Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory disease characterized by airway inflammation and abnormal alveolar enlargement. It is the third leading cause of death around the world. Although extensive research efforts have been made, there is still no curable treatment available for lung tissue damage in patients with COPD. Therefore, it is of great significance to elucidate the mechanisms of tissue damage and repair in COPD. As the first barrier against environmental insults and pathogens, pulmonary epithelial cells play an essential role in regulating injury response and repair. However, how pulmonary epithelial cells contribute to irreversible alveolar destruction in COPD is not well understood. In this study, we elucidated the mechanisms of epithelial cell damage in both cigarette smoke-induced COPD and alpha1 antitrypsin deficiency (AATD)-associated genetic COPD. To investigate alveolar epithelial cell damage and repair in cigarette smoke-induced emphysema, a lineage tracing model was utilized to fluorescently label and chase alveolar type II (AT2) epithelial cells, the adult progenitor cells in the alveolar epithelium. An assessment of cigarette smoke-induced changes in cellular composition and regenerative capacity of the alveolar epithelial cells was performed. Cigarette smoke was found to impede the AT2-directed alveolar epithelial regeneration and repair process, and this impaired progenitor cell function was not restored after smoke cessation. Moreover, comparison analysis between stains that are sensitive and resistant to smoke-induced damage revealed that deficiency in lipid metabolism may contribute to the dysregulation of alveolar epithelial repair by AT2 cells. Restoring alveolar progenitor functions through lipid metabolism may serve as a novel therapeutic for alveolar destruction in smoke-induced COPD. To explore the mechanism of epithelial damage in AATD-associated genetic COPD, we utilized a PiZ (p.Glu342Lys) transgenic mouse model expressing human ZAAT protein. Morphometric analysis of PiZ lungs suggests that the accumulation of ZAAT polymers in the lung directly leads to the spontaneous development of emphysema. To investigate epithelial damage induced by zAAT accumulation, we isolated the epithelial cell population from the lung of PiZ mice. We identified epithelial-specific expression of cleaved caspase 3, indicating a direct cytotoxic effect of ZAAT in impairing epithelial function and inducing epithelial cell death. Future therapeutics could directly target the cytotoxicity of pulmonary epithelial cells in AATD to reduce lung tissue damage. Overall, our findings suggest that pulmonary epithelial damage plays an essential role in the pathogenesis of lung tissue damage in COPD. Future epithelial cell-based therapies may contribute to pulmonary re-epithelialization and tissue repair in both cigarette smoke-induced and AATD-associated COPD.

Thesis (PhD (Sport Science))--Stellenbosch University, 2008. / The benefits of exercise training for patients with chronic obstructive pulmonary disease (COPD) are well-documented. In South Africa, exercise programmes for COPD patients are limited and often expensive and inaccessible to the broader community. The purpose of this study was to assess the responses of COPD patients to an exercise programme and to determine if the same results can be obtained through a less costly programme. In the primary programme of the study, 22 subjects were subjected to 12 weeks of exercise training. Each subject underwent comprehensive pre- and post-intervention assessments, which included the measurement of overall health status by a physician, level of dyspnoea, forced expiratory lung function, exercise capacity, body mass index and health-related quality of life. Exercise sessions included aerobic and strength training exercises and involved three, hour-long exercise sessions a week. In the modified programme, 18 subjects were randomly divided into an experimental and control group. Eleven subjects were included in the experimental group and seven subjects in the control group. Subjects had to complete 32, hour-long exercise sessions in a 10-week period. The experimental group’s exercise programme was adapted so that no specialised equipment was used, while the control group exercised in a well-equipped exercise- and rehabilitation centre.

