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A nursing concern for patients with chronic obstructive airway disease (COAD) is to assist the patient/family in improving adaptation strategies and self-care abilities. Identification of emotional and behavioral characteristics impacting on symptoms and life quality may predict individuals at risk for greater utilization of health care resources. The purpose of this descriptive study was to apply Traver's Prediction Formula for Emergent Use to a more general COAD population to determine if the formula would accurately predict those subjects who have high versus low emergent use of institutional health care resources. Fifty subjects with a range of COAD severity were studied. Subjects completed instruments which measured symptoms and life quality: the Bronchitis-Emphysema Symptom Checklist and the Sickness-Impact Profile. Findings demonstrated Traver's Formula predicted low emergent subjects with 76 percent accuracy, high emergent subjects with 53 percent accuracy and predicted the overall emergent status of subjects with 67 percent accuracy.

A dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg for the degree of Master of Science in Medicine. / A study was undertaken to ascertain whether a low intensity, long term home walking exercise programme could produce physiological changes in patients with chronic obstructive pulmonary disease (COPD). Subjective psychological effects of such a programme were also evaluated. (Abbreviation abstract) / AC2017

Yeung Fai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 125-138). / Abstracts in English and Chinese; questionnaires also in Chinese. / Acknowledgement --- p.iii / Declaration --- p.iv / List of Tables --- p.v / List of Figures --- p.viii / Abstract --- p.ix / Abbreviation --- p.xiv / Chapter Chapter One --- Introduction / Background --- p.1 / Chapter 1.1 --- Definition / Chapter 1.2 --- Disease Prevalence / Chapter 1.3 --- Associated Disability / Chapter 1.4 --- Treatment-effectiveness / Chapter 1.5 --- Rehabilitation / Chapter Chapter Two --- Hong Kong Situation --- p.56 / Chapter 2.1 --- What is known --- Hong Kong elderly population database / Chapter 2.2 --- Service provision for the elderly in Hong Kong / Chapter Chapter Three --- Methodology --- p.68 / Chapter 3.1 --- Aims / Chapter 3.2 --- Subject and methodology / Chapter Chapter Four --- Results --- p.93 / Chapter 4.1 --- Results at baseline / Chapter 4.2 --- "Trend with time (0,12,48 weeks) between the exercise group and the control group" / Chapter 4.3 --- Results at first follow up (12 weeks) / Chapter 4.4 --- Results at second follow up (48 weeks) / Chapter 4.5 --- Results from baseline to second follow up within the exercise group or within the control group / Chapter Chapter Five --- Discussion --- p.113 / Chapter 5.1 --- Short-term efficacy of pulmonary program / Chapter 5.2 --- Long-term efficacy of pulmonary program / Chapter 5.3 --- The characteristics of pulmonary program / Chapter Chapter Six --- Conclusion --- p.124 / Reference --- p.125 / Appendix The Questionnaire Used in Interviews --- p.139

