Typescript (photocopy). / Digitized by Kansas Correctional Industries

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The aims of this project were to develop a system for monitoring a continuous stream of high grade purified water for potential contamination by bacterial endotoxins. The monitoring system was to be designed so that it could be readily integrated within a closed water purification processing system. The project was viewed as a developmental stage towards the development of a commercial sensor with wide ranging applications within the pharmaceutical and environmental sectors. This text details the development of testing protocols for the examination of ultra pure water using different sensing matrices. The endotoxin structure is comprised of three main sections with specific chemistry. These regions have each been considered as potential areas for detection. The development of surface plasmon resonance (SPR) systems and protocols for the detection of endotoxin was shown both to be possible and practical within given experimental parameters. In order to assess the potential for this sensing within a more established experimental system and to further expand the potential sensing layers for endotoxins, further experiments were carried out using a BIAcore system. The use of the BIAcore allowed the examination of alternative sensing surfaces based on the specific nature of the endotoxin molecule rather than the use of literature based reactants that have previously displayed an affinity for the endotoxin molecules. The methods used within this project have concentrated on the overall chemistry of the endotoxin molecule. The potential binding/complexing agents have been targeted at the three principal regions of the endotoxin structure using the chemical nature of these regions as an attractive surface to the sensing layer.

A research report submitted to the faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in the partial fulfillment of the requirements for the Degree of Master of Science in Dentistry, Johannesburg, 2017 / Chemotherapy and radiation therapy are the most widely used interventions for the treatment of cancer. Several adverse effects including mucositis are associated with these therapies, which affect a patient’s quality of life, resulting in morbidity and mortality. Cancer therapy also causes an imbalance in the oral flora which allows colonization of the oral cavity with uncommon bacteria, including aerobic gram negative bacteria and less commonly, Candida. These organisms can become established in the lesions of oral mucositis. These gram negative bacteria produce endotoxins. Although the involvement of endotoxins in the development of systemic infections is well described, the role of endotoxins in oral mucositis is not known. Therefore, this study investigated the presence of aerobic gram negative bacteria and endotoxins in the oral cavities of patients receiving cancer treatment and their role in the development of oral mucositis. Oral cavity rinse samples were collected from 100 cancer patients on cancer treatment and 50 healthy individuals. Ethical clearance was obtained from The Committee for Research on Human Subjects (Medical). The demographic and clinical data were recorded. Samples were serially diluted and cultured onto Mitis Salivarius Agar for Streptococci, Baird Parker Agar for Staphylococcus aureus, MacConkey Agar for aerobic gram negative bacteria (AGNB) and Chromagar for Candida species. Colony counts were obtained and the cultures of AGNB and Candida species were further identified at the species level using the API technique. An antimicrobial susceptibility test was performed on AGNB. Oral rinse samples were further tested for the presence of endotoxin using the Hycult Biotech Limulus Amebocyte Lysate (LAL) assay. Results were analysed using the Mann-Whitney and chi-square test. P-values of ≤ 0.05% were considered significant. Eighty percent of cancer patients were females with breast (58%) or cervical cancer (9%). The majority of these patients were on chemotherapy (61%), were receiving a combination of chemotherapeutic drugs and had completed many cycles of chemotherapy treatment. Twelve percent of patients had oral mucositis of various grades. Healthy individuals also comprised of mainly females (76%). All cancer patients and 98% of healthy individuals carried Streptococci. No significant difference in the carriage of S. aureus was found between the two groups. However, the Candida carrier rate was significantly high in cancer patients (55%) compared to the healthy (20%) individuals (p<0.01). Although the Candida counts were not different between the groups (p>0.05), cancer patients carried a variety of Candida species and some patients carried more than one type of Candida species in their oral cavity. In addition, C. glabrata was only found in cancer patients. Between the groups of cancer patients and healthy individuals, no significant difference in the carrier rate of AGNB was found (cancer 24% vs 14% healthy). However, cancer patients carried a variety of AGNB. Enterobacter cloacae and Klebsiella pneumonia was isolated from the oral cavities of both the study groups. These bacteria were resistant to many antibiotics. When the prevalence of these oral bacteria was compared between patients with and without oral mucositis, it was found that the percentage prevalence of Candida species was significantly high in patients with oral mucositis. A mean endotoxin concentration of 3.65ng/ml and 3.37ng/ml was detected in the oral rinse samples of cancer patients and healthy individuals respectively. The difference in the endotoxin between the two groups was not significant (p=0.5). Mean values of 4.1ng/ml and 3.53ng/ml were found in cancer patients with and without oral mucositis respectively. The difference in the quantities of endotoxins between the two groups was not significant (p=0.6). In addition, endotoxin present in cancer patients with AGNB (3.39ng/ml) and without AGNB (3.8ng/ml) was also not significantly different. These results suggest that although cancer patients carry aerobic gram negative bacteria and endotoxins in their oral cavities, they may not contribute in the exacerbation of oral mucositis. However, Candida species may contribute in the exacerbation of oral mucositis and therefore, during cancer treatment, it is important to take preventative measures to reduce the colonization of Candida to prevent infection. / MT2017

