This study is an historical analysis of the education for students with mild intellectual disabilities in Saskatchewan from 1900-2002. The thesis analyzed the beginnings of thought on the construct of intelligence, its hereditarian orientation, and the IQ test that originated in 1904 to measure individual differences in intelligence. The use of the IQ test was traced as it progressed through the eugenics movement that dominated from approximately 1900-1940, as well as the mental hygiene movement that was present during roughly the same time period. The importance of the concept of intelligence and the IQ test was analyzed for how it affected the identification of individuals with an intellectual disability, and how the identification process affected their treatment and education. The classification and educational placement of students identified with an intellectual disability had parallel affects on the curriculum for these students. The changes in attitudes from eugenics and institutionalization of those identified with an intellectual disability and their subsequent deinstitutionalization, beginning in the 1960s, are examined for the effects these attitudinal shifts had on the education for these individuals. Education developed a system of special education that was based on measuring individual differences and making placement and curriculum decisions based upon these results. The education system in Saskatchewan developed from a segregationist philosophy to integration beginning in the 1970s. As the belief in the educability of these individuals and information on how to educate the intellectually disabled increased, a move towards full inclusion of these students began in the 1990s. As early as the 1970s, Saskatchewan Education began to develop specific curriculum guides and policies on the education of students with an intellectual disability. The progression of these documents up to 2002 is analyzed to determine the shifts in curriculum and student placement policy that occurred during this time period. The continuance of a reliance on the IQ test to identify and place students with an intellectual disability in the education system was analyzed. The attempt of Saskatchewan Education to deal with difficulties in providing for an appropriate education for students with an intellectual disability and suggestions for future directions are discussed.

This study is an historical analysis of the education for students with mild intellectual disabilities in Saskatchewan from 1900-2002. The thesis analyzed the beginnings of thought on the construct of intelligence, its hereditarian orientation, and the IQ test that originated in 1904 to measure individual differences in intelligence. The use of the IQ test was traced as it progressed through the eugenics movement that dominated from approximately 1900-1940, as well as the mental hygiene movement that was present during roughly the same time period. The importance of the concept of intelligence and the IQ test was analyzed for how it affected the identification of individuals with an intellectual disability, and how the identification process affected their treatment and education. The classification and educational placement of students identified with an intellectual disability had parallel affects on the curriculum for these students. The changes in attitudes from eugenics and institutionalization of those identified with an intellectual disability and their subsequent deinstitutionalization, beginning in the 1960s, are examined for the effects these attitudinal shifts had on the education for these individuals. Education developed a system of special education that was based on measuring individual differences and making placement and curriculum decisions based upon these results. The education system in Saskatchewan developed from a segregationist philosophy to integration beginning in the 1970s. As the belief in the educability of these individuals and information on how to educate the intellectually disabled increased, a move towards full inclusion of these students began in the 1990s. As early as the 1970s, Saskatchewan Education began to develop specific curriculum guides and policies on the education of students with an intellectual disability. The progression of these documents up to 2002 is analyzed to determine the shifts in curriculum and student placement policy that occurred during this time period. The continuance of a reliance on the IQ test to identify and place students with an intellectual disability in the education system was analyzed. The attempt of Saskatchewan Education to deal with difficulties in providing for an appropriate education for students with an intellectual disability and suggestions for future directions are discussed.

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Computer models are nowadays routinely used in harbor engineering applications. Models based on the two-dimensional elliptic mild-slope equation can simultaneously simulate refraction, diffraction, reflection, and dissipation in completely arbitrary coastal domains. However, floating structures such as floating breakwaters and docks are often encountered in the modeling domain. This makes the problem locally 3- dimensional. Hence it is problematic to incorporate a floating structure into the 2-d model. Tsay and Liu (1983) proposed a highly simplified but approximate approach to handle this problem practically. The validity of their approach is examined in detail and it is found that the actual solutions deviate considerably from the theoretical solutions, although their approximation provides results with the correct trend. Therefore, correction factors have been developed and may be used to produce more reliable results using the framework of Tsay and Liu (1983). The resulting method is applied to Douglas harbor in Alaska. The result shows that docks in the harbor distort the wave field considerably and create a reflective pattern that can affect navigation safety in some areas. Also plots are developed for the transmission coefficients for waves propagating past rectangular and cylindrical floating objects of infinite extent for a wide range of conditions encountered in practice.

M. Tech. Metallurgical Engineering / Mild steel is vulnerable to corrosion; this behaviour affects the material strength and electrochemical behaviour during industrial application. Mild steel also has poor tribological resistance; its application for the components of machines, however, requires good tribological property. The cost incurred from equipment failures, properties loss and increased production overheads makes is imperative to enhance mild steel's electrochemical and tribological properties. Electroless nickel plating has found extensive use in various industries attesting to its exceptional properties. The effect of bath parameters on the electroless plating process is of importance as this affects the adhesion, morphological behaviour, electrochemical properties and uniformity of coating. The key aim of this research is: To generally improve the understanding of the effect of electroless binary and ternary alloys on the corrosion and wear resistance of mild steel using weight loss method, potential measurement, linear polarization and tribological sliding wear tests. This work studies the effect of temperature, concentration, deposition time and the inclusion of Tin (Sn) as a third addition to the electroless bath. Corrosion and wear behaviour of the electroless plated mild steel was studied.

