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It has long been identified that relative deprivation increases prejudice. Guimond and Dambrun (2002) demonstrated that relative gratification, as the opposite of relative deprivation, is also an important variable in predicting intergroup discrimination. Guimond and Dambrun (2002), further suggest that in order to prevent destructive conflicts between groups, such as intergroup discrimination, the goal of equality rather than economic improvements has to be kept in mind. The present paper will report three experiments which aimed to replicate Guimond and Dambrun’s (2002) findings on relative deprivation and relative gratification and which further aimed to test their proposal that equality would reduce prejudice. The results of the three experiments confirmed the predicted effects of relative deprivation and relative gratification on intergroup discrimination. However, the results did not confirm that equality reduces prejudice. Methodological and theoretical reasons for these results are provided and discussed in detail.

The ability to navigate with limited vision is a skill that is often employed in our daily lives. Navigating without vision to a remembered target has previously been studied. However, not much is known about the attention required to perform blind navigation. We examined the effect of aging and presence of obstacles on the attentional demands of blind navigation. We evaluated reaction time, navigation errors and average walking speed in an 8 meter walking path, with or without obstacles, in the absence of vision. Results showed that older participants had increased reaction time and increased linear distance travelled as opposed to young participants, that obstacles increased reaction time and decreased average walking speed in all participants, and that emitting the reaction time stimulus early in the trial increased the linear distance travelled. Interpretation of the results suggests that aging and presence of obstacles augments the attentional demands of blind navigation.

There is increasing evidence that inflammatory processes play a pivotal role in the pathophysiology of ischaemic brain injury. Cerebrovascular endothelial cells that form the blood-brain barrier are critical for maintaining brain homeostasis, however, during cerebral ischaemia they contribute to the post-ischaemic inflammatory responses. It is not yet fully understood how different cerebral cells interact during this inflammatory response. This study aimed to test the hypothesis that oxygen-glucose deprivation (OGD) induces the inflammatory activation of the cerebrovascular endothelium and glial cells in vitro and that intercommunication between these cells regulate their responses to OGD. Primary murine brain endothelial cells (MBECs) monocultures, murine mixed-glial monocultures and MBEC-glial co-cultures were exposed to OGD for up to 24 hours (h), then reperfused cultures were returned to normoxia for a further 24 hours. MBECs and glia remained viable over a 24 h OGD exposure and during reperfusion. OGD induced a time-dependent increase in MBEC glucose transporter 1 (GLUT-1) expression but a time-dependent decline in expression and secretion of monocyte chemoattractant protein-1 (MCP-1). A significant increase in keratinocyte-derived chemokine (KC) secretion by MBEC monocultures was observed during reperfusion after prolonged exposure (18-24 h) to OGD whereas, KC secretion by co-cultured MBECs was increased during reperfusion after short exposure (4 h) to OGD. Co-cultured MBECs displayed a significant increase in intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in response to a short or prolonged exposure to OGD with 24 h of reperfusion. Neither OGD nor reperfusion had any effect on permeability of the MBEC monolayer. OGD induced a time-dependent increase in nuclear stabilisation of hypoxia inducible factor-1 alpha (HIF-1α) in glial cells which correlated to vascular endothelial growth factor (VEGF) secretion during OGD and subsequent reperfusion. Nuclear stabilisation of the nuclear factor kappa B (NFκB)p65 subunit by glial cells was dependent upon the duration of OGD. Reperfusion induced a significant increase in KC secretion by co-cultured glial cells after short exposure to OGD. Inflammatory activation of co-cultured MBECs and glia after 4 or 24 h OGD caused a significant increase in neutrophil transendothelial migration which correlated with MBEC expression of ICAM-1 and VCAM-1. A combination of these cell adhesion molecules with neutrophil integrins and soluble glial-derived mediators contributed to neutrophil transendothelial migration. These studies provide evidence that combined hypoxia and glucose withdrawal induces the activation of MBECs and glial cells in vitro. Cross-talk between these two cell types may further regulate their activation. As a result of this inflammatory activation, soluble MBEC and glial-derived mediators may contribute to neutrophil transendothelial migration through the regulation of MBEC cell adhesion molecule expression.

