symptom burden. Although exercise is well-known to improve quality of life and mitigate adverse outcomes in cancer care, exercise programming in advanced pancreatic cancer care remains limited. This thesis used a pragmatic qualitative interpretive description approach to explore the exercise experiences and perspectives of individuals living with advanced pancreatic cancer in Canada. Six individuals diagnosed with stage III/IV exocrine pancreatic cancer from across Canada were interviewed and a reflexive thematic analysis was conducted. Three themes were identified impacting how exercise was perceived and experienced: (1) Taking control of my journey; (2) Building the motivation; and (3) A program for me. Connections to the Behaviour Change Wheel and Theoretical Domains Framework were identified and explored within each theme. Findings from this study will be integrated within an exploratory sequential mixed methods project to co-create and implement a tailored exercise program for advanced pancreatic cancer care in Canada.
The Impact of Frailty on Fitness Gains from an Exercise Oncology Program
(2025-07-02) Pedrick, Denelle; No; Master of Science; School of Health & Human Performance; Not Applicable; Dr. Myles O'Brien; Not Applicable; Dr. Melanie Keats; Dr. Stefan Heinze; Dr. Scott Grandy
This study examined the impact of frailty on fitness gains among individuals living with and beyond cancer who participated in a 12-week multimodal exercise oncology program (ACCESS). Using secondary data from a sample with a mean age of 59.8 years (SD= 11.6), participants were classified as frail or non-frail based on Frailty Index scores derived from the Pictorial Fit-Frail Scale. Physical fitness outcomes—including walking distance, muscular endurance, grip strength, and balance—were assessed pre- and post-intervention. Participants were also stratified by age (<65 vs. ≥65) to explore age-related effects. Correlational analyses and repeated measures ANOVA were conducted. Findings revealed that frailty was weakly associated with reduced improvements in aerobic and muscular endurance, particularly among older adults. However, frail individuals still demonstrated meaningful gains, and frailty did not significantly limit improvements over time. These results suggest that structured exercise programs can benefit frail individuals living with and beyond cancer, reinforcing the value of inclusive exercise interventions and the need for tailored approaches in oncological rehabilitation.
HYPOXIA MEDIATES N-METHYL-D-ASPARTATE SIGNALING RELATED SUSCEPTIBILITY TO TRAUMATIC BRAIN INJURY
(2025-07-02) Muradov, Jamil; Not Applicable; Doctor of Philosophy; Department of Medical Neuroscience; Received; Jamie Hutchison; Yes; Lutz Weise; William Baldridge; Alon Friedman
Cortical spreading depolarizations (CSDs) are an early hallmark of traumatic brain injury
(TBI) and are associated with poor clinical outcomes, yet their underlying mechanisms
remain poorly understood. We hypothesized that post-traumatic hypoxia promotes CSDs
and impairs neurovascular responses. This study examined how hypoxia and CSDs affect
neurobehavioral outcomes post-TBI and evaluated the effects of NMDAR antagonists as
potential therapeutics.
Using an animal model of single moderate TBI (N=67), we assessed its outcome
variability (Chapter 2). TBI impaired neurological scores at 48 h post-impact (p<0.0001)
and disrupted the neurovascular response to CSDs. Behavioral scores showed a bimodal
distribution (R²=0.88; trough=7.01), categorizing animals into “susceptible” and
“resilient” groups. Susceptible animals exhibited early cardiorespiratory dysfunction
(lower HR and SpO₂ at hind paw and neck; p=0.02, p<0.001, p=0.01) and a significantly
reduced neurovascular response to triggered CSDs, along with prolonged post-CSD
oligemia.
To explore the relationship between hypoxia and CSDs (Chapter 3), I used epidural
electrodes and cranial window surgery. Animals that developed CSDs had lower mean
SpO₂ (83.6%) compared to those that did not (92.2%). The co-occurrence of CSDs and
hypoxia significantly altered the neurovascular response, with a 16% reduction in
cerebral blood flow during the expected hyperemic phase, suggesting potential
hypoperfusion and ischemia.
In Chapter 4, I studied CSD-induced vascular responses in resilient vs. susceptible
animals under hypoxia or following NMDAR antagonist treatment. Memantine reduced
CSD incidence by 42–73% and mitigated cortical hypoperfusion. In a randomized pre-
clinical trial, memantine treatment improved behavioral outcomes and preserved
neurovascular function.
This multi-modal investigation identified post-impact hypoxia as a key driver of CSDs
and demonstrated that hypoxia and CSDs synergistically impair neurovascular regulation.
Targeting these processes through oxygen support and NMDAR antagonism prevented
secondary injury and improved outcomes. These findings may inform mechanism-based
strategies for mitigating TBI susceptibility across injury severities.
Health Rays, Vol. 43, No. 5, June 1962
(Nova Scotia Sanatorium, Kentville, N.S., 1962) Nova Scotia Sanatorium
Health Rays, Vol. 43, No. 6, July 1962
(Nova Scotia Sanatorium, Kentville, N.S., 1962) Nova Scotia Sanatorium
Health Rays, Vol. 43, No. 7, August 1962
(Nova Scotia Sanatorium, Kentville, N.S., 1962) Nova Scotia Sanatorium