M. Tech. Chemical Engineering. / Discusses the corrosion of mild steel due to sulphate ions together with chloride ions in concrete reinforcement in alkaline media can be limited or even eliminated by the introduction of laser surface irradiation on the mild steel material.

The majority of patients with chronic obstructive pulmonary disease (COPD) have milder airway obstruction and are not diagnosed in a timely fashion. Nevertheless, these patients are largely under-studied; this, despite new evidence of increased morbidity and mortality in this sub-population. Recent studies have highlighted the increased ventilatory requirements and abnormalities in respiratory mechanics as important features to explain the relatively reduced exercise tolerance and greater exertional dyspnea in these patients. However, it remains uncertain whether such abnormal mechanical factors actually limit exercise capacity in mild COPD. Accordingly, the objective of this study was to determine whether ventilatory constraints represent a primary factor in exercise limitation and increased dyspnea in this patient group. To determine the role of mechanical factors in exercise limitation in mild COPD, we selectively loaded the respiratory system by adding dead space (DS) to the breathing circuit. We compared ventilation, breathing pattern, operating lung volumes, and dyspnea intensity during incremental cycle exercise in 20 patients with GOLD stage I COPD (post-bronchodilator FEV1/FVC=61±5%, and FEV1=95±11% predicted; mean±SD) and 20 healthy age-, sex- and BMI-matched subjects under two conditions, in randomized order: unloaded control (CTRL) or ventilatory stimulation by 600mL of an added DS. Compared to the CTRL condition, both healthy and COPD participants had small decreases in peak work rate and no significant increase in peak ventilation with the added DS. At the highest equivalent work rate of 60 watts, DS caused a smaller increase in tidal volume (VT) in COPD compared with healthy subjects (+0.26±0.29 vs. +0.56±0.22 L respectively, p<0.01) with a correspondingly greater increase in dyspnea intensity (+1.8±1.8 vs. +0.2±0.6 Borg units, respectively, p<0.0001). At peak exercise, COPD patients failed to significantly increase VT, reflecting the fact that end-inspiratory lung volume (EILV) could not increase with DS vs. CTRL (5.25±0.91 vs. 5.16±0.84 L, respectively, p=0.41). This contrasts the results in health where EILV increased with DS vs. CTRL (5.40±1.01 vs. 5.13±0.90 L, respectively, p<0.05). We conclude that the lower exercise performance in mild COPD, compared with health, is explained by critical respiratory mechanical constraints which limit further increases in ventilation to support a higher metabolic load. / Thesis (Master, Physiology) -- Queen's University, 2012-09-28 12:04:50.507

The integrity of brain white matter is vital for the interneuronal signalling between distinct brain regions required for normal cognitive function. White matter integrity is compromised with ageing and could contribute to age-related cognitive decline. Chronic cerebral hypoperfusion is thought to underlie the development of white matter pathology and cognitive changes, often seen in the elderly. Additionally, the development of regional hypoperfusion and white matter damage are thought to be early events in Alzheimer’s disease (AD) pathogenesis. This thesis set out to test the hypothesis that chronic cerebral hypoperfusion underlies the development of white matter pathology and cognitive decline and also that chronic cerebral hypoperfusion causes the development of Ab pathology in AD. The first aim was to investigate the impact of hypoperfusion on the development of white matter damage and different aspects of cognition in a mouse model of chronic cerebral hypoperfusion. Two studies were undertaken to address this. The first study examined the temporal development of pathology following hypoperfusion induced by bilateral carotid artery stenosis (BCAS) using microcoils Hypoperfusion was induced in wild type (WT) mice and the pathological changes examined at one week, two weeks, one month and two months. Hypoperfused animals developed a diffuse and widespread white matter pathology, present from one week, which occurred predominantly in the myelin component of white matter; this was accompanied by minimal axonal damage. A second study examined the impact of hypoperfusion on different aspects of spatial memory and further investigated pathological changes in the model at one and two months. Behavioural testing revealed a significant impairment in spatial working memory but not episodic memory or spatial reference memory in hypoperfused animals. In the same mice, pathological assessment indicated that there was a significant increase in levels of myelin damage and elevated levels of microglial activation as compared to shams. These results demonstrate that modest reductions in cerebral blood flow are sufficient to cause the development of white matter damage and the development of cognitive deficits. The second aim was to investigate the impact of hypoperfusion on the development of white matter and amyloid pathology in a mouse model (3xTg-AD) of AD. To address this, using 2 different sizes of microcoils (0.18mm and 0.16mm internal diameter) BCAS of varying severities was induced in 3xTg-AD mice and white matter and Ab pathology were assessed at one month. Circle of Willis (CoW) architecture was also compared between WT and 3xTg-AD mice. Overall white matter pathology was not exacerbated in experimental 3xTg-AD mice with BCAS induced by 0.18mm coils. However with a greater level of stenosis (0.16mm coil) ischaemic damage to neuronal perikarya was present in most experimental animals. In addition to ischaemic damage, localised areas of severe white matter pathology were also observed in conjunction with subtle changes to white matter Ab levels. Hypoperfusion did not impact on the development of intraneuronal Ab pathology, other than in the presence of ischaemic damage when levels were reduced. Comparison of CoW architecture between WT and 3xTg-AD mice revealed strain specific differences in the presence and morphology of the posterior communicating artery which may explain the lack of pathology in 3xTg-AD mice as compared to WT following BCAS induced using 0.18mm dia. microcoils. The third aim was to investigate whether white matter protein composition changed with age and also whether ageing conferred increased vulnerability to hypoperfusion. To address this, white matter protein levels were compared between young (3-4 months) and old (12-13 months) 3xTg-AD mice. White matter pathology was compared between sham and hypoperfused animals in the aged cohort. Levels of myelin basic protein and 2', 3'-cyclic nucleotide 3'- phosphodiesterase were found to be significantly increased whilst levels of myelin associated glycoprotein were significantly reduced with ageing. These results suggest that changes in myelin protein composition may contribute to the development of age related white matter pathology. White matter pathology was not exacerbated in aged hypoperfused animals following one month of hypoperfusion as compared to shams. The results presented within the thesis demonstrate that chronic cerebral hypoperfusion precipitates the development of selective white matter damage and impacts on cognition. Also it has been shown that where hypoperfusion is severe enough to cause ischaemic damage to neuronal perikarya and localised areas of severe white matter pathology, alterations in white matter Ab levels can occur. Hypoperfusion does not impact on APP processing or on intraneuronal levels of APP or Ab, other than in the presence of ischaemic damage to neuronal perikarya, when levels are reduced. These findings highlight the importance of early intervention strategies in the treatment of vascular risk factors which can lead to hypoperfusion and the development of white matter damage and a decline in cognitive function in later life. These findings also suggest that repair or prevention of white matter damage may be an appropriate strategy for the attenuation of cognitive decline following onset of hypoperfusion. This thesis also highlights some of the limitations of animal models of human disease.