Morphological, electrophysiological and biochemical changes have been shown to occur in the retina, lateral geniculate nucleus, and visual cortex of light deprived animals. We attempted to determine whether the dark-rearing of rats from birth to 15, 30 and 60 days of age alters the ability of noradrenaline (NA) 30 μM, potassium chloride (KCI) 50 μM, adenosine 30 μM and combinations of NA and KCI with adenosine to stimulate the _in vitro formation of cyclic AMP (cAMP) in visual cortical slices and, as an internal control, in frontal cortical slices. At 15 and 30 days of age there was an 11% and 2170 reduction, respectively, compared to normally reared controls, in the stimulation of cAMP formation in a 5 minute incubation with NA in both frontal and visual cortical slices. After 60 days of dark-rearing, however, this was reversed in that the NA stimulation of cAMP formation was 23% and 357» higher than controls in frontal and visual cortical slices. In frontal cortical slices of rats dark-reared for 15 and 30 days there was a significant reduction in the stimulation of cAMP formation in a 20 minute incubation with NA. No differences were observed between 30 day old experimental and control animals in studies of the accumulation of cAMP in frontal and visual cortical slices incubated for various times with KCI. The stimulation of cAMP formation induced by KCI and adenosine in a 5 minute incubation was 5770 and 397o higher, respectively, in frontal cortical slices of 60 day old experimental animals than controls while the response in visual cortical slices was unaffected. The differences found between 60 day old experimental and control animals were abolished in both visual and frontal cortical slices when adenosine was used in combination with NA or KCI. Studies of the accumulation of cAMP in slices incubated for various times with NA revealed that the effect observed in the visual cortex after 30 days of light deprivation was due to a decrease in the maximum level of cAMP reached within a 20 minute incubation period, whereas in the frontal cortex the maximum level attained within a 20 minute incubation period was unaffected. These results are discussed in terms of our present knowledge concerning supersensitivity and plasticity in the central nervous system and the role of cAMP in nerve. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate

A number of studies have shown that sensory deprivation is associated with selective decreases in GABA, GAD, and GABA receptors, in deprived areas of visual and somatosensory cortex. Those studies focused on layer 4, a recipient of direct thalamocortical sensory input. However, supragranular layers 2/3 have been recently identified as a major locus of functional plasticity in sensory deprivation and long-term potentiation. To examine whether GABAA receptors in layers 2/3 are affected by sensory deprivation, rats had mystacial vibrissae in middle row C or rows ABDE trimmed for 6 weeks beginning in early adulthood. Layers 2/3 above the deprived and adjacent whisker barrels were located in tangential sections, using patterns of radial blood vessels as fiducial marks. In deprived whisker barrel columns, [3H]muscimol binding to GABAA receptors decreased by 12.8% ± 1.2 (P &lt; 0.001) in layers 2/3 and 11.4% ± 1.2 (P<0.001) in layer 4. Altered levels of GABAA α1 subunit (Fritschy et al., 1994) were indicated by reduced optical density of immunostaining, both in deprived layers 2/3 (6.4% ± 0.7; P&lt; 0.001) and in layer 4 (3.4% ± 1.0; P &lt; 0.005). Interestingly, Nissl staining density also decreased in deprived layers 2/3 (12.7% ± 1.8 P &lt; 0.001) and in 4 (6.0 ± 0.7 (P &lt; 0.001). The percent decreases were greater in layers 2/3 than in 4 for both GABAA α1 (P &lt; 0.05) and Nissl substance (P &lt; 0.005). The present results suggest that down-regulation in GABAA receptors may underlie the physiological signs of disinhibition observed in neurons of layer 2/3 and 4 in deprived whisker barrel columns.

The soil-nematode Caenorhabditis elegans survives oxygen deprivation (anoxia < 0.001 kPa of O2, 0% O2) by entering into a state of suspended animation during which cell cycle progression at interphase, prophase and metaphase stage of mitosis is arrested. I conducted cell biological characterization of embryos exposed to various anoxia exposure times, to demonstrate the requirement and functional role of spindle checkpoint gene san-1 during brief anoxia exposure. I conducted a synthetic lethal screen, which has identified genetic interactions between san-1, other spindle checkpoint genes, and the kinetochore gene hcp-1. Furthermore, I investigated the genetic and cellular mechanisms involved in anoxia-induced prophase arrest, a hallmark of which includes chromosomes docked at the nuclear membrane. First, I conducted in vivo analysis of embryos carried inside the uterus of an adult and exposed to anoxic conditions. These studies demonstrated that anoxia exposure prevents nuclear envelope breakdown (NEBD) in prophase blastomeres. Second, I exposed C. elegans embryos to other conditions of mitotic stress such as microtubule depolymerizing agent nocodazole and mitochondrial inhibitor sodium azide. Results demonstrate that NEBD and chromosome docking are independent of microtubule function. Additionally, unlike anoxia, exposure to sodium azide causes chromosome docking in prophase blastomeres but severely affects embryonic viability. Finally, to identify the genetic mechanism(s) of anoxia-induced prophase arrest, I conducted extensive RNA interference (RNAi) screen of a subset of kinetochore and inner nuclear membrane genes. RNAi analysis has identified the novel role of 2 nucleoporins in anoxia-induced prophase arrest.

