Thesis (Ph. D.)--University of Kentucky, 2000. / Title from document title page. Document formatted into pages; contains vi, 137 p. : ill. Includes abstract. Includes bibliographical references (p. 108-135).

Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 143-163).

Thesis (Ph. D.)--University of Texas at Austin, 2002. / Vita. Includes bibliographical references. Available also from UMI Company.

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Humoral immune responses arise when B lymphocytes respond to activation signals, enter mitosis and proliferate rapidly. Concurrent differentiation to antibody secreting and isotype switched effector cells is tightly linked to cell division, such that the degree of proliferation strongly influences the nature of the response that is mounted. Previous versions of a quantitative model of lymphocyte proliferation based on inherent variation in the time cells take to divide or die were able to accurately describe the entry of naïve, resting cells into division and subsequent population expansion. In the work described here, the model was tested and extended by investigating the proliferation cessation and population contraction phases of in vitro B cell responses. Experiments designed to assess the distribution of times to die of cells that had ceased proliferating revealed that the number of divisions achieved by individual cells is stochastically distributed in the population and varied in response to different stimuli. Both the concentration and duration of stimulation regulate the number of divisions undergone. A cell that stops dividing is described as having reached its division destiny. Further investigation revealed that cells reach a maximum division destiny even during repeated high-dose stimulation. This limit is dictated by cellular progression through divisions, and is not dependent on the survival capacity of the cells or time. Incorporation of division destiny in the quantitative model allows proliferation cessation to be described and the distribution of times to die after this point to be assessed. This extended model can describe the full course of in vitro lymphocyte proliferative responses to various different stimuli. (For complete abstract open document)

Title page, abstract and table of contents only. The complete thesis in print form is available from the University of Adelaide Library. / Salmonella is a genus of Gram-negative bacteria responsible for food-borne enteritis and systemic fever. Salmonellosis continues to be a serious health burden worldwide. Lipopolysaccharide (LPS) is the dominant lipid component of the outer membrane of Salmonella. LPS is composed of lipid A, an oligosaccharide core, and a polymer of O units known as O antigen. Wzz proteins control the length of O antigen by an unknown mechanism. While O antigen is essential for S. typhimurium virulence, the significance of length regulation by Wzz is not known. This study investigates the pathogenic relevance of the wzz genes in S. typhimurium. In addition to the previously recognised wzz gene (WZZ[subscript]ST), a second gene with this function (WZZ[subscript]fepE) was identified in the S. typhimurium genome. Whereas WZZ[subscript]ST specifies the production of long LPS chains with a modal length of 16-35 O antigen repeat units, WZZ[subscript]fepE conferred very long chains containing> 100 O antigen repeat units. Strains carrying mutations in one or both wzz genes were constructed to investigate the role of wzz genes in virulence. It was found that wzz-controlled regulation of O antigen length was essential for resistance to the bactericidal activity of serum complement, while studies in the mouse model of infection found that wzz genes are essential for full virulence. The wzz double mutant was complemented with heterologous wzz genes from a variety of bacterial sources. Despite variable sequence similarity of the encoded Wzz proteins each was functional in the S. typhimurium host, generating a panel of isogenic O antigen length variants. This panel of variants was used to define a minimum length requirement for complement resistance and identified relationships between O antigen length and complement consumption. Finally, the regulation of O antigen chain length was investigated. It was found that growth either in iron limiting conditions or in serum caused an increased production of LPS with very long O antigen chains (conferred by WZZ[subscript]fepE), resulting in increased complement resistance. The constitutive activation mutation of the phoPQ regulator (Phop) results in an altered O antigen distribution phenotype consistent with down-regulation of wzz genes. However PhoPQ had no effect on production of Wzz[subscript]sT as determined by immunoblotting with an antiWZZ[subscript]ST antiserum. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1152141 / Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2005

Proefschrift Universiteit van Amsterdam. / Met lit. opg. - Met samenvatting in het Nederlands.

Thesis (Ph. D.)--University of New South Wales, 1999. / Also available online.