Thesis (MSc(HlthSc)) -- Flinders University, Faculty of Health Science. / Typescript (bound). "A thesis in two parts." Includes bibliographical references (leaves 222 - 245). Also available online.

Dissertation (Ph.D.)--University of South Florida, 2007. / Title from PDF of title page. Document formatted into pages; contains 104 pages. Includes vita. Includes bibliographical references.

Prediking is 'n dialoog. Dit dompel die preek in 'n direkte krisis. Wat kan die prediker doen om hierdie dialoog te bevorder? Die deelnemers in die erediens word kortliks bespreek. God spreek met die prediker deur die teks. Die prediker moet hierdie teks aan die hoorder in die erediens oordra. Om die oorspronklike teks te verstaan het daar drie hoofstrome in die tradisionele hermeneuse ontstaan: Krities-histories, Tekskrities en Hoorders hermeneutiek. Die probleem is egter nie opgelos nie. Hoe kan die prediker die boodskap effektief aan die hoorder oordra? Daar word voorgestel dat die kreatiewe proses gebruik word in die voorbereiding van die preek. Die breinkaart kan gebruik word om die teks en hoorder van die teks, beter te verstaan. Hulpmiddelle moet gebruik word om die teks aan die hoorder oor te dra. Hier word die gebruik van literatuur en drama bestudeer. / Preaching is a dialogue. This states the current problem of preaching. How can the preacher improve this dialogue in the sermon? The participants in the sermon are shortly discussed: The preacher listens to the text. God speaks through the text. The preacher must communicate this text to the listener in the sermon. Three major streams have evolved in the tradisional hermeneutics: Critical-historical, Textual and Listeners hermeneutics. There is however, still a problem. How does the preacher present this message effectivly to the listener? It is suggested that the creative process must be considered in preparing a sermon. The mind map can be used to understand the text and listener of the text better. More aids can be used to reach the listener effectivly. In this thesis the use of literature and drama in the preparing and delivering of the sermon will be studied. / Philosophy, Practical and Systematic Theology / M.Th. (Practical theology)

This thesis proposes a mechanism for the induction of peripheral tolerance to protein antigens. I have investigated the mechanism of tolerance induction to soluble protein antigens by targeting an antigen to small, resting B cells. For this purpose I have used a rabbit antibody directed at the IgD molecule found on the surface of most small, resting B cells but missing or lowered on activated B cells. Intravenous injection of normal mice with 100 μg of an ultracentrifuged Fab fragment of rabbit anti-mouse IgD (Fab anti-δ) makes these mice profoundly tolerant to challenge with nonimmune rabbit Fab (Fab NRG) fragments. This tolerance is antigen specific since treated mice make normal responses to an irrelevant antigen, chicken immunoglobulin (Ig). Fab fragments of rabbit Ig (rabbit Fab) not targeted to B cells do not induce tolerance as well as Fab anti-δ. Evidence suggests that the B cells must remain in a resting state for tolerance to be induced, since injection of F(ab)'2 anti-δ does not induce tolerance. Investigation of the mechanisms of the tolerance, by adoptive transfer, have shown that rabbit Fab specific B cell function has been impaired. The major effect however is in helper T cell function, as shown by adoptive transfer and lack of help for a hapten response. In vitro proliferation experiments show that the T cell response has not been shifted toward activation of different T cell subsets which do not help Ig production, nor is there any change in the Ig isotypes produced. Suppression does not appear to be the major cause of the helper T cell defect as shown by cell mixing experiments. This work shows that an antigen targeted to small B cells can induce tolerance to a soluble protein antigen, and suggests a role for small B cells in tolerance to self-proteins not presented in the thymus.

The purpose of this study was to gain a better understanding of the effect that attribution style and presenting symptoms has on the self-reported readiness to change of female survivors of childhood sexual abuse. The aim was to demonstrate that the stages of change are a useful concept in understanding how to approach treatment with female child sexual abuse survivors seeking psychotherapy. One factor that influences the effectiveness of psychotherapy is a client's degree of motivation. The concept of "stage of change" has been used as a measure of client motivation. Stage of change consists of four basic stages; precontemplative, contemplative, action, and maintenance. Prior research has demonstrated that assisting clients in transitioning from a lower to a higher stage of change early in psychotherapy can improve outcomes. Assigning clients a "readiness to change" score is a simple method of categorizing their stage of change. There are many variables that could impact a client's readiness to change. The two selected for this study were attributional style and presenting symptoms. The statistical analysis consisted of using correlation to determine the strength of the relationship between readiness to change, overall attribution styles, and presenting symptoms. Multiple regression was used to see how much of the variance in readiness to change could be accounted for by different levels of attributions or symptomatology. No correlation was found between readiness to change and the other variables, although internal attribution style, external attribution style, and symptomatology were all correlated with each other. Likewise, the different levels of attribution and symptomatology did not account for a significant amount of variance in readiness to change. A secondary analysis into the relationship between total attributions endorsed and symptomatology provided evidence that individuals who make more attributions report significantly more presenting symptoms than individuals who make fewer attributions. The conclusions drawn from this study focus on the importance of utilizing client motivation in the initial sessions of therapy, and propose that focusing on reducing the number of attributions made could be more beneficial to clients than helping them move from one attribution style to another.

