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1
McAllister, David Anthony. "Chronic obstructive pulmonary disease, pulmonary function and cardiovascular disease". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5615.
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Cardiovascular disease is common in Chronic Obstructive Pulmonary Disease (COPD), and forced expiratory volume in one second (FEV1) independently predicts cardiovascular morbidity and mortality. Pathological changes in the systemic vasculature have been proposed as potential mechanisms linking COPD to cardiovascular disease, and patients with COPD may be at increased risk of acute myocardial infarction during acute exacerbations. Notwithstanding causation, FEV1 may be a useful prognostic marker in patients undergoing cardiac surgery. This thesis examined these three aspects of cardiovascular co-morbidity in relation to COPD and FEV1. In 2,241 consecutive cardiac surgery patients, FEV1 was associated with length of hospital stay (p<0.001) and mortality (p<0.001) adjusting for age, sex, height, body mass index, socioeconomic status, smoking, cardiovascular risk factors, chronic pulmonary disease, and type/urgency of surgery. In a survey of Scottish Respiratory Consultants there was no consensus regarding the investigation and management of acute coronary syndrome in exacerbation of COPD. In a case-series of 242 patients with exacerbations 2.5% (95% CI 1.0 to 5.6%) had chest pain, raised serum troponin and serial electrocardiogram changes suggestive of acute coronary syndrome. However, over half reported chest pain, while raised troponin was not associated with chest pain or serial ECG changes. Carotid-radial pulse wave velocity (PWV), aortic distensibility, and aortic calcification were measured to assess the relationship of the systemic vasculature to FEV1 and emphysema severity on CT. In adjusted analyses, emphysema was associated with PWV in patients with COPD (p = 0.006) and, in population based samples, with extent of distal aortic calcification (p=0.02) but not with aortic distensibility (p=0.60). This thesis found that FEV1 was associated with mortality and length of hospital stay in patients undergoing cardiac surgery, and that chest pain and raised troponin were common but unrelated in exacerbation of COPD. In the vascular studies distal but not proximal vascular pathology was associated with FEV1, and if COPD is truly related to systemic arterial disease, the distal arterial tree is implicated.
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Murphy, Nicola. "Chronic obstructive pulmonary disease and anxiety". Thesis, Coventry University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368862.
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Solomon, Brahm Kevin. "Psychological Aspects of Pulmonary Rehabilitation in Chronic Obstructive Pulmonary Disease". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34292.
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As a leading cause of disability that often leads to death, chronic obstructive pulmonary disease (COPD) can be characterized as both a chronic illness and a life-threatening one. As a result, the experience of individuals with COPD can include psychological concerns that are associated with both rehabilitation and palliative care. At the same time, the often-uncertain trajectory of COPD obscures a clear transition from rehabilitation to palliative care. It is not surprising, therefore, that treatments aimed at addressing patients’ rehabilitative and palliative needs largely proceed independently of each other.
This dissertation contains two studies conducted with patients participating in a pulmonary rehabilitation program for COPD (N = 242). Separately, each study stems from a research tradition grounded in either the rehabilitative or palliative approach to treatment. Together, the studies highlight an opportunity for a model of more integrated care. Study 1 is derived from the rehabilitation literature and focuses on the issue of “catastrophizing” about breathlessness. Catastrophizing is characterized by a magnification of a symptom’s threat value, rumination about its perceived negative impact, and a sense of helplessness in addressing it. In some medical conditions with a primary symptom, such as chronic pain, catastrophizing demonstrates a strong relationship with the development of disability. Study 1 examines whether this relationship is found in the context of breathlessness. The study also reports the initial validation of the Breathlessness Catastrophizing Scale (BCS) as a means of assessing this phenomenon.
Study 2 has its conceptual basis in the palliative care literature and highlights patients’ existential concerns around loss of dignity. Loss of dignity is a central construct in recent health care debates, because it is a primary reason underlying the requests of terminally ill individuals to seek medically hastened deaths (i.e., euthanasia or assisted suicide). Until now, however, loss of dignity has only been examined among patients with cancer. Study 2 examines whether loss of dignity is as prevalent among those with advanced COPD, and whether it improves with treatment.
