Thesis (Ph. D.)--University of Hong Kong, 2008. / Also available in print.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leave 126-134). Also available in print.

Thesis (M. Phil.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves [59]-61).

Thesis--Columbia University.

Thesis--Wisconsin. / Vita. Includes bibliographical references (leaves 160-164).

Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2006. / Includes bibliographical references. Also available in electronic version.

No description available.

BACKGROUND: The piezoelectric knife was developed for atraumatic bone surgery utilizing ultrasonic vibrations as an alternative to mechanical instruments in conventional oral surgery. Recently it has been used in surgically facilitated orthodontics with Piezocision™. This technique requires alveolar decortication with the piezoelectric knife that cuts through the cortical bone to reach the medullary space. We hypothesized that Its clinical effectiveness is “depth dependent” hence the need to reach the medullary bone and not rely on a “superficial scratch”. This study tested the hypothesis that the extent of the regional acceleratory phenomenon (RAP) following bone injury is depth dependent by comparing superficial and deep corticotomies on the rat tibia. MATERIAL & METHOD: Twenty-six, 9-10 week male Sprague-Dawley rats, weighing approximately 300g, were used in this study approved by the Boston University Medical Center Institutional Animal Care and Use Committee. The piezoelectric knife (Piezotome 2, Acteon, BSL1 insert) with a fixed D 1 power setting and a 30Hz modulation frequency was used to create a decortication on the tibia of the animal. This procedure was carried out with a 1mm penetration depth on the right tibia (deep corticotomy reaching the medullary space) and 0.5mm penetration depth on the left tibia (shallow corticotomy not reaching the medullary space). Tissue response was analyzed at day 1, 3, 7, 14, and 28 using Hematoxylin/Eosin, Masson trichrome, TRAP and picro sirus red stains. Untreated rats were used as controls. The samples were fixed in 4% formaldehyde and the location of the surgical defect underneath the soft tissue was confirmed using Computed Tomography (CT). RESULTS: The CT image analysis was used to cut the samples with extreme precision in the sagittal plane and prepare the tissues for histological analysis. Hematoxylin & Eosin staining highlighted the following sequence of events: 1) establishment of a fibrin clot and granulation tissue (activation phase) 2) increased osteoclastic activity at the site of decortication (resorption phase) 3) increased osteogenic activity (formation phase). Deep corticotomy sites showed extensive morphological changes for both soft and hard tissues. They were characterized by significant osteoclastic activity at day 7 and intense angiogenesis visible both at the entry and exit of the surgical wound. In contrast, the shallow sites showed none of these findings. The new bone that formed at the deep corticotomy site in the medullary space resorbed by at day 14, while the new that bone formed below the periosteum persisted at day 28. None of these phenomena were observed at the shallow sites, where repair had occurred at day 14 or earlier showing minimal RAP activity. CONCLUSION: The extent of the RAP following bone injury is depth dependent. The deep corticotomy sites showed more dramatic biological responses than the shallow osteotomy sites.

A dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg. in fulfilment of the requirements for the degree of Doctor of Philosophy / This thesis describes and discusses oxidants and anti-oxidants and their relation to human disease. Cigarette smoking is used as the model for the study of chronic inflammatory processes, firstly, to establish a causative link between oxidants and disease viz. lung function abnormalities in smokers, secondly to evaluate the interaction between hyperactive phagocytes and anti-oxidant defences and thirdly, to investigate the possibility that intervention with anti-oxidants may ameliorate the effects of chronic inflammation. / IT2018

<p><strong>Introduction</strong></p> <p>The airway epithelium, which acts as a protective barrier, is impaired in asthmatic patients and may contribute to abnormal airway function. Chronic inflammation, a feature of asthma, is associated with structural changes in the airway epithelium including the transformation of columnar epithelial cells into mucin secreting goblet cells. Human epithelial cells exposed to Interleukin-13 (IL-13) <em>in vitro</em> resulted in goblet cell metaplasia and a significant drop in transepithelial resistance, indicating that barrier function is impaired.</p> <p><strong>Aim</strong></p> <p>We sought to determine whether goblet cell metaplasia alone is sufficient to impair airway epithelial barrier function <em>in vivo</em>.</p> <p><strong>Methods</strong></p> <p>Female BALB/c mice were infected with an adenovirus to overexpress IL-13, a control adenovirus, or no virus. Barrier integrity was assessed via single-photon emission computed tomography (SPECT) imaging by measuring the dispersion of technetium-labeled diethylene triamine pentaacetic acid (^99mTc-DTPA) out of the lungs over time. Lung sections were stained by Periodic acid-Schiff to detect the presence of mucin-containing goblet cells.</p> <p><strong>Results</strong></p> <p>IL-13 exposure resulted in goblet cell metaplasia and associated airway hyperresponsiveness to methacholine. However, there was no significant increase in dispersion of ^99mTc-DTPA over time from the airways in IL-13 overexpressed mice compared to control mice.</p> <p><strong>Conclusion</strong></p> <p>IL-13 induced goblet cell metaplasia did not impair the airway epithelial barrier to ^99mTc-DTPA in our <em>in vivo</em> mouse model. Therefore, we conclude that epithelial dysfunction to DTPA observed in human asthmatics and in animal models of asthma are not due to IL-13 induced goblet cell metaplasia.</p> / Master of Science (MSc)