Thesis (M.A. in educational administration)--Washington State University, May 2010. / Title from PDF title page (viewed on June 29, 2010). "Department of Educational Leadership and Counseling Psychology." Includes bibliographical references (p. 51-56).

Inaug.--Diss.--Bonn. / Vita. Includes bibliographical references (p. 337-374).

Thesis (M.Arch.)--University of Hong Kong, 1999. / Includes special report study entitled : Planning for flexible design. Includes bibliographical references. Also available in print.

Thesis (Ph. D.)--University of Chicago, Dept. of Education, March, 2001. / Includes bibliographical references. Also available on the Internet.

M.A. / New job and study opportunities were created for many people because of political changes in South Africa. This implied that many people left their homes and moved to new areas. Research indicated that 60% to 70% of first year students suffered from homesickness during their first semester at university. For some of them it was only a light experience; for others it was an intense negative experience with serious social-, academic-, and financial implications which could result in illness or even death. The role of salutogenic factors (factors that contribute to health) in the occurrence of homesickness, experienced by Afrikaans- and English speaking male and female first year students at the Rand Afrikaans Universiy, was investigated. It was found that the experience of homesickness was diminished by the salutogenic factors "sense of coherence", "self-efficacy", learned resourcefulness" and social support. These factors thus contributed to health. The factor "hardiness" did not play a salutogenic role in this study. Although the multicultural context of South Africa was not taken into account, the study should be useful in identifying students who would be prone to homesickness and illness during their first year at university.

No description available.

Plagiarism is a modern Western construct which arose with the introduction of copyright laws in the eighteenth century. Before this time, there was little sense of artistic "ownership". Since then, the ideas of "originality" in writing as well as the "autonomous text" have been highly valued. In the theoretical section of this dissertation I deal with plagiarism and referencing from three perspectives. After looking at problems of definition of plagiarism, I turn to the first perspective, the historical development of the notions of plagiarism and originality. Alongside this I discuss the notions of "autonomous text" and "decontextualized" language, and attempt to show that these concepts are problematic, and that language is intensely social at the levels of discourses, genres, and the word. The second angle is a snapshot of present-day writing genres, and how they deal with documentation in different ways. The third point of focus is on the development of the student writer, on whom present-day genres of academic writing, and the historically constructed notions of plagiarism converge. Here I centre on the development of the undergraduate student as a writer, and some of the things that may be happening when a student is seen to be plagiarizing. Some of these are the "alienness" of academic discourses, the hybridization of discourses, the need to "try on" academic discourses, the lack of authority of the student writer and her relationship to the authority of the sources, and the way in which languages are learned and reproduced in chunks. I look finally at what the meaning of authorship might be in an intensely social view of language, and at the complexity of developing authorial voice in writing. The dissertation is located in a postpositivist paradigm, and seeks to interpret as well as being oriented towards praxis. The research took place within the Political Studies Department at the University of Cape Town. The study included a discourse analysis of the departmental handbook, as well as analysis of academic essays, at the first year and third year level, which were selected for having problems with referencing, or having plagiarized. A few were selected for good referencing. Students who had written these essays, and tutors and lecturers who had marked them, were then interviewed. In the analysis I explore differing understandings of the role of referencing in the academic essay, what negative and positive consequences the practice of referencing and the monitoring of plagiarism have, with regard to authority and voice in student writing, what might be happening when students are thought to be plagiarizing, and what difficulties are experienced by students in developing an authorial voice when using multiple sources. The study found that there are a range of underlying causes for plagiarism in student writing, which indicate that plagiarism is more a problem of academic literacy than academic dishonesty. It also found that marking practices in detecting plagiarism may sometimes be based on problematic assumptions about the amount of background knowledge and independent ideas which students bring to their writing. I conclude by putting forward a pedagogy for plagiarism and referencing, which is based on 1) the negotiation of shared meaning around the concept of plagiarism, including an examination of assumptions linked to this concept in its monitoring and enforcement, leading to the development of written policy and guidelines emerging from this shared understanding. 2) The development of an academic literacy programme within the curriculum, with attention to the complexities of developing authorial voice whilst constructing a text based on the texts of others, with a focus on authors, which moves students towards an understanding of how knowledge is constructed.