In Study 1 the BCS was found to be a reliable measure of breathlessness catastrophizing, with good convergent validity and sensitivity to change. Interestingly, it appears that breathlessness catastrophizing need not be a barrier to functional improvement in COPD. In Study 2, a “fractured” sense of dignity was found among 13% of patients with advanced COPD, suggesting that it is at least as prevalent as among those receiving palliative cancer care. It was also evident that loss of dignity is amenable to change with appropriate rehabilitation. This finding is important for societal debates regarding the provision of medically hastened deaths, which are often described as offering “death with dignity”. Together these studies demonstrate that in an interdisciplinary environment, such as the pulmonary rehabilitation program, not only is collaboration possible, but the distinct rehabilitative and palliative needs of patients can be met.
4
Greening, Neil James. "Early pulmonary rehabilitation for exacerbations of chronic obstructive pulmonary disease". Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/29155.
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Exacerbations are key events in the natural history of chronic obstructive pulmonary disease (COPD), with limited recovery of physical performance, and the highest cause of readmission in the UK. This thesis explores the impact of exacerbations in COPD and chronic respiratory disease. In the first study I have investigated the effects of an early rehabilitation intervention on healthcare utilisation, strength and exercise capacity by conducting a large randomised control trial. Using a sub-group of this cohort I have then explored factors that predict hospital readmission. Finally I have conducted a study of single leg neuromuscular electrical stimulation (NMES) in stable COPD, alongside a resistance training group. No difference was seen following early rehabilitation in hospitalisation, healthcare utilisation or physical performance. A number of unexpected findings were noted, including an increase in 12 month mortality in the intervention group and large functional recovery in the usual care group. Using multivariate analysis three risk factors for hospital readmission were identified, including quadriceps cross sectional area, using ultrasound. In the stable state NMES was seen to significantly increase muscle mass from baseline, comparable to changes seen using resistance training. In summary early rehabilitation in chronic respiratory disease does not impact on future hospitalisation. Identification of those with rehabilitation potential is required as the hospitalised population represent a frail group, with advanced disease.
5
John, Michelle. "The extra-pulmonary effects of chronic obstructive pulmonary disease (COPD)". Thesis, University of Nottingham, 2014. http://eprints.nottingham.ac.uk/14405/.
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Rationale Cardiovascular disease (CVD) is a leading cause of mortality in patients with COPD. Aortic stiffness, measured using aortic pulse wave velocity (PWV), an independent, non-invasive, predictor of CV risk; and inflammatory markers are increased in COPD. Screening tools for community based identification of increased CVD risk, and a proactive approach to addressing primary prevention of CVD is needed. Statins modulate aortic stiffness and are anti-inflammatory, but are not currently used for primary prevention in COPD. Objectives Proof of principle double-blind Randomised Control Trial (RCT) to determine if six weeks simvastatin 20mg od reduces aortic stiffness, systemic and airway inflammation in COPD. Cross-sectional pilot study comparing a non-invasive measure of oxidative stress (skin “AGE”) in COPD and controls, to lung function and aortic stiffness. Methods Stable patients (n=70) were randomised to simvastatin or placebo treatment. Pre- and post-treatment aortic stiffness, blood pressure, spirometry, circulating inflammatory mediators and lipids were measured; airway inflammatory markers were performed where possible. Predefined subgroup analysis was performed where baseline aortic PWV >10m/s. For the cross-sectional study stable COPD patients (n=84) and controls (n=36) had lung function, arterial stiffness and skin AGE measured. Results In the RCT the active group achieved significantly lower total cholesterol, but no significant drop in aortic PWV compared to placebo group: -0.7(95%CI -1.8,0.5)m/s, p=0.24; or inflammatory markers. In those with higher baseline aortic PWV, n=22, aortic PWV improved in the active group compared to placebo: -2.8(-5.2,-0.3)m/s, p=0.03. Skin AGE was increased in COPD compared to controls, inversely related to lung function, and directly related to aortic stiffness. Conclusions We could not detect any significant difference in the change in aortic PWV in patients with COPD taking simvastatin compared to placebo. We did, however, report a significant and clinically relevant reduction in aortic PWV in those with high baseline aortic stiffness, suggesting a potential for statins to reduce CV morbidity in high risk individuals. The pilot cross-sectional study suggests there is an indication to assess the potential role of skin AGE in patients with COPD as a non-invasive measure of CV risk.
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Roos-Engstrand, Ester. "T cells in chronic obstructive pulmonary disease". Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33677.