Thesis (MScSportSc)--University of Stellenbosch, 2004. / ENGLISH ABSTRACT: The purpose of the study was to measure the responses of chronic obstructive pulmonary disease patients to an exercise programme in a South Africa setting. Nine subjects were evaluated before and after aerobic and resistance training three times a week for the total of 12 weeks. Each evaluation measured forced expiratory lung function; health-related quality of life; functional capacity; level of dyspnea; body composition; physician global evaluation; and the patient global evaluation. The exercise programme consisted of one-hour exercise sessions, three times a week for 12 weeks. The exercise sessions included elements of aerobic and resistance training of the upper and lower extremities. Functional capacity improved drastically (p < 0.01), as did the physician and the patient global evaluations (p < 0.01 and p < 0.01, respectively). Levels of dyspnea also improved (p < 0.01). Health-related quality of life improved marginally (p = 0.03). No significant change was noted in lung function and body composition. The study concluded that an exercise programme consisting of aerobic and resistance training improves chronic obstructive pulmonary disease patients' health-related quality of life, functional capacity and levels of dyspnea. Exercise also reduces the symptoms of chronic obstructive pulmonary disease as are perceived by the physician and patient alike. Exercise does not change lung function or body composition of chronic obstructive pulmonary disease patients. Exercise in conjunction with appropriate medical treatment has the potential to benefit all chronic obstructive patients in South Africa. Keywords: COPD, quality oflife, functional capacity, rehabilitation, exercise. / AFRIKAANSE OPSOMMING: Die doel van die studie was om die reaksies te meet van pasiënte met chroniese obstruktiewe pulmonêre siekte op 'n oefenprogram in 'n Suid-Afrikaanse konteks. Nege proefpersone is voor en na aërobiese en weerstandsoefening drie keer per week vir 'n totaal van 12 weke geëvalueer. Elke evaluering het die volgende gemeet: geforseerde ekspiratoriese longfunksie, gesondheidsverwante lewenskwalitiet, funksionele kapasiteit; dispneevlak, liggaamsamestelling; geneesheer algehele evaluering asook pasiënt algehele evaluering. Die oefenprogram het uit een-uur sessies bestaan, wat drie keer per week vir 12 weke plaasgevind het. Die oefensessies het elemente van aërobiese en weerstandsoefeninge van die boonste en onderste ledemate ingesluit. Funksionele kapasiteit het drasties verbeter (p < 0.01), net so ook die geneesheer en pasiënt algehele evaluerings (p < 0.01 en p < 0.01, respektiewelik). Dispneevlakke het ook verbeter (p < 0.01). Gesondheidsverwante lewenskwaliteit het marginaal verbeter (p = 0.03). Geen beduidende veranderinge is in die longfunksie en liggaamsamestelling gevind nie. Die studie het bevind dat 'n oefenprogram wat uit aërobiese en weerstandsoefening bestaan gesondheidsverwante lewenskwaliteit, funksionele kapasiteit asook dispneevlakke van pasiënte met chroniese obstruktiewe pulmonêre siekte verbeter. Oefening verminder ook die simptome van chroniese obstruktiewe pulmonêre siekte soos waargeneem deur beide die geneesheer en pasiënt. Oefening verander ook nie longfunksie of liggaamsamestelling van pasiënte met chroniese obstruktiewe pulmonêre siekte nie. Oefening tesame met die geskikte mediese behandeling kan voordelig wees vir chronies obstruktiewe pasiënte in Suid- Afrika. Keywords: KOPS, lewenskwaliteit, funksionele kapasiteit, rehabilitasie, oefening.

The present study was initiated to evaluate the pulmonary inflammatory and fibrotic responses induced by single and repeated exposures to glass fibers. Single and repeated intratracheal injections of glass fibers induced an acute inflammatory response which progressed to a chronic inflammatory and fibrotic response. Mice exposed to glass fibers in single or repeated doses demonstrated elevated numbers of eosinophils, neutrophils and macrophages and increases in cell-free protein in lung lavage fluid at five days post-exposure. These parameters, in addition to relative lung/body weight ratios and lung tissue hydroxyproline levels, were elevated in comparison to saline control animals at five weeks post-exposure. Although repeated exposures to glass fibers did not potentiate the cellular inflammatory response, they did induce a marked infiltration of eosinophils, a response not observed with either asbestos or silica exposures. These observations suggest that glass fibers may be more toxic to the lungs than previously thought.