published_or_final_version / Nursing Studies / Master / Master of Nursing

Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD) with chronic airway inflammation as a key feature. Currently, no effective treatment can reduce the protracted inflammation in the lung of COPD. Further research on the inflammatory mechanisms would therefore be important in determining new potential therapeutic targets in COPD. Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter that plays an important role in pulmonary functions and inflammatory responses. The serotoninergic system including serotonin transporter (SERT), serotonin receptors (5-HTR) and its metabolic enzyme monoamine oxidase (MAO) have been reported to associate with cigarette smoking and/or COPD. Blockade of serotonin receptor 2A (5-HTR2A) with its selective antagonist ketanserin has been shown to improve lung function in COPD patients. In this study, we hypothesize that the serotoninergic system is involved in cigarette smoke-induced oxidative stress, inflammation and COPD. Exposure to cigarette smoke medium (CSM) caused the elevation of interleukin (IL)-8 levels in primary normal human bronchial epithelial (NHBE) cells and a human bronchial epithelial cell line (BEAS-2B) in vitro via activation of p38 and extracellular signal-regulated kinases 1 and 2 (ERK1/2) signaling pathway. Besides, CSM was found to disrupt the glutathione (GSH) system, resulting in the translocation of nuclear factor-erythroid 2 related factor 2 (Nrf2) to the nucleus. Knock-down of Nrf2 by small interference RNA (siRNA) blocked CSM-induced IL-8 release. Pretreatment with ketanserin was found to attenuate CSM-induced IL-8 release by inhibiting the p38, ERK1/2, and Nrf2 signaling pathways, and by partially restoring the GSH system. On the other hand, CSM reduced MAO activity in BEAS-2B, indicating a reduced catabolism of 5-HT. Furthermore, 5-HT was found to share the common p38 and ERK1/2 signaling pathway with CSM in IL-8 release. In the cigarette smoke-exposed rat model, the GSH system in the lung was found to be disrupted compared to the sham-air control, supporting our in vitro findings. Interestingly, we found an increased MAO-A activity in the lung of cigarette smoke-exposed rats in comparison to sham air-exposed rats. The increased MAO-A activity in the lung was associated with the reduction of 5-HT levels in bronchoalveolar lavage (BAL) and lung homogenates, while the increased metabolism of 5-HT may be involved in cigarette smoke-induced superoxide anion levels. On the other hand, serum, but not plasma level of 5-HT was elevated in cigarette smoke-exposed group, which may be due to platelet activation caused by cigarette smoke. In the clinical study, the elevated plasma 5-HT levels were found to be associated with an increased odds ratio for COPD and positively correlated with age in COPD patients. Furthermore, plasma 5-HT was also demonstrated to be a significant mediator on the relation between cigarette smoking and COPD. In summary, our study supports the hypothesis that the serotoninergic system contributes to cigarette smoke-induced oxidative stress, inflammation and COPD. The serotoninergic system (e.g. 5-HTR2A) may constitute potential therapeutic targets for the treatment of COPD, which is worthy for further investigation. / published_or_final_version / Medicine / Doctoral / Doctor of Philosophy

Chronic obstructive pulmonary disease (COPD) is one of the world’s most common chronic diseases, and consists of chronic bronchitis that involves chronic inflammation of the bronchi, or emphysema that involves destruction of lung alveoli. In COPD patients, the airways become narrowed, and the airflow is irreversibly obstructed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea), as well as abnormal inflammatory response in the lung. Nowadays, COPD is often under-diagnosed, as spirometry was not performed until patient has significant symptoms of dyspnea, cough and sputum production. At that stage, the COPD patients may have reached an advanced stage with considerable loss of lung function. Thus, biomarkers are of great interest for research and clinical purposes in COPD, especially for early diagnosis of COPD. In this study, the relationship between plasma levels of different biomarkers, including monocyte chemoattractant protein-1 (MCP)-1 (a primary chemoattractant biomarker), matrix metalloproteinase nine (MMP)-9, vascular endothelial growth factor (VEGF), and hepatocyte growth factor (HGF) (injury and repair biomarkers), and growth differentiation factor 15 (GDF)-15 (a novel biomarker), in 29 healthy ever-smokers and 116 COPD patients was investigated using commercially available enzyme-linked immunosorbent assay (ELISA) kits. We also investigated the correlations between these biomarkers and lung function. There were significant increases in plasma MCP-1, MMP-9, HGF and GDF-15 in COPD patients compared to healthy smokers. Among ever-smokers with or without COPD, plasma MCP-1, MMP-9 and HGF levels were inversely correlated with force expiratory volume in one second![FEV1 (% predicted)] after adjustment for age, smoking status and packyears smoked. Correlation was also found between plasma MCP-1 and HGF, plasma MMP-9 and HGF or GDF-15, plasma HGF and GDF-15 after adjustment for age, smoking status and pack-years smoked. Further multiple linear regression analyses demonstrated that plasma MMP-9 level increased with the COPD GOLD stages. In conclusion, our findings suggest that MMP-9 might be as an important biomarker for COPD initiation and progression. As this study provides only evidence of association rather than of causation, prospective studies are required to assess biological significance of these associations between the plasma biomarkers. / published_or_final_version / Medicine / Master / Master of Medical Sciences

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