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Stevenson, Nicola Jane. "Lung mechanics in chronic obstructive pulmonary disease". Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432977.
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Wodehouse, Theresa. "Ciliary aspects of chronic sino-pulmonary disease". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271952.
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Al-shair, Khaled. "Systemic Manifestations of Chronic Obstructive Pulmonary Disease". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509061.
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Revill, Susan M. "Endurance exercise in chronic obstructive pulmonary disease". Thesis, Loughborough University, 1997. https://dspace.lboro.ac.uk/2134/15388.
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Polkey, Michael Iain. "Diaphragm function in chronic obstructive pulmonary disease". Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286262.
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Donaldson, Anna. "Circulating microRNA in Chronic Obstructive Pulmonary Disease". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24776.
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Skeletal muscle dysfunction in COPD is associated with increased morbidity. Novel agents might reverse skeletal muscle dysfunction through different mechanisms since the biopsy picture in COPD patients is heterogenous. Thus there is a need for a biomarker of skeletal muscle dysfunction which could both be measured in blood and obviate the need for a biopsy. Previous work has found that muscle-specific microRNA (miR-1, miR-499, miR-206 and miR-133) are down-regulated in the quadriceps of COPD patients. Tissue specific miRNA circulate in the blood at detectable levels and are currently under investigation as biomarkers of other diseases. I therefore hypothesised that muscle-specific microRNA might be clinically viable biomarkers of skeletal muscle dysfunction. The studies in this thesis found that: 1. Levels of circulating muscle-specific microRNA (miR-1, miR-133, miR-206 and miR-499) were increased in stable COPD patients. The increase in muscle-specific microRNA in the stable COPD patients suggests that continual muscle turnover occurs outside of times of disease exacerbation. 2. Plasma levels of muscle-specific miRNA were not different in COPD patients admitted to hospital for an exacerbation of their disease compared to stable COPD patients. 3. Most muscle-specific microRNA did not change in muscle with acute exercise. I demonstrated an increase in miR-181 (an miRNA not restricted to, but with known function in muscle) one hour after acute exercise in the quadriceps muscle of COPD patients. However when fold change was calculated for the COPD patients and controls, there was no statistical difference found. There were no detectable miR-181 changes measured in blood. 4. Finally, I used a microarray approach to investigate other circulating microRNA that might to be useful to separate patients based on their lean muscle-mass. COPD patients with a reduced skeletal muscle mass had a reduced number of microRNA associated with growth and cell pluripotency, further studies are required to validate these findings. Taken together, the results from this thesis suggest that the microRNA analysed were detectable in blood, but they could not be usefully used (based on current analysis) as biomarkers of quadriceps dysfunction.
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Taylor, Abigail Elizabeth. "Macrophage phagocytosis in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/7374.
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The hypothesis examined in this thesis stated that macrophages from COPD subjects are defective in their ability to phagocytose. To investigate this hypothesis, engulfment by COPD macrophages was compared to that of cells from controls (smokers without COPD and non-smokers). Phagocytosis of polystyrene beads by monocytes-derived-macrophages (MDM) was comparable to that of alveolar macrophages, thus validating the MDM model. There was no difference in uptake of beads by any subject group, however, COPD MDM phagocytosed significantly less E. coli, H. influenzae and S. pneumoniae than cells from controls. This was not due to current medications as commonly prescribed therapies did not reduce phagocytosis of these bacteria. To identify the mechanism of this defeat, cytoskeletal arrangement was investigated. Actin polymerisation was not altered by disease, but COPD MDM had a greater susceptibility to microtubule disruptors and reduced levels of acetylated tubulin compared to control cells. Increasing microtubule acetylation enhanced uptake of H. influenzae, suggesting that this may be a novel mechanism for improving phagocytosis. Other mechanisms investigated included sphingosine-1-phosphate (S1P) signalling, as production of this molecule was increased by COPD MDM and inhibition of S1P signalling cascade increased uptake of H. influenzae. Microarray analysis demonstrated that following exposure to H. influenzae, COPD MDM expressed significantly more inflammatory genes than control cells, suggesting that these macrophages respond differently to bacteria. These findings suggest that COPD macrophages have a reduced phagocytic ability, which may result in bacterial colonisation, inflammation and exacerbations. Improving this macrophage function would offer therapeutic potential in this disease.
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Baldrick, Francina Rose. "Diet and chronic obstructive pulmonary disease (COPD)". Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527657.