Thesis (MScEng)--Stellenbosch University, 2013. / ENGLISH ABSTRACT: Pleural effusion is a common respiratory condition that is characterized by an abnormal collection of fluid in the lung cavity. In this study, an innovation using the transmission of sound into the respiratory system as a novel tool to detect fluid in the lung was developed. First, the method was evaluated on a phantom model of a lung. Based on the results of this test model, the appropriate technique was used in a clinical study. This method has several advantages, such as that is non-invasive, low cost, and easy for clinical review. Two techniques, including analysis of the frequency response of the model and the transient time of transmitted sound in the lung, were evaluated in the phantom models of the human lung. Two phantom models with similar geometry to the human lung, including a healthy model (without fluid in the model) and a pleural effusion model (with bulk of fluid in the model) were developed. These models have acoustical properties similar to the lung parenchyma. To obtain the frequency responses of the model, a sine sweep signal was transmitted into the model and the frequency response of the model was then calculated using the fast Fourier transform. The transient time of the transmitted sound was calculated using a cross correlation method. The results show that the locations of fluid in the model were detectable using both techniques. However, the transient time technique is better than the frequency response technique because it is simple, fast, and has potential for use in a clinical enviorment. Based on the results obtained from the phantoms, the transient time method was performed on both 22 healthy participants and four patients diagnosed with pleural effusion. To perform this technique on human subjects, a data acquisition system was developed. Two types of sound, including a complex chirp sound and a polyphonic sound, were transmitted into the respiratory systems of the participants. The time delay between a reference microphone, located on the trachea of the subject, and eight microphones attached to the chest was computed using a cross correlation method, and the effect of inhalation and lung size on the transient time of transmitted sound on the healthy subject was evaluated. The results show that using transmission of sound in the lung is a promising technique in the diagnosis of pleural effusion. / AFRIKAANSE OPSOMMING: Pleurale effusie is 'n algemene respiratoriese toestand wat gekenmerk word deur 'n abnormale versameling van vloeistof in die longholte. In hierdie studie is 'n innoverende manier ontwikkel om vloeistof in die long met behulp van die transmissie van klank te bespeur. Die metode is eers op 'n fantoommodel van 'n long geëvalueer. Op grond van die resultate van hierdie toetsmodel is die geskikte tegniek in 'n kliniese studie gebruik. Hierdie metode het verskeie voordele, soos dat dit ingreepsvry is, nie duur is nie en kliniese evaluering moontlik maak. Twee tegnieke, naamlik ontleding van die frekwensierespons van die model en die oorgangstyd van versende klank in die long, is in die fantoommodel van die menselong geëvalueer. Twee fantoommodelle met soortgelyke geometrie aan die menselong, met inbegrip van 'n gesonde model (sonder vloeistof in die model) en 'n pleurale-effusie-model (met 'n massa vloeistof in die model), is ontwikkel. Hierdie modelle het akoestiese eienskappe soortgelyk aan die longparenchiem. Om die frekwensieresponse van die model te verkry, is 'n sinuskrommesein tot in die model versend. Die frekwensierespons van die model is met behulp van die vinnige Fourier-transformasie bereken. Die oorgangstyd van die versende klank is deur 'n kruiskorrelasie-metode bereken. Die resultate toon dat die ligging van die vloeistof in die model met albei tegnieke bespeur kan word. Die oorgangstyd-tegniek is egter beter as die frekwensierespons-tegniek, aangesien dit eenvoudig en vinnig is en maklik in 'n kliniese omgewing gebruik kan word. Op grond van die resultate wat van die fantome verkry is, is die oorgangstyd-metode op 22 gesonde deelnemers en vier pasiënte wat met pleurale effusie gediagnoseer is, uitgevoer. 'n Dataverkrygingstelsel is ontwikkel ten einde hierdie tegniek op proefpersone uit te voer. Twee soorte klank, naamlik 'n komplekse tjirpgeluid en 'n polifoniese klank, is na die respiratoriese stelsels van die deelnemers versend. Die tydvertraging tussen 'n verwysingsmikrofoon in die tragea van die proefpersoon en agt mikrofone wat aan die bors vasgeheg is, is met 'n kruiskorrelasie-metode bereken, en die uitwerking van inaseming en longgrootte op die oorgangstyd van versende klank op die gesonde proefpersone is geëvalueer. Die resultate toon dat die gebruik van transmissie van klank in die long 'n belowende tegniek vir die diagnose van pleurale effusie is.