Staging Sleep: Labor, Care, and Rest in Contemporary Performance examines an archive of plays and performances from the past forty years—which I term sleep theatre—including dramatic literature that foregrounds sleep and sleeplessness and performance art in which the artist sleeps in front of an audience. Contemporary theatre about sleep exposes the roots of sleep loss in overwork, healthcare disparities, and housing insecurity and imagines alternative social possibilities for sustainable rest. I understand the concerns and possibilities raised by sleep theatre through the framework of social reproduction theory, a feminist analysis of the vital forms of labor antecedent to commodity production, including housework and dependent care, that keep us all alive. I reorient theatre scholarship on sleep away from psychoanalytic readings of staged dreams and toward an understanding of sleep as a political act shaped by social and material contexts. In Staging Sleep, I argue that studying sleep in theatre and performance art offers new insights into social relations of care and interdependence among performers and spectators, and that sleep onstage not only critiques inhumane economic arrangements but also imagines myriad new social configurations that value rest over work. Staging Sleep begins in 1980, in the immediate aftermath of two decades of international Marxist feminist organizing that saw politicized housewives agitating for recognition of the value of both their work and their leisure. I demonstrate how sleep theatre expands and complicates this political legacy, beginning with the continuing global assault on welfare and unions in the 1980s. In my first chapter, I track how pioneering socialist feminist playwright Caryl Churchill develops the sleepless housewife as a character type, bringing sleep to the stage in a new way as a linchpin of her critique of the family. I then track sleep in theatre as a site of experimentation informed by feminist, queer, and disability studies through the 2010s. Chapter 2 explores sleep in plays by Sarah Kane, Maria Irene Fornes, and Peggy Shaw at the nexus of illness, friendship, and a fraying welfare state. Chapter 3 examines how directors stage homeless sleep in four recent adaptations of Cymbeline from the UK and South Sudan. My final chapter asks how performance itself creates the care and attention necessary to sustain sleep in the globe-touring, iterative performance artworks Best Place to Sleep and Black Power Naps. Sleep performances imagine, enact, and test the limits of very different configurations of labor and rest: ways of life in which caretaking labor is redistributed, and resilience and health become collective concerns rather than individual responsibilities. I suggest that sleep performance is a nascent theatrical phenomenon that will continue to reappear as politically-minded artists work through the theatrical possibilities of spectatorship, site, and immersion in the context of deep questions of everyday justice and equity. Staging Sleep shows how theatre can exploit and transform the weirdness of watching someone sleep, or of falling asleep in the audience, into a restructuring of our practices of work and rest, space and shelter, toward ensuring safe and restorative sleep as a universal right.

Selynn Yan Ting Lim Abstract The thesis endeavours to use the concept of relative deprivation to explain and account for the reasons behind the various manifestations of political and religious tension in Indonesia. From the most recent series of bombings in Surabaya in 2018, to the conflicts in the Maluku Islands back in 1999, it is undeniable that Indonesia is not immune to extremist activities or religious- political conflicts. The involvement of Political Entrepreneurs (PEs), such as giving a frame to people's perceived grievances, drive sentiments of being deprived in relative to other groups. Such feelings are especially made salient with the influence of social media. At the same time, the Indonesian government's advocacy of the wasatiyyah concept, which means middle-path Islam, appears to be its most effective tool in countering the trend of extremism in the society. However, such an interpretation of Islam is potentially at odds with the "right" form of Islam as practiced by the Muslims in Saudi Arabia. Faced with increasing pressure from Islamic hardliners in the society, the Indonesian state ideology - Pancasila - is under much threat as people are gradually becoming disillusioned with it.

The effects of constant food deprivation, terminated at different times of day were examined with respect to percent body weight loss (%BWL), plasma corticosterone (PC) and plasma glucose (PG). A 19-hour food deprivation paradigm schedule staggered around varying times of the day-night cycle was used. Patterns of %BWL related to nocturnal lipogenesis and diurnal lipolysis showed the greatest loss (10%) occurring at 0700 hr, while in evening hours, there was an increasing pattern of weight loss, with the greatest amount (7%) occurring at 2200 hr. A pattern suggestive of neuroregulatory cycles of glucocorticoid release was evident for PC levels; maximum levels for PC (23.2 μg%) were reported at 0700 hr and at 1900 hr (16.6 μg%). Similar patterns were also noted in PG levels, with respective maximum levels of 138.0 mg% and 125.8 mg% occurring at 0700 hr and 1900 hr. These results indicate that the time of day that a deprivation schedule is initiated and terminated is an important consideration due to the impact of circadian photoperiodism. Time of day should be an essential consideration when utilizing deprivation paradigms.