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Santiago, Pia Bantegui. "Adherence to exercise following pulmonary rehabilitation of chronic obstructive pulmonary disease /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3130214.
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Puhan, Milo Alan. "Patient-oriented research in chronic obstructive pulmonary disease /". Zürich, 2005. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253399.
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Roberts, Della Kim. "The family experience with chronic obstructive pulmonary disease". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24422.
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This study was designed to gain an understanding of the family experience when an adult member has chronic obstructive pulmonary disease (COPD). It is recognized that illness within the family affects the well-being of the family unit and the health of all members. To understand the impact of COPD upon the family, however, the literature provides only knowledge of the experience of the individual who has COPD and the spouse, not that of the family unit. Thus, the purpose of this study was to describe and explain the COPD experience from the perspective of the family unit.
A qualitative method, phenomenology, was chosen for this investigation. Data were collected through semi-structured interviews with eight families who shared their experiences. From the content analysis of these data, three themes that were common throughout the families' accounts were identified and developed to describe and explain family life with COPD.
The first theme, disease-dictated family life, describes four aspects of a common lifestyle that is imposed on the family by the characteristics of COPD. The second theme, isolation, describes the isolation that accompanies the illness experience, for the family group and the individual members within the group. The final theme, family work, describes the four primary challenges the families face and the coping strategies they use to deal with them. These findings revealed that COPD acts as an intense stressor within the family, requiring extensive family work to cope with COPD in a way that maintains the well-being of the family unit. Furthermore, it was found that living with COPD in many ways inhibits the resources within the family and those external sources of support that foster the family's ability to manage the stress associated with living with COPD. The implications for nursing practice and nursing research were delineated in light of the research findings.Applied Science, Faculty of
Nursing, School of
Graduate
18
Thomas, Catherine. "Defective innate immunity in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/40171.
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Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease, comprising chronic bronchitis, small airways fibrosis and emphysema. The primary risk factor for developing COPD, in industrialised nations is cigarette smoking. Exacerbations of COPD, of which approximately half are due to bacterial infection, are associated with worsening quality of life, more rapid decline in FEV1 and increased mortality. In healthy individuals, alveolar macrophages (AM) clear inhaled bacterial pathogens from the lung by phagocytosis, resulting in sterility of the lower respiratory tract. However, COPD patients have increased bacterial colonisation of the lower airways compared to healthy smokers and non-smokers. The increased rates of bacterial colonisation in COPD, suggests that there may be a mechanistic defect in the clearance of bacteria by phagocytic cells. The main aim of this thesis was to investigate the hypothesis that defective innate immunity in COPD patients results in reduction in bacterial phagocytosis, with increased frequency of acute exacerbation, and that this defective phagocytosis may be explained by instability of microtubules. Phagocytic ability of both macrophages and neutrophils from COPD patients was compared to age-matched, non-smokers and smokers. Monocyte-derived-macrophages (MDMs) were used as a model of AM. Both MDMs and neutrophils from all subject groups displayed equivalent phagocytosis of inert beads, showing that cells from all subject groups are capable of phagocytosis. However, both MDMs and neutrophils from smokers and COPD patients showed reduced uptake of both Haemophilus influenzae (by 48%, p < 0.001 and 28%, p < 0.01 respectively) and Streptococcus pneumoniae (by 52%, p < 0.001 and 32%, p<0.05 respectively). Whilst MDMs showed defective phagocytosis of bacteria, intracellular killing remained intact. When COPD patients were divided into those with a history of frequent (≥2/y) or infrequent exacerbations (< 1/y), frequent exacerbators had significantly reduced phagocytosis of bacteria compared to infrequent exacerbators. No differences were seen when phagocytosis at baseline was compared to phagocytosis at times of exacerbation. As COPD patients appear to have defective phagocytosis, and with recent meta-analyses showing an increased risk of