The aim of this study is to establish a brief screening tool to classify PD patients as PD with normal cognition (PD-N), PD patients with mild cognitive impairment (PD-MCI) and PD patients with dementia (PD-D). There has been emerging evidence that the MoCA (Montreal Cognitive Assessment) shows potential for the brief assessment of cognition to differentiate among PD patients. One possible solution to further improve the discrimination among PD-D, PD-MCI and PD-N groups is to examine Instrumental Activities of Daily Living (IADL) measures in conjunction with the MoCA. A convenience sample of 162 patients suffering from PD and 53 volunteer control subjects were examined in a movement disorders center. Extensive neuropsychological testing was done to classify the PD patients into PD-N, PD-MCI or PD-D. The 24 patients were diagnosed as PD-D based on the Movement Disorders Society Task Force criteria. For PD-MCI, two criteria were used: 1.5SD:2 in one-domain (1.5 SD below the norms on two measures in at least one of four cognitive domains) and 1.5SD:1 in two-domains (1.5 SD below normative data in at least one measure but in two domains) which made a diagnosis of 34 and 39 PD-MCI patients respectively. The remaining patients were classified as PD-N. For both the MCI criteria, the results suggest that 1) for discriminating PD-MCI from PD-N, the MoCA is a sufficiently suitable screening measure that is not improved by adding ADL measures, 2) for distinguishing PD-D from PD-MCI, the MoCA and the full ADL-IS questionnaire can be administered to a patient suffering from PD. When time is limited and depending on the possibility of answering the questions regarding the ADL-IS items, the MoCA along with the Muddled and Complex Medication ADL-IS items should be administered. When no scores are obtained for Muddled, then MoCA along with Complex Medication ADL-IS item is sufficient to discriminate PD-D from PD-MCI. However, if no scores are obtained for Complex Medication item, then an average of four ADL-IS items should be taken along with the MoCA. This attractive brief screening tool helps in detection of cognitive impairment in the elderly.

Individuals with mild cognitive impairment (MCI) show variable impairment in autobiographical memory function, source memory function and reduced integrity in the brain’s default mode network (DMN). There is overlap between the DMN, such as the medial posterior cortical hub, and brain regions that are active when participants recall autobiographical memories. To assess the association between autobiographical memory and the DMN, 14 MCI and eleven age and education-matched healthy control participants were assessed using the autobiographical memory interview (AMI) and underwent resting state fMRI scans. The same participants underwent a test of source memory which assessed both recognition and source memory. The MCI group showed significantly increased semantic as well episodic memory impairments using the AMI, evident across the lifespan for episodic memory but not for childhood semantic memory. Significantly poorer DMN connectivity, using a goodness of fit index (GOF) of the DMN template, was evident in the MCI group. MCI participants showed poorer performance on both recognition and source memory relative to HC participants. A modest association between AMI semantic memory (r=0.4) scores, but not episodic memory scores (r=0.09), and DMN connectivity was found in these participants. For future study the predictive value of MR imaging in the DMN of MCI participants should be explored.