Hospital readmission rates are considered to be an important indicator of quality of care because they may be a consequence of actions of commission or omission made during the initial hospitalization of the patient, or as a consequence of poorly managed transition of the patient back into the community. The negative impact on patient quality of life and huge burden on healthcare system have made reducing hospital readmissions a central goal of healthcare delivery and payment reform efforts. In this project, we will focus on COPD (Chronic Obstructive Pulmonary Disease) which is one of the leading causes of disability and mortality worldwide. This project will design and develop a prognostic COPD healthcare management system which is a sustainable clinical decision-support system to reduce the number of readmissions by identifying those patients who need preventive interventions to reduce the probability of being readmitted. Based on patient’s clinical records and discharge summary, our system would be able to determine the readmission risk profile of patients treated for COPD. Suitable interventions could then be initiated with the objective of providing quality and timely care that helps prevent avoidable readmission. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2014. / FAU Electronic Theses and Dissertations Collection

Orientador: Silke Anna Theresa Weber / Banca: Camila Renata Corrêa Camacho / Banca: Márcia Guimarães da Silva / Banca: Ricardo Beneti / Banca: Aline Roberta Danaga / Resumo: Introdução: A prevalência da DPOC e da SAOS e o comportamento das atividades inflamatória e metabólica destas doenças, isoladamente, já foi estudada. Entretanto, a sobreposição entre elas (Overlap) e a associação com a obesidade, ainda necessita de investigações. Objetivos: Verificar a incidência da SAOS em portadores de DPOC obeso e as atividades inflamatória e metabólica desta tríade. Métodos: Foram incluídos portadores de DPOC moderado e grave com índice de massa corpórea (IMC) ≥ 27 Kg/cm2 . Além da espirometria que classificou a DPOC, foi realizada polissonografia que diagnosticou ou não a SAOS. Foram avaliados os marcadores bioquímicos de glicemia, hemoglobina glicada (HBC), insulina, leptina, adiponectina, grelina, proteína C-reativa (PCR) e interleucina 6 (IL-6). Resultados: Este estudo transversal incluiu portadores de DPOC com (N=46) e sem (N=20) SAOS com médias de idade, IMC e VEF1, respectivamente, 61.57±11.31 x 59.75±9.68 anos, 34.00±5.67 x 33.89±6.75 kg/cm2, 57.20±16.81 x 53.85±17.65 %pred. As médias de glicemia, HBC, insulina, leptina e adiponectina com ou sem SAOS foram semelhantes. A grelina aumentou com a maior gravidade da SAOS na overlap (186.16±25.56 x 137.10±21.78 pg/ml). Não foi observado aumento da PCR para nenhum grupo. A maior gravidade da DPOC aumentou a IL-6 (5.17±5.79 x 11.18±13.10). Conclusão: A prevalência de SAOS é elevada em pacientes portadores de DPOC com obesidade. A SAOS grave elevou a atividade metabólica pelo aumento da grelina, sem influencia na expressão inflamatória, na tríade com DPOC e obesidade. A gravidade da DPOC produziu maior atividade inflamatória de IL-6. / Abstract: Introduction: The prevalence of COPD and OSA and the behaviour of inflammatory and metabolic activities of each diseases has already been studied. However, the overlap between OSA and COPD, associated to obesity, still needs investigation. Objectives: To determine the incidence of OSA in obese patients with COPD, and