The effect of protein-energy malnutrition on reactive gliosis following global ischemia
dc.contributor.advisor | Paterson, Phyllis G. | en_US |
dc.contributor.committeeMember | Nichol, Helen | en_US |
dc.contributor.committeeMember | Juurlink, Bernhard H. J. | en_US |
dc.contributor.committeeMember | Zello, Gordon A. | en_US |
dc.creator | Harmon, Monique Iona | en_US |
dc.date.accessioned | 2007-12-01T10:25:36Z | en_US |
dc.date.accessioned | 2013-01-04T05:09:31Z | |
dc.date.available | 2008-12-03T08:00:00Z | en_US |
dc.date.available | 2013-01-04T05:09:31Z | |
dc.date.created | 2007 | en_US |
dc.date.issued | 2007 | en_US |
dc.date.submitted | 2007 | en_US |
dc.description.abstract | Protein-energy malnutrition (PEM) has been found in up to 16.3% of acute stroke patients upon admission to hospital. Our laboratory has previously shown that PEM impairs functional outcome in a gerbil model of global ischemia, but the mechanism has not been established. The purpose of the current study was to characterize the marked reactive gliosis apparent in a subset of these animals that could represent an increased inflammatory response. A second objective was to validate a screening protocol for assessing completeness of ischemia in this model. Male Mongolian gerbils, aged 11-12 weeks, were randomized to PEM (2% protein) or control diet (12.5% protein) for 28d. PEM animals lost 12.2% of their initial body weight, and feed intake and serum albumin concentration were 12.3% and 17.8% lower than controls, respectively. At day 28, animals underwent 5 min bilateral common carotid artery occlusion (ischemia) or sham surgery. Activity was monitored using infrared beam interruptions for 20h post-surgery to screen for complete ischemia on the basis of persistent hyperactivity. Brain sections were stained with hematoxylin & eosin, and viable hippocampal CA1 neurons were counted at 10d post-ischemia. Immunohistochemistry for glial-fibrillary acidic protein (GFAP) and ricinus communis agglutinin -120 (RCA-120), markers for astrocytes and microglia, respectively, and the inflammatory cytokine TNF-alpha was performed on brain sections at 6h, 24h, 3d and 10d post-surgery (Ischemic, n=8; Sham, n=3). The activity monitoring procedure for detecting complete ischemia validated against hippocampal CA1 neuronal loss at 10d demonstrated an accuracy of 84.6%. Temporal changes in GFAP and RCA-120 immunoreactivity characteristic of reactive gliosis were demonstrated following ischemia, but this was not exacerbated by PEM. TNF-alpha immunoreactivity following ischemia was also unaltered by PEM. Ischemia significantly reduced surviving CA1 neurons at 10 days post-ischemia (two-way ANOVA; p | en_US |
dc.identifier.uri | http://hdl.handle.net/10388/etd-12012007-102536 | en_US |
dc.language.iso | en_US | en_US |
dc.subject | protein-energy malnutrion | en_US |
dc.subject | reactive gliosis | en_US |
dc.subject | gerbil | en_US |
dc.title | The effect of protein-energy malnutrition on reactive gliosis following global ischemia | en_US |
dc.type.genre | Thesis | en_US |
dc.type.material | text | en_US |
thesis.degree.department | Nutrition | en_US |
thesis.degree.discipline | Nutrition | en_US |
thesis.degree.grantor | University of Saskatchewan | en_US |
thesis.degree.level | Masters | en_US |
thesis.degree.name | Master of Science (M.Sc.) | en_US |