pneumonia with fluticasone propionate (FP), the effects of both budesonide (BUD) and FP on phagocytosis by MDMs and neutrophils from COPD patients was assessed. No differences were found in phagocytosis of bacteria by MDMs in the presence of either steroid, or in the ability of these cells to perform functions of intracellular killing. In the presence of BUD, neutrophils showed significantly improved uptake of H. influenzae (with a maximal effect of 67%, p<0.05), but neither FP nor BUD had any impact on phagocytosis of beads or S. pneumoniae. Further investigation into the mechanisms underlying defective phagocytosis revealed increased susceptibility of COPD MDMs to microtubule disruption. Associated with this finding was a reduced level of acetylated tubulin in COPD MDMs. Addition of a microtubule stabiliser increased acetylated tubulin and significantly increased bacterial phagocytosis (maximal increase of 20% and 40% in phagocytosis of Haemophilus influenzae and Streptococcus pneumoniae respectively). In contrast, neutrophils displayed no differences in acetylated tubulin and showed no improvement in phagocytosis after exposure to microtubule stabilisers, suggesting an alternative mechanistic defect in neutrophils compared to MDMs. Acetylated microtubules are deacetylated by the enzymes HDAC6 and SIRT2. Exposure to the deacetylase inhibitors, tubacin (HDAC6 inhibitor) or AGK2 (SIRT2 inhibitor), led to increases in levels of acetylation of tubulin but no improvements in phagocytosis, whilst knockdown of either HDAC6 or SIRT2 revealed a similar picture, with increased acetylation but no improvements in phagocytosis. These findings suggest that increased acetylation of tubulin alone is not sufficient to improve phagocytosis, but rather that the defect in phagocytosis is related to microtubule instability. Knockdown of C6orf134, a newly discovered tubulin acetyl-transferase, in healthy MDMs led to reductions in levels of acetylated tubulin and reduced bacterial, but not inert bead, phagocytosis, mimicking the defect seen in COPD MDMs. This suggests that alterations in activity or expression of this protein may account for the defective phagocytosis seen in COPD MDMs. Improving phagocytosis by stabilisation of microtubules may therefore lead to reduced levels of bacterial colonisation and improved exacerbation frequency in COPD patients.
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Camp, Patricia. "Sex and gender in chronic obstructive pulmonary disease". Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1410.
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Research on sex and gender in chronic obstructive pulmonary disease (COPD) has primarily focused on differences in pulmonary function. Detailed gender- and sex-based analyses of other aspects of COPD, including epidemiology, risk factors other than cigarette smoke, pathophysiology, and measurement tools are warranted. In Chapter Two we analyzed administrative health services data to compare the prevalence, mortality and use of drugs and spirometry in men and women with COPD. Contrary to recent predictions, we did not detect a dramatic increase in the prevalence or mortality of COPD over time in women compared to men. We discuss how different coding practices in medical billing can impact the results. In Chapter Three we examined sex differences in COPD phenotypes. We hypothesized that male smokers would have more emphysema whereas female smokers would have more airway wall remodeling using data from high resolution computed tomography (HRCT) scans. We did detect more emphysema in male smokers but there was no evidence of increased airway remodeling in women. We discuss the limits of HRCT to detect airway differences in women and men. In Chapter Four we examined the use of HRCT in assessing emphysema. We hypothesized that the computer-derived estimates of emphysema (the fractal value and the % low attenuation area (%LAA)) would differentiate COPD from non-COPD as accurately as the radiologist’s emphysema scores, and would provide similar predictions in both men and women. Instead, we found that the subjective rating of emphysema best differentiated COPD, and the fractal value (a measure of emphysematous lesion size) better differentiated COPD compared with an established objective measurement, the %LAA. These results were generally the same in men and women. In Chapter Five we examined characteristics of COPD in women exposed to biomass smoke. We hypothesized that biomass smoke would induce an airway disease-predominant phenotype. We found that women with biomass smoke-exposed COPD had greater airway remodeling and less emphysema than women with tobacco smoke-exposed COPD. In summary, these findings suggest that sex and gender differences are present in COPD epidemiology and pathophysiology. However, current research measurement tools may limit the ability to accurately measure these differences.
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Sze, Marc Alexander. "The lung microbiome in chronic obstructive pulmonary disease". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/36343.