inflammatory and metabolic activities of this triad. Methods: moderate and severe COPD patients were included with a body mass index (BMI) ≥ 27 kg / cm2. In addition to spirometry which ranked COPD, polysomnography was performed for OSA diagnosis. Blood glucose, glycated hemoglobin (GH), insulin, leptina, adiponectin, ghrelin, C-reactive protein (CRP) and interleukin 6 (IL-6) were assesed. Results: This cross-sectional study included COPD patients with (N = 46) and without (N = 20) OSA mean age, BMI and FEV1, respectively, 61.57 ±11.31 x 59.75 ±9.68 years, 34.00 ±5.67 x 33.89 ±6.75 kg/cm2, 57.20 ±16.81 x 53.85 ±17.65% pred. Mean blood glucose, GH, insulin, adiponectin and leptin with or without OSA were similar. Ghrelin increased with greater severity of OSA in the overlap group(186.16 ±25.56 x 137.10 ±21.78 pg/ml). There was no difference for CRP, but IL-6 (5.17 ±5.79 x 18.11 ±10.13) was increased in the more severe COPD. Conclusion: The prevalence of OSA is high in COPD patients with obesity. The severe OSAS increased metabolic activity by increasing ghrelin. The severity of COPD produced greater inflammatory activity. / Doutor

Orientador: Alexandra Ivo de Medeiros / Banca: Alexandre Salgado Basso / Banca: Alexander Batista-Duharte / Resumo: A fagocitose, por células dendríticas (CD), de células apoptóticas (CA) infectadas induz a produção de TGF-β, IL-6 e IL-23, propiciando um microambiente com condições ideais para diferenciação de células Th17. Recentes resultados obtidos por nosso grupo demonstram que a fagocitose, por CD, de células apoptóticas infectadas resulta também na produção de altos IL- 1 e PGE2. A presença destes mediadores solúveis foi capaz de induzir a diferenciação de células Th17, in vitro, no entanto, a inibição da síntese de PGE2, pelo tratamento com inibidor não seletivo da COX (Indometacina), resultou no aumento da porcentagem destes linfócitos. Neste estudo foi avaliado o efeito da fagocitose de células apoptóticas infectadas com Escherichia coli (CA+Ec) na diferenciação de células Th17 in vivo e o efeito de PGE2 neste processo. A instilação de animais com CA+Ec, induziu a produção das citocinas IL-6, IL-1β e TGF-β no pulmão, o que sugere que a presença de CA+Ec é capaz de gerar um microambiente favorável para induzir a diferenciação Th17. A instilação de CA+Ec promoveu a diferenciação de células Th17, assim como a produção de IL-17. Porém, o tratamento com inibidor de COX resultou no aumento na porcentagem e no número de células Th17 no pulmão. A presença destas células resultou no aumento na porcentagem de neutrófilos no tecido pulmonar que parece refletir na diminuição da carga bacteriana recuperada do pulmão, quando comparado com animais que não receberam o tratamento. Assim, o conjunto destes resultados sugere que a fagocitose de CA+E. coli promove a diferenciação de células Th17. No entanto, a secreção de PGE2, pela fagocitose destas CA+Ec suprime a diferenciação e/ou migração de células Th17 para o pulmão, levando a inibição do recrutamento de neutrófilos e aumento da suscetibilidade às infecções pulmonares. / Abstract: The phagocytosis of infected-apoptotic cells (iAC) by dendritic cells (DC) induces the production of TGF-β, IL-6 and IL-23, providing a microenvironment to Th17 cell differentiation. Recent data obtained in our group showed that the phagocytosis of infected- apoptotic cells by CD also results in high levels of IL-1β and PGE2. The presence of these soluble mediators was