The rat pineal gland provides a convenient model for investigating nor adrenergic receptor neurotransmission and the effects of various drugs on these processes in health and disease. The effect of a variety of antidepressant drugs on rat pineal gland function following acute and chronic administration is described. Antidepressants from several different classes increase melatonin synthesis in rat pineal gland cultures when administered acutely. This effect appears to be mediated by noradrenaline acting on postsynaptic β-adrenoceptors. Activation of these receptors, in turn, activates the enzyme serotonin N-acetyltransferase via a cyclic adenosine monophosphate (cAMP) second messenger system. Serotonin N-acetyltransferase catalyses the rate-limiting conversion of serotonin to melatonin. Blockade of postsynaptic β-adrenoceptors prevents the antidepressant-induced increase in melatonin synthesis. The possibility that atypical antidepressants as well as those that selectively inhibit serotonin reuptake may increase melatonin synthesis via a β-adrenoceptor mechanism is discussed. In contrast, however, antidepressants from different classes have variable effects on rat pineal gland function when administered repeatedly. Chronic treatment with antidepressants that selectively inhibit noradrenaline reuptake appear to down-regulate the β-adrenoceptor system while, simultaneously, increasing melatonin output. Atypical antidepressants and those that selectively inhibit serotonin reuptake appear to be without these effects when administered repeatedly. The pineal gland of normal rats may therefore not represent a suitable model for evaluating the biochemical effects of chronic antidepressant treatment. In an attempt to investigatc pineal gland function in rats with "model depression" , antidepressants were administered to chronically reserpinized rats. Treatment with reserpine produced an increase in the density of pineal β-adrenoceptors. In addition, pineal cyclic AMP accumulation and N-acetyltransferase activity were increased in reserpinized rats following exogenous catecholamine stimulation. Reserpine, by depleting intraneuronal catecholamine stores, prevented the nocturnal induction of N-acetyltransferase activity and reduced the synthesis of melatonin in pineal gland cultures. A variety of antidepressants, irrespective of their acute pharmacological actions, reversed these effects when administered chronically to resepinized rats. Acute antidepressant administration was not associated with a reversal of the reserpine-induced effects. These findings provide additional evidence against the hypothesis that antidepressant drugs act by reducing noradrenergic neurotransmission and casts doubt on the importance of β-adrenoceptor down-regulation in the mechanism of antidepressant action. The possibility that the pineal gland of the reserpinized rat may represent an alternative model for evaluating antidepressant therapies is discussed.

Alteration of serum tryptophan leads to parallel alterations in brain tryptophan levels. Such changes in brain tryptophan levels has been shown to lead to mood disturbances. The primary enzyme responsible for altering serum tryptophan levels is the liver cytosolic enzyme, tryptophan pyrrolase. Activation of this enzyme is responsible for the enhanced catabolism of circulating tryptophan. The purpose of the present study was firstly to establish whether there is a link between sex steroids and tryptophan pyrrolase activity especially since sex steroids are also known to cause mood disturbances and secondly to determine the effects of sex steroids on brain indolamine metabolism. The results show that all three sex steroids induce the activity of tryptophan pyrrolase implying that they decrease serum tryptophan levels by the activation of tryptophan pyrrolase, thus making less tryptophan available for uptake by the brain. It was also shown that the sex steroids enhance the uptake of ¹⁴C-tryptophan by brain synatopsomes. In addition, the sex steroids influenced the pattern of metabolism of serotonin by organ cultures of rat pineal glands. It is possible that the sex steroids regulate the availability and uptake of indoleamines in the brain.

Embryos from the annual killifish Austrofundulus limnaeus have a unique and unequalled ability among vertebrates to withstand extended periods of anoxia (maximum lethal time to 50% mortality of 65 days at 25°C). In addition, tolerance of anoxia is gained and subsequently lost during the normal development of this species. Thus, anoxia tolerant and anoxia sensitive individuals can be compared within the same species, making A. limnaeus an excellent model for studying the molecular changes associated with survival of oxygen deprivation in vertebrates. The aim of this project is to analyze the molecular changes associated with anoxia tolerance in the embryos of A. limnaeus. Understanding how the cells of these embryos become tolerant to anoxia will aid in identifying novel therapeutic targets to reduce cell death following periods of ischemia in heart, brain or other tissues. Three major analyses were used to investigate the molecular changes associated with anoxia tolerance in this species. The first was a cell cycle and cell cycle arrest analysis using flow cytometry along with an immunoblot analysis of both positive and negative regulators of cell cycle progression. The second was a cell death analysis utilizing caspase-3/7 activity as well as TUNEL staining. The third was an immunoblot analysis of three different post-translational modifers (ubiquitin, SUMO-1 and SUMO-2/3). The overall findings from this study indicate that the embryos of A. limnaeus do indeed experience some degree of cellular stress (i.e. increase in ubiquitinated proteins, increase in p53 expression, evidence of DNA damage from TUNEL staining and increases in caspase activity) in response to anoxic treatment, even in their most protective state of diapause II. However, despite these observations, the whole organisms are still able to recover from anoxia and do not succumb to death. The overall low levels of TUNEL-positive cells and caspase activity relative to the positive controls indicates that the damage accrued in response to anoxic treatment is minimal. It appears that embryos are able to either "sacrifice" a certain portion of cells or they are able to repair the damage required for resumed development following anoxia.