Building on the logic of issue selling, my dissertation explores the micro-processes of shareholder social activism through which shareholders interact with targeted firms and also addresses which micro-processes could affect the effectiveness and the success of shareholder social activism. To do this, my dissertation develops a theory with respect to the approaches of linguistically framing the contents of and of presenting shareholder social activism. Based on a qualitative (descriptive) analysis on 1,612 shareholder social proposals, my dissertation identifies six packaging strategies that are used by the proponents to linguistically frame the contents of their proposals and two selling strategies used by the proponents to present their proposals. Subsequently, a quantitative analysis demonstrates that the effectiveness of shareholder social proposals would be largely determined by the joint effects of opportunity framing, threat framing, coalition building, and repeated submitting and that other packaging strategies would have little unique contribution to the effectiveness and the success of shareholder social activism. I argue that my dissertation would make contributions to the understanding of shareholder social activism and also offer some theoretical considerations for future studies on issue selling, although my dissertation might not directly contribute to the body of work of issue selling. / Ph. D.

京都大学 / 新制・課程博士 / 博士(医学) / 甲第24515号 / 医博第4957号 / 新制||医||1064(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 森信 暁雄, 教授 竹内 理, 教授 濵﨑 洋子 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

Indiana University-Purdue University Indianapolis (IUPUI) / CD1d is a cell surface glycolipid that, like Major Histocompatibility Complex (MHC) class I and MHC class II molecules, presents antigen. However, instead of peptides, CD1d presents lipids to Natural Killer (NK) T cells, a subset of T cells that express both NK cell markers and the T cell receptor and produces both T helper (Th) 1 and Th2 cytokines. Our lab focuses on the regulation CD1d-mediated antigen presentation. TGF beta is a known regulator of the immune system, such as controlling MHC class II antigen presentation. Further, TGF beta can activate the mitogen activated protein kinase (MAPK) p38, a known negative regulator of CD1d-mediated antigen presentation. Therefore, we hypothesized that TGF beta would be a negative regulator of CD1d-mediated antigen presentation, and our results showed a decrease in antigen presentation by CD1d in response to TGF beta treatment. However, this inhibition was not through p38 activation, as indicated by the absence of a rescue of CD1d-mediated antigen presentation in, TGF beta-treated, p38 dominant negative-expressing cells. Alternatively, the Smad pathway, the canonical pathway activated by TGF beta, was investigated through a lentivirus shRNA-mediated knockdown of Smad2, Smad3 and Smad4 proteins. Smad2 shRNA-expressing cells showed in an increase in CD1d-mediated antigen presentation, suggesting an inhibitory role for Smad2. In contrast, Smad3 shRNA-expressing cells did not differ from control cells. However, as in the case of Smad2, CD1d+ cells in which Smad4 was knocked down, were substantially better at CD1d-mediated antigen presentation than control cells, suggesting that it also negatively regulates antigen presentation. Overall, these studies demonstrate that the canonical TGF beta/Smad pathway regulates an important part of the host’s innate immune response, vis-à-vis CD1d-mediated antigen presentation.

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Vaccination against intracellular pathogens requires generation of pool of memory T cells, which can respond upon infection and mediate immune responses by either killing of infected host cells or induce killing mechanisms in infected cells. T cell-inducing vaccines aim to deliver the antigen to antigen presenting cells (APCs) by presenting on MHC molecules thus bridging innate and adaptive immunity. The intracellular pathogen Edwardsiella ictaluri causes enteric septicemia of catfish (ESC), which is a devastating disease in catfish industry. E. ictaluri can survive in professional phagocytes and use them as an infection source. Two new live attenuated vaccine (LAV) strains, EiDELTAevpB and ESC-NDKL, were developed by our group. However, the role of LAVs in phagocytosis, bacterial killing, and antigen presentation is unexplored. Therefore, further research is necessary to determine immune responses in channel catfish against LAVs. The long-term goal of this project is to identify immunological APC-dependent mechanisms that underscore E. ictaluri pathogenesis to enable development of effective control strategies for ESC. The overall goal of this project is to assess the role of three professional APCs, dendritic cells (DCs), macrophages and B cells in the LAV-induced innate and adaptive immune responses in catfish. The central hypothesis is that efficacious LAV strains will enhance phagocytosis and microbial killing, and promote the generation of T cells that regulate and control protective B cell-mediated immunity. The rationale for this research is that more detailed knowledge about phenotype and function of catfish APCs will not only help gain insight into the evolution of vertebrate adaptive immune system but will provide valuable information for development and optimization of immunotherapies and vaccination protocols for aquaculture use. In this study, we first identified DC-like cells in immune-related organs of catfish and assessed their expression patterns in lymphoid organs of catfish in E. ictaluri infection. Although WT strain induces the functional inability of DC-like cells in migration and maturation, LAVs strains promote the migration and maturation of DC-like cells for antigen presentation. Two LAVs enhanced the phagocytosis and killing activity in catfish macrophages and B cells. Also, LAVs induce high expression of T cell-related genes without causing inflammation.