Thesis (Ph. D.)--University of Chicago, Committee on Immunology, June 2001. / Includes bibliographical references. Also available on the Internet.

Project (D. Min.)--Emmanuel School of Religion, Johnson City, Tennessee, 2000. / Abstract and vita. Includes bibliographical references (leaves 555-564).

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.

Starch is the main storage biopolymer in cereal plants. Several enzymes and carrier proteins are involved in the starch biosynthesis process. ADP-glucose pyrophosphorylase (AGPase) has been characterized as a key factor in this process, which catalyzes the conversion of glucose 1-phosphate into ADP-glucose in the cytosol of the endospermic cell. The freshly synthesized ADP-glucose must be transported into amyloplasts by the activity of ADP-glucose transporter. In the current research, we have characterized HvBT1 biochemically in E. coli system. HvBT1 shows high affinity to ADP-glucose as a transport substrate in counter-exchange with ADP with affinities of 614 and 334 µM, respectively. The cellular and subcellular localization of HvBT1 indicated its target the amyloplasts envelopes. The comparison between two barley cultivars; Harrington and Golden Promise shed some light on the impact of HvBT1 on starch accumulation. Higher expression of AGPase and HvBT1 (10 fold) provide an ideal combination for improving starch yield, where starch content was higher by 2.5% in Harrington. Unlike Harrington, the expression of soluble starch synthase encoded genes was higher in Golden Promise which accumulates less starch. This result provided evidence of the importance of HvBT1 in starch synthesis process along with AGPase. Down-regulation of HvBT1 also provided a cement evidence of its effect on the starch accumulation process, where the knock down lines showed 17% lower starch and altered starch composition. Also, as a result of decreasing starch, protein content increased in the transgenic grains by 4-5 % of its content in the wild type, while β-glucan was 37% lower than the wild type control. Down-regulation of HvBT1 led to decrease the grain yield by ~ 30% as a result of increase the grain size. Also, it seems to have pleotropic effects on other starch synthesis genes, where AGPLs was down-regulated while the plastidial SSU genes, AGPS1b and S2 were up-regulated. Soluble starch synthases SS2a and SS3a were down-regulated, while SS2b was up-regulated in the transgenic plants. The accumulated evidences indicated that HvBT1 is a key factor in starch biosynthesis process. / February 2015

This thesis presents a search for the rare B meson decay B -> pi l⁺l⁻ (l=e or mu) using 428 fb⁻¹ of data collected at the Upsilon(4S) resonance by the BaBar detector at the PEP-II asymmetric energy e⁺e⁻ storage rings located located at SLAC National Accelerator Laboratory in Menlo Park, California. Four exclusive modes are studied: B⁺ -> pi+ e⁺e⁻, B⁺ -> pi⁺ mu⁺mu⁻, B0 -> pi⁰ e⁺e⁻, and B0 -> pi⁰ mu⁺mu⁻. Branching fraction upper limits at the 90% confidence level are presented for the exclusive modes B⁺ -> pi⁺ mu⁺mu⁻ and B0 -> pi0 mu⁺mu⁻, and the combined mode B -> pi mu⁺mu⁻. / text

Kaposi’s Sarcoma-associated Herpes Virus (KSHV) is a human herpesvirus associated with cancers. To date, KSHV miRNAs have been mostly identified via analysis of cells that are undergoing latent infection. This work presented here is a novel approach to profile small RNAs from populations of cells undergoing predominantly lytic infection. Using two different next generation sequencing platforms, I cloned and sequenced both pre-microRNAs and derivative microRNAs (miRNAs). This analysis shows that the vast majority of viral and host 5p miRNAs are co-terminal with the 5 prime end of the cloned pre-miRNAs, consistent with both being defined by microprocessor cleavage. I report the complete repertoire (25 total) of 5p and 3p derivative miRNAs from all 12 previously described KSHV pre-miRNAs. Two KSHV pre-miRNAs, pre-miRs-K8 and K12, encode abundant derivative miRNAs from the previously unreported strands of the pre-miRNA. I identify several novel small RNAs of low abundance, including viral microRNA-offset-RNAs (moRNAs), and antisense viral miRNAs (miRNA-AS) that are encoded antisense to previously reported KSHV pre-miRNAs. This work also shows that much of the KSHV genome is transcribed in both the top and bottom strand orientations during lytic replication. Despite the enormous potential to form double-stranded RNA in KSHV-infected cells, I observe no evidence for the existence of abundant viral-derived small interfering RNAs (siRNAs). From the small RNA deep-sequencing, I also detected a low abundant small RNA fragment (23 nt) that maps to a putative hairpin structure (named hairpin K) within the KSHV PAN transcript. I demonstrate that hairpin K is a cis-negative regulatory element in PAN. It is well-appreciated that viruses utilize host effectors for macromolecular synthesis and as regulators of viral gene expression. Viruses can encode their own regulators, but often utilize host-encoded factors to optimize replication. This work shows that Drosha, an endoribonuclease best known for its role in the biogenesis of miRNAs, can also function to directly regulate viral gene expression. Kaposin B (KapB) is a KSHV-encoded protein associated with cytokine production and cytotoxicity. I demonstrate that in addition to previously known transcriptional mechanisms, differences in Drosha levels contribute to low levels of KapB expression in latency and robust increases in expression during lytic replication. Thus, KSHV modulates Drosha activity differentially depending on the mode of replication. This regulation is dependent on Drosha-mediated cleavage, and KapB transcripts lacking the Drosha cleavage sites express higher levels of KapB resulting in increased cell death. This work increases the known functions of Drosha and implies that tying viral gene expression to Drosha activity is advantageous for viruses. / text

