Thesis (M.P.H.)--University of Adelaide, Dept. of Community Medicine, 1988. / Includes bibliographical references (leaves 161-192).

Senior Honors Thesis (Nursing)--Ohio State University, 2004. / Title from first page of PDF file. Document formatted into pages; contains 20 p.; also includes graphics Includes bibliographical references (p. 15-18 ).

Thesis (M. Phil.)--University of Hong Kong, 1994. / Includes bibliographical references (leaves 192-201).

Thesis (M.P.H.)--University of Hong Kong, 2009. / Includes bibliographical references (p. 96-110).

Thesis (MSocSc)--University of South Australia, 1995

Thesis (Ph. D.)--University of Adelaide, Dept. of Community Medicine, 1988. / Includes bibliographical references (leaves 215-236).

Nasal AEC cultures were established from children (0.6-14.9 years) undergoing elective surgical procedures under general anaesthetic, categorised as atopic asthmatics (n=12), virus-induced wheezers (n=8) or healthy controls (n=32) using questionnaire and serum IgE levels. All subjects were free of current respiratory symptoms. Successful AEC cultures were maintained to passage 2 or 41 (79%) subjects. AEC from children with a history of wheeze produced significantly less IL-8, IL-6, MCP-1 and G-CSF than AEC from healthy controls. When the wheezing phenotypes were considered separately, AEC from atopic asthmatic children released significantly less IL-8, IL-6, MCP-1 and G-CSF than AEC from controls but there were no significant differences between AEC mediator release from children with virus-induced wheeze and either atopic asthmatics or controls. Similar results were found for cytokine-stimulated AEC. In non-wheezy subjects, there were no differences in AEC mediator release between atopic and non-atopic individuals. There were no differences between the study groups in the percentage increments in mediator release in response to stimulation. In multivariate analysis, taking into account age, gender, passive smoke exposure, use of inhaled corticosteroids, total serum IgE and specific responses to inhaled aeroallergens as possible confounders, wheeze was the only significant predictor of AEC mediator release. It was concluded that there are intrinsic differences in AEC from children with a history of wheeze compared to healthy controls and these are independent of atopic status. This study provides further evidence that the airway epithelium is implicated in the pathogenesis of childhood wheezing. It is hypothesised that different systemic factors, such as atopy and viral responsiveness, interact with common epithelial abnormalities to give rise to different wheezing phenotypes. Further work is required to establish whether these abnormalities are primary or secondary and to confirm these findings in well-differentiated AEC cultured with an air-liquid interface.

The effects of household exposure to cigarette smoke on the incidence of respiratory illness were examined among 1007 18 month old children at Lu-wan District, Shanghai City, People's Republic China. The passive smoking quantity was estimated by summing the total daily cigarette consumption of family members. No mothers who smoked were found. A significant dose-response relationship of passive smoking to hospitalization for respiratory illness during the children's first 18 months of life was found, for which no confounding factors were discovered. The relative risk was 2.4 for children living in families including people who smoked 20 or more cigarettes a day compared with those living in nonsmoking families. The children who were boys or artificially (bottle) fed were more affected than those who were girls or breast fed. The cumulative incidence of bronchitis and pneumonia increased significantly with increasing cigarette smoking of family members, that did not change when sex, birth weight, type of feeding, coal for cooking, or parental education were taken into account. Family smoking status was not found to be significantly associated with the cumulative incidence of asthma, whooping cough, sinusitis or measles. / Graduation date: 1993

published_or_final_version / Community Medicine / Master / Master of Public Health

The present study was performed to determine whether ongoing oxidative stress in some BPD infants contributes to their increased energy expenditure leading to growth failure. The study consisted of two parts. The first is a descriptive census of BPD infants (n = 38) followed at the outpatient clinics at The Montreal Children's Hospital (MCH). The second is a cross-sectional study of fifteen patients wherein anthropometric parameters, energy intake, and oxidative stress measures (red cell glutathione (GSH) and plasma malondialdehyde (MDA)) were assessed. Nine infants with growth failure were compared to six thriving infants with respect to their nutritional and oxidative stress status. Growth failure was defined as weight for age and weight for height for age less than the tenth percentile (z score $ leq - 1).$ Results revealed that the prevalence of growth failure in the BPD infants followed at MCH ranged between 45% and 55%. The mean ($ pm$ SD) energy intakes for thriving and failing to thrive infants expressed as a percent of the recommended nutrient intake were 104 $ pm$ 46% and 133 $ pm$ 35% respectively. Six infants had reduced mean ($ pm$ SD) blood glutathione per hemoglobin (3.63 $ pm$ 0.37 umol/g) compared to adult controls (6.57 $ pm$ 1.04 umol/g). Four of the six infants had growth failure while two were thriving. Fourteen Infants including all failing to thrive infants had elevated mean ($ pm$ SD) plasma MDA levels compared to adult controls (129 $ pm$ 48 vs 55 $ pm$ 3 nmol/l). Differences in oxidative stress markers were not observed between the two groups. These results suggest that growth failure is associated with an increase in caloric consumption and not with a decrease in caloric intake. The preliminary findings on oxidative stress markers suggest a depletion of the GSH antioxidant in some infants and marked lipid peroxidation in the BPD population.