able to induce the differentiation of Th17 cells, in vitro. However, the inhibition of PGE2 synthesis, by non-selective COX inhibitor (indomethacin), result the increase of percentage of Th17. In this study, it was evaluated the effect of phagocytosis of infected-apoptotic cells (AC+E. coli) during the Th17 cell differentiation, in vivo, and the effect of PGE2 in this process. The inoculation of AC+ Ec (in.) into lung induced the production of IL-6, IL-1β and TGF-β in lung, suggesting that the presence of AC+Ec is able to induce a microenvironment favorable to Th17 cell differentiation. The instillation of AC+Ec induced the differentiation of Th17 cells. However, the treatment of the animals with COX inhibitor resulted in an increase in the percentage, and number, of Th17 cells in the lung. The presence of these cells increased in the percentage of neutrophils in the lung and that apparently reflect in bacterial clearance from the lung, compared to animals that received no treatment. Taken all together, the phagocytosis of AC+Ec promotes the Th17 cell differentiation. However, the production of PGE2 by efferocytosis suppresses the differentiation and / or migration of Th17 cells to the lungs, impair the recruitment of neutrophils and increase the susceptibility to lung infections. / Mestre

by Martin Li. / Year shown on spine: 1997. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 150-157). / DECLARATION --- p.II / ABSTRACT --- p.III / ACKNOWLEDGEMENTS --- p.VII / CONTENTS --- p.VIII / LIST OF ABBREVIATIONS --- p.XIV / LIST OF TABLES --- p.XVI / LIST OF CHART --- p.XXIII / LIST OF FIGURES --- p.XXIV / Chapter CHAPTER 1 --- OBSTRUCTIVE AIRWAY DISEASE: PUBLIC HEALTH AND CLINICAL ASPECTS --- p.1 / Chapter 1.1. --- Background --- p.1 / Chapter 1.2. --- Magnitude of the problem --- p.2 / Chapter 1.2.1. --- Asthma --- p.2 / Chapter 1.2.2. --- Chronic obstructive pulmonary disease --- p.3 / Chapter 1.2.3. --- Prevalence of osteoporosis in Hong Kong --- p.4 / Chapter 1.2.4. --- History of asthma care --- p.5 / Chapter 1.2.5. --- Treatment of OAD --- p.5 / Chapter 1.3. --- Side effects of Glucocorticoid in OAD patients --- p.6 / Chapter 1.4. --- Side effccts of inhaled corticosteroids in OAD patients --- p.7 / Chapter 1.5. --- Trend of asthma therapy in Hong Kong --- p.8 / Chapter CHAPTER 2: --- OSTEOPOROSIS: PUBLIC HEALTH AND CLINICAL ASPECTS --- p.11 / Chapter 2.1. --- Bone Biology --- p.11 / Chapter 2.2. --- Skeletal Organisation --- p.11 / Chapter 2.3. --- Bone remodelling --- p.12 / Chapter 2.4. --- Effect of corticosteroids on bone remodelling --- p.13 / Chapter 2.5. --- Corticosteroids induccs osteoporosis --- p.13 / Chapter 2.6. --- Factors affecting BMD --- p.14 / Chapter 2.6.1. --- Peak bone mass --- p.14 / Chapter 2.6.2. --- Ethnic factors --- p.14 / Chapter 2.6.3. --- Aging --- p.15 / Chapter 2.6.4. --- Calcium intake --- p.15 / Chapter 2.6.5. --- Oestrogen --- p.16 / Chapter 2.6.6. --- Alcohol consumption --- p.17 / Chapter 2.6.7. --- Cigarette smoking --- p.17 / Chapter 2.7. --- Physical activity and BMD --- p.17 / Chapter 2.8. --- Body composition in Chinese subjects --- p.18 / Chapter CHAPTER 3 --- "PHASE I: BODY COMPOSITION AND BONE MINERAL DENSITY IN OBSTRUCTIVE AIRWAY DISEASE PATIENT AND NORMAL CONTROL SUBJECTS: OBJECTIVES, SUBJECTS AND METHODS" --- p.20 / Chapter 3.1. --- Objectives --- p.20 / Chapter 3.2. --- Subjects and methods --- p.21 / Chapter 3.2.1 --- OAD patients --- p.21 / Chapter 3.2.1.1 --- Disease