Interleukin (IL)-10-secreting regulatory Bcells(B10) are acknowledged to play important roles in balancing cellular immunity and fighting against autoimmune diseases. Since the early discovery of the potential of B cells in suppressing autoimmunity by secreting IL-10 in a murine model of experimental autoimmune encephalomyelitis(EAE),accumulating evidences have revealed the existence and regulatory function of B10 cells in the progression of several autoimmune diseases including multiple sclerosis (MS), lupus and autoimmune arthritis, suggesting potential values of therapeutic intervention. Autoimmune diabetes is an autoimmune disease in animal models characterized by progressive insulitis and mass destruction of βcells in pancreatic islets. However, the role of Bregsin the development of this disease remains largely unclear. To explore whether Bregs possess a regulatory function in suppressing diabetes, B10 cells were generated from B-cell activation factor (BAFF)-stimulated B cells of Non-obese diabetic (NOD)mice. Notably, NOD mice receiving B10 transfer exhibited delayed diabetes onset and substantially reduced incidence, suggesting some therapeutic effect against autoimmune diabetes. As an important contributor to inflammation and autoimmune disorders, the pathogenic function of IL-17 producing CD4+cells (Th17) in autoimmune diabetes has been increasingly identified, which attracts me to investigate whether B10 cells can contribute to amelioration of autoimmune diabetes via suppressing Th17 cells. During the development of autoimmune diabetes in NOD mice, both B10 and Th17 significantly increased at prediabetic stage and rapidly declined after disease onset. Upon adoptive transfer of B10 cells into prediabetic NOD mice, Th17 cells in pancreatic lymph nodes and pancreas were profoundly reduced. To verify whether B10 cells can directly inhibit Th17 generation in vitro, CFSE-dilution assay combined to Th17 polarization assay was performed. Results indicated that B10 cells suppress Th17 polarization in an IL-10 independent manner, but inhibit Th17 proliferation in an partially IL-10 dependent way. Finally I transferred B10 together with naive CD4+T cells reactive to islets into lymphopenic NOD-SCID mice and detected substantially reduced Th17 frequencies in pancreatic lymph nodes and pancreas, suggesting a potential way of developing new therapeutic strategies in treating Type 1 diabetes in humans. / published_or_final_version / Pathology / Master / Master of Philosophy

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There has been a movement towards research on the therapist and their capacity in providing treatment for eating disorders (Garner, 1985; Thompson & Sherman, 1989). This Doctoral Thesis Portfolio attempts to provide insight into therapy with the eating disordered population from therapists’ subjective experiences. It attempts to approach eating disorders from both a scientific and practitioner perspective using counselling psychology philosophy to understand and enlighten the therapeutic process when working with these clients. Rizq (2005) said that counselling psychology concentrates on two aspects in therapy, as it promotes the use of the therapist’s self as a tool for therapeutic change alongside adopting psychological theory for the enquiry of this experience. This portfolio will focus on the integration of these two aspects. Therapy with eating disorders was analysed from a theoretical, personal, and professional perspective. This will be explored in this portfolio via three individual components. Firstly, research is presented that investigated therapists’ emotional experience after sessions with a client being treated for anorexia. Secondly, the literature on alexithymia in anorexia is critically reviewed with particular reference to inform counselling psychology and to develop understanding of the therapeutic process with this client group. In the final section a case study will be presented in relation to the concept projective identification in order to illustrate the inter-subjective nature oftherapy with a bulimic client.

No description available.