Diss. (sammanfattning) Stockholm : Karolinska institutet, 2009. / Härtill 4 uppsatser.

Thesis (Ph.D.) - Health Research Methodology -- McMaster University, 2002. / Bibliography: leaves 241-259. Also available via World Wide Web.

Diss. (sammanfattning) Stockholm : Karol. inst., 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 4 uppsatser.

<p>Please remove prior submission under the same title</p> / <p>Diabetes mellitus (DM) is associated with a significantly increased risk of microvascular complications, such as retinopathy, nephropathy, and neuropathy, as well as macrovascular disorders, including cerebro- and cardiovascular disease. Traditionally, the micro- and macro- vascular complications of DM have been considered distinct and independent disorders; however, data from several epidemiological and pathophysiological studies suggest they may be linked. It has been suggested that the <em>vasa vasorum</em>, a microvascular network which nourishes the walls of large muscular arteries, may play a role in macrovascular atherosclerosis. The effect of hyperglycemia on the microvessels of the vasa vasorum, and the potential impact of these effects on macrovascular atherosclerosis are not known.</p> <p>Here, we use a multiple-low-dose streptozotocin (STZ) injected apolipoprotein-E deficient mouse model to investigate the effects of hyperglycemia on the vasa vasorum, and to correlate such effects to atherosclerotic plaque progression. Hyperglycemia significantly increased plaque size and necrotic area (3- and 4-fold, respectively) relative to controls by 15 weeks of age. However, the density of vasa vasorum microvessels in the aortic wall of hyperglycemic mice was reduced at each time point examined. A similar vasa vasorum deficiency was also seen in STZ-induced hyperglycemic C57Bl/6J mice and hyperglycemic Ins2^Akita mice, and microvessel density could be corrected by insulin-mediated glucose normalization, suggesting a hyperglycema-specific effect. A localized deficiency in VEGF appears to be responsible for the reduced neovascularisation. Lastly, hyperglycemic mice fed standard chow supplemented with benfotiamine, a drug used to treat microvascular disorders in DM, appear to have reduced atherosclerosis.</p> <p>These findings provide the first indication that, in addition to retinal and glomerular capillary beds, hyperglycemia alters the microvessel structure of the vasa vasorum. Such microvascular changes directly correlate to the development and progression of atherosclerosis in hyperglycemic ApoE-deficient mice.</p> / Master of Science (MSc)

<p>Background</p> <p>Adults with cerebral palsy (CP) may have special health care considerations related to an increased prevalence of risk factors for chronic diseases. In particular, disability-related sedentary time may increase the risk of cardiovascular disease and the related major adverse cardiovascular events (MACE) in this population.</p> <p>Methods</p> <p>Part I: A systematic review of major databases, trial registries, and conference abstracts identified randomized trials and observational studies exploring the prevalence and evaluating the prevention of MACE and risk factors for MACE in adults with CP. Title and abstract, data extraction, and quality of reporting assessment were completed in duplicate.</p> <p>Part II: A secondary analysis of Canadian census data evaluated the crude and adjusted risk of stroke in adults with CP and compared the crude risk with other Canadian adults with spinal cord injury, acquired brain injury, and epilepsy. All risks were reported as an odds ratio (OR) with 95% confidence intervals.</p> <p>Results</p> <p>Part I: 2281 unique articles were screened to provide 10 cross-sectional studies. No studies evaluated any interventions for MACE or risk factors for MACE. The most common risk factor studied was obesity. Two studies showed an increased in death due to circulatory diseases.</p> <p>Part II: Crude risk of stroke to CP was OR=12.5 (12.2-12.9). Mediation effects or multicollinearity was not observed. The adjusted risk of stroke was OR=7.9 (1.8-34.2). Elevated crude risk of stroke was also noted in patients with acquired brain injury (OR=16.2 [16.0-16.5]), spinal cord injury (OR=6.1 [6.0-6.3]), and epilepsy (OR=6.2 [6.0-6.3]).</p> <p>Conclusions</p> <p>This thesis provides a preliminary overview of the risk of MACE in adults with CP and hypothesis generating evidence for further research in this population. A prospective cohort study is urgently needed assess the implications of these findings. Adults with CP should minimize exposure to modifiable risk factors as much as possible.</p> / Master of Science (MSc)