definition and selection criteria --- p.21 / Chapter 3.2.1.2. --- Normal Control subjects --- p.21 / Chapter 3.3. --- Power of estimation --- p.22 / Chapter 3.4. --- Survey methods --- p.22 / Chapter 3.5. --- Questionnaire --- p.23 / Chapter 3.6. --- Body composition and bone mineral density measurement --- p.23 / Chapter 3.6.1. --- Body composition analysis --- p.24 / Chapter 3.6.2. --- Lumbar spine and proximal hip bone mineral density analysis --- p.24 / Chapter 3.6.3. --- Routine quality control of measurements --- p.24 / Chapter 3.6.4. --- Precision on patient repositioning --- p.25 / Chapter 3.7. --- Statistical methods --- p.25 / Chapter 3.8. --- Bone mineral density of normal control subjects --- p.25 / Chapter CHAPTER 4 --- PHASE II: FLUORIDE IN THE TREATMENT OF OSTEOPOROSIS --- p.27 / Chapter 4.1. --- Introduction --- p.27 / Chapter 4.2. --- Mechanisms of action --- p.28 / Chapter 4.2.1. --- Antiresorptive effect of fluoride --- p.28 / Chapter 4.2.2. --- Force-oriented osteogenic effect of fluoride --- p.28 / Chapter 4.2.3. --- Biochemical osteogenic effect --- p.29 / Chapter 4.3. --- Effect of fluoride salts on BMD: results of clinical trials --- p.29 / Chapter 4.4. --- Effcct of fluoride on bone histomorphology --- p.30 / Chapter 4.5. --- Compliance with sodium fluoride therapy --- p.31 / Chapter 4.6. --- Contradiction of fluoride treatment --- p.31 / Chapter 4.7. --- Sodium monofluorophosphate preparation --- p.32 / Chapter CHAPTER 5 --- PHASE II: THE EFFECTS OF FLUORIDE ON BONE MINERAL DENSITY OF OAD PATIENTS ON STEROID TREATMENT --- p.37 / Chapter 5.1. --- Objectives --- p.37 / Chapter 5.2. --- Subjects and methods --- p.37 / Chapter 5.2.1. --- Power of the study --- p.37 / Chapter 5.2.2. --- Subjects --- p.37 / Chapter 5.2.3. --- Method of randomisation --- p.38 / Chapter 5.2.4. --- Treatment modalities --- p.39 / Chapter 5.2.4.1. --- Treatment group --- p.39 / Chapter 5.2.4.2. --- Control group --- p.39 / Chapter 5.2.5. --- Bone mineral density measurements --- p.39 / Chapter 5.2.6. --- Routine quality control of measurement and precision on patient repositioning --- p.40 / Chapter 5.2.7. --- Methods of monitoring drug compliance --- p.40 / Chapter 5.2.8 --- Statistical methods --- p.40 / Chapter CHAPTER 6 --- RESULTS FOR PHASE I --- p.42 / Chapter 6.1. --- Statistical power of this phase of the study --- p.42 / Chapter 6.2. --- Clinical features of OAD subjects on inhaled steroid --- p.42 / Chapter 6.3. --- Anthropometric measurements and bone mineral density --- p.45 / Chapter 6.4. --- Analysis of covariance for BMDs differences --- p.48 / Chapter 6.5. --- Multiple regression --- p.50 / Chapter 6.6 --- Correlation --- p.51 / Chapter CHAPTER 7 --- RESULTS FOR PHASE II: FLUORIDE AND CALCIUM TRIAL --- p.81 / Chapter 7.1. --- Factors affects the power of studies --- p.81 / Chapter 7.2. --- Clinical findings --- p.82 / Chapter 7.3. --- Body measurements and bone mineral densitometry --- p.85 / Chapter CHAPTER 8: --- DISCUSSION FOR PHASE I --- p.117 / Chapter CHAPTER 9: --- DISCUSSION FOR PHASE II: TRIDIN AND CALCIUM TRIAL --- p.124 / APPENDIX 1: QUESTIONNAIRE FOR OAD BONE MINERAL DENSITY STUDY --- p.132 / APPENDIX 2: BONE SCANS FROM HOLOGIC QDR2000 --- p.137 / APPENDIX 3. TABLES AND REFERENCE CURVES FOR NORMAL HONG KONG CHINESE FEMALE OR MALE BMD --- p.142 / REFERENCE --- p.150

Thesis. 1976. Sc.D.--Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Vita. / Includes bibliographical references. / Sc.D.