No description available.

Thesis (doctoral)--University of Turku, 1980. / Bibliography: p. 125-144.

Thesis (M. Phil.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.

No description available.

No description available.

Abstract Ischemic stroke is associated with cardiovascular autonomic nervous system (ANS) disturbances, including reduced heart rate (HR) variability and acute phase neurohumoral activation with elevated stress hormone levels. The impact of HR variability and neurohumoral factors such as natriuretic peptides on the long-term survival of patients with ischemic stroke has not been studied previously. This study was designed to evaluate cardiovascular autonomic regulation in ischemic stroke patients by assessing HR dynamics and various neurohumoral factors. The values of the assessed variables in predicting mortality were evaluated. HR variability assessments were performed in the acute phase of ischemic stroke and for a general elderly population. Various neurohumoral factors were also assessed in the acute phase of stroke. After follow-up, the survival of the subjects was assessed and the prognostic values of the measured factors were evaluated. Stroke patients were found to have cardiovascular autonomic and hormonal disturbances manifested as reduced traditional time and frequency domain measures of HR variability, altered long-term HR dynamics and elevated levels of natriuretic peptides in the acute phase. Altered long-term HR dynamics in the acute phase of stroke predicted long-term mortality after stroke and cerebrovascular mortality in the general elderly population. Neuroendocrine activation involving elevated natriuretic peptide values that were associated with high cortisol and catecholamine levels was observed in the acute phase of ischemic stroke. Neurohumoral disturbance was prognostically unfavourable. The most powerful predictors of poststroke mortality were altered long-term HR dynamics and elevated levels of natriuretic peptides and cortisol, which predicted mortality independently of the conventional risk factors in multivariate analysis. Prognostically unfavourable cardiovascular autonomic dysfunction with disturbances in the long-term behaviour of HR dynamics was found to be related to ischemic stroke. Neurohormonal activation with elevated natriuretic peptide and cortisol levels in the acute phase predicts long-term mortality after ischemic stroke.

published_or_final_version / abstract / Diagnostic Radiology / Master / Master of Philosophy

Purpose: In the United States, stroke is the leading cause of disability. The majority of survivors sustain permanent physical and/or cognitive impairments. Stroke survivors with impairments experience depression, loss of functional independence, and poor quality of life (QOL). Stroke disparities exist among different racial and ethnic groups of the US population. Latinos experience a first time stroke at a younger age compared to non-Latino Whites. As a result, Latinos live with impairments for a greater number of years. The vast majority of stroke survivors return to live in their communities. Reintegrating into home and social activities is key to survivors’ perceived QOL. This dissertation project sought to understand from an ecological framework the post-stroke community reintegration experiences of Latino older adults in an urban New York City neighborhood. The study also sought to examine the viewpoints of health and social service providers, whose opinions, actions, and programs can support stroke survivors’ reintegration into community. Methods: Qualitative in-depth interviews were conducted with 30 Latino stroke survivors 50 years of age and older who had experienced a disabling stroke within 36 months. In addition, 20 health and social service providers based in a large medical center, and multiple senior centers in the northern Manhattan section of New York City were interviewed. The stroke survivor data was analyzed using a phenomenological approach. A thematic analysis approach was used to analyze the data from the health and social service informants. Data analysis identified physical, psychological, social, and environmental factors pertinent to stroke survivors’ community integration experiences. These identified factors were categorized into macro-, exo-, meso-, and micro-levels to capture the psycho, social, and environmental ecology in which community reintegration takes place for Latino stroke survivors. Results: Qualitative accounts of survivors revealed several microsystem factors, including a struggle to maintain a positive self-concept and to engage in activities associated with valued identities and roles, while simultaneously suffering chronic pain, fatigue, and functional limitations. Changes in their affect lead survivors to socially isolate themselves. In addition, they relied more on women than men for social support, a salient mesosystem factor. Survivors encountered significant exosystem level barriers in the environment that limited their ability to travel and access activities. For some, these barriers inadvertently left survivors homebound. Survivors also encountered a societal culture, a macrosystem factor, which stigmatized them due to their impairments. Interviews with health and social service professionals revealed various factors that influenced community reintegration of people with stroke. At the macrosystem level, funding for programs and healthcare financing dictated services and eligibility criteria. In the exosystem, a segmented medical model of care postponed the conversation on community integration. Professional practices, organizational level constraints and culture were mesosystem level factors that influenced community reintegration. The confluence of these factors created an ecological system that influenced stroke survivors’ opportunities to socially engage in their home and community life. Conclusion: An ecological approach provides a useful framework to understand the complexity and potential interplay of factors that contribute to community integration post-stroke for Latino older adults in an urban area.

No description available.

<p>In a mouse model of ischemic stroke, infarct volume is highly variable and strain dependent, but the natural genetic determinants responsible for this difference remain unknown. To identify genetic determinants regulating ischemic neuronal damage and to dissect apart the role of individual genes and physiological mechanisms in infarction in mice, we performed forward genetic mapping analyses of surgically induced cerebral infarct volume. We have identified multiple quantitative trait loci (QTL) that modulate infarct volume, with a major locus (<italic>Civq1 </italic>) on chromosome 7 accounting for over 50% of the variation, with a combined LOD score of 21.7. Measurement of infarct volume in chromosome substitution strains (CSS) and two additional intercrosses validate that <italic>Civq1</italic> on chromosome 7 is present in multiple inbred strains. Interval-specific ancestral SNP haplotype analysis for <italic>Civq1</italic> results in 5 candidate genes. A causative gene underlying <italic>Civq1</italic> may regulate collateral artery formation and genetic variations in the gene may result in the differential outcome of cerebral infarction. Additionally, we have identified a locus of large effect, <italic>Civq4</italic>, modulating infarct volume through a mechanism different from collateral circulation. In conclusion, the extent of ischemic tissue damage after distal middle cerebral artery occlusion (MCAO) in inbred strains of mice is regulated by genetic variation mapping to at least 4 different loci. A single locus on chromosome 7 determines the majority of the observed variation in the trait in multiple mouse strains. <italic>Civq1</italic> appears to be identical to <italic>Lsq1</italic>, a locus conferring limb salvage and reperfusion in hindlimb ischemia. The identification of the genes underlying these loci may uncover novel genetic and physiological pathways that modulate cerebral infarction and provide new targets for therapeutic intervention in ischemic stroke, and possibly other human vascular occlusive diseases.</p> / Dissertation