"December 2002" / Bibliography: leaves 99-118. / ix, 118 leaves : ill. (some col.), plates (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / The major aim of this study was to investigate the possible molecular mechanism of resistance against Bt-toxin based on observations that Bt-toxin binds to a soluble immune-defence component. The binding of Bt-toxin to glycosylated lipophorin in the gut was found to be consistent with a model where the toxin is inserted into the membrane by an endocytosis mechanism. In resistant insects, the primary Bt-target is an immune-complex in the gut lumen and at the peritrophic membrane, which inactivates the toxin by a coagulation process. / Thesis (Ph.D.)--University of Adelaide, Dept. of Applied and Molecular Ecology, 2003

M.S. / Physiology / There has been a controversy among both clinicians and physiologists for a long time concerning the effects of various toxins on the thyroid gland. / The first sentence serves as the abstract for this thesis. The poor quality of the text is due to the onion skin paper the thesis was scanned from.

Thesis (M. Phil.)--University of Hong Kong, 1988.

Porphyromonas gingivalis is a keystone periodontopathogen and its lipopolysacharide (LPS) is strongly associated with periodontal disease. A long-standing controversy occurs on the role of P. gingivalis LPS in induction of innate host response in different cell types. It has recently been found that P. gingivalis LPS displays remarkable heterogeneity with both tetra- (LPS1435/1449) and penta-acylated (LPS1690) lipid A structures. However, the potential effects of heterogeneous structures of P. gingivalis LPS on modulating host innate responses in human gingival fibrobalsts (HGFs) - the most abundant cells in gingiva remain unclear. To fulfill this research gap, a comprehensive study on the P. gingivalis LPS-HGFs interations was undertaken. The effects of P. gingivalis LPS1435/1449 and LPS1690 on the expression profiles of pro-inflammatory cytokines were investigated (Chapter III). P. gingivalis LPS1690 (not LPS1435/1449) significantly upregulated the expression of IL-6, IL-8 and TNF-α, suggesting that P. gingivalis LPS may differentially modulate the expression of pro-inflammatory cytokines. The effects of P. gingivalis LPS on the expression of MMPs 1-3 and TIMP-1, and regulation of MMP-3 were then determined (Chapter IV). P. gingivalis LPS1690 markedly induced MMP-3 expression through p38 MAPK and ERK signal pathways, whereas TIMP-1 was greatly upregulated by P. gingivalis LPS1435/1449. These findings suggest that P. gingivalis LPS heterogeneity may differentially modulate the expression and regulation of MMP-3. Based on these findings, the involvements of TLR2/4 and the downstream signaling pathways were explored (Chapter V). P. gingivalis LPS1690 induced TLR4 expression, whereas TLR2 was upregulated by P. gingivalis LPS1435/1449. NF-κB pathway played a dominant role in P. gingivalis LPS1690-induced expression of IL-6 and IL-8. These findings suggest that the two isoforms of P. gingivalis LPS critically interact with TLR2 and TLR4, and may determine the subsequent activation of signal transduction cascades that differentially modulate immuno-inflammatory response. P. gingivalis could thereby evade innate host defense and contribute to periodontal pathogenesis. To obtain a holistic profile of heterogeneous P. gingivalis LPS-HGFs interactions, a systems biology-based study through proteomics, metabolomics and bioinformatics approaches was undertaken (Chapter VI). Pro-inflammatory proteins (e.g. Cyclophilin, Annexins, IL-6 and Cathepsins) were induced by P. gingivalis LPS1690. In contrast, anti-inflammatory proteins (e.g. ANXA1, ANXA2 and Gal-1) were upregulated by P. gingivalis LPS1435/1449. P. gingivalis LPS1690 also induced antioxidant defense molecules like MnSOD and PRDXs. Secretomic analysis showed that immuno-inflammatory mediators, extra-cellular proteases and matrix proteins were differentially modulated by the two isoforms of P. gingivalis LPS as well. These findings demonstrate that host responses such as immuno-inflammatory activity, oxidative stress and anti-oxidant defense may be differentially modulated and regulated by the heterogeneous P. gingivalis LPS. Further study shows that P. gingivalis LPS1435/1449 and LPS1690 differentially modulate oxidative stress response and antioxidant expression, and differential regulation of MnSOD could be a critical determinant of periodontal homeostasis (Chapter VII). The present findings may bring new insight into the molecular mechanisms of periodontal pathogenesis. Targeting the mechanisms of shift in lipid A structures of P. gingivalis LPS may be a potential strategy to develop novel approaches to control and prevent periodontal diseases. / published_or_final_version / Dentistry / Doctoral / Doctor of Philosophy

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