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Until recently the normal human lung was thought to be sterile below the larynx, but recent reports from other laboratories indicate that a diverse microbiome exists and becomes less diverse in smokers. These reports led naturally to the hypothesis that pathogens emerging from the abnormal microbiome in smokers could drive the innate and adaptive immune response that has been associated with the pathology of peripheral lung abnormalities observed in Chronic Obstructive Pulmonary Disease (COPD). The purpose of the present study was to examine this hypothesis in human lung tissue. This began with a preliminary experiment in which DNA isolated from 2 samples from a control lung were compared to DNA isolated from 5 different samples of a severe COPD lung, using 75 based pair-end tag sequencing (metagenomic sequencing). For bacteria, a weighted average genome size representing bacterial species identified was applied and the results validated using PCR and qPCR assays. This preliminary experiment was followed by a qPCR, T-RFLP, and targeted sequencing analysis of the bacterial 16S rRNA gene in DNA isolated from single samples of frozen lung tissue obtained from 8 non-smoking and 8 smoking controls, 8 COPD (GOLD 4), and 8 cystic fibrosis patients. The metagenomic sequencing conducted in the preliminary study showed that the 5 samples from a single COPD patient had an average of 2.4 ± 0.7 bacteria/1000 human genomes while the smoking control had 1.6 ± 0.8 bacteria/1000 human genomes. The qPCR results obtained from a single sample from 32 different subjects showed that on average the 8 samples/group of non-smokers, smokers, and COPD (GOLD 4) patients had 34.5 ± 21.8, 44.3 ± 47.0, and 24.1 ± 36.9 bacteria/1000 human cells, respectively, while cystic fibrosis patients had (20 ± 54) x 10 4 bacteria /1000 human cells. T-RFLP analysis showed three distinct community compositions: smokers and non-smokers, cystic fibrosis, and COPD (GOLD 4) patients. These results confirm the presence of a small number of bacteria within the human lung of non-smoker and smoker controls and in COPD patients with a shift in bacterial composition in lungs of those with COPD (GOLD 4).
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Hopkinson, Nicholas Shaun. "Skeletal muscle dysfunction in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417140.
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Urbanowicz, Richard Antoni. "Peripheral cytotoxic cells in chronic obstructive pulmonary disease". Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490982.
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Chronic obstructive pulmonary disease (COPD) is a treatable and preventable disease state, characterised by progressive airflow limitation that is not fully reversible. Although primarily a disease that affects the airways, COPD is increasingly recognised as a systemic disease. It is a current and growing cause of mortality and morbidity worldwide, with the World Health Organization (WHO) projecting that total deaths attributed to COPD will increase by more than 30% in the next 10 years, making it the third major cause of death worldwide.
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Swallow, Elisabeth. "Skeletal muscle dysfunction in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508993.
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Eltboli, Osama M. I. "Eosinophilic airways inflammation in Chronic Obstructive Pulmonary Disease". Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32546.
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Background: Eosinophilic airway inflammation (>3% sputum eosinophils) is a feature of subgroup of subjects with chronic obstructive pulmonary disease (COPD). My objectives were to investigate the clinical characteristics of eosinophilic COPD, its stability over time and extent in bronchial tissue, whether it is related to parasite exposure or atopy and whether its persistence is due to abnormal clearance by macrophages. Methods: Subjects were studied that had participated in previous observational studies. The repeatability of sputum eosinophils was measured between 3 monthly visits for 1 year. The extent of eosinophilic inflammation in bronchial tissue was assessed using immunohistology on bronchial tissue from COPD and control subjects. Positive serology for parasites was tested in serum samples for 4 helminth species. Atopy was assessed in the subjects using serum total Ig-E and skin prick test. Eosinophil efferocytosis by macrophages was investigated in vivo using cytoplasmic area of red hue of macrophages and in vitro using apoptotic eosinophils fed to monocyte-derived macrophages from COPD and healthy controls. The dynamics of eosinophil clearance during exacerbations was explored using the red hue technique. Results: Eosinophilic and non-eosinophilic COPD have similar lung function and exacerbation frequency. In eosinophilic COPD the health status is better and bacterial colonisation is lower. This phenotype is stable over time. Airway tissue eosinophilis are increased in COPD subjects with high blood eosinophils and are positively correlated with features of remodelling. Eosinophilic COPD is not associated with helminth exposure, but is related to elevated total Ig-E. Macrophage efferocytosis of eosinophils is impaired in COPD and is associated with the severity and frequency of COPD exacerbations. Efferocytosis of eosinophils by macrophages is increased following oral corticosteroid therapy at exacerbation. Conclusion: Eosinophilic COPD is a distinct and stable phenotype that persists in the blood, bronchus and sputum. Its persistence is partly related to atopy and impaired clearance by macrophages with the latter associated with COPD exacerbation severity and frequency.
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Hobbs, Brian. "Exome Array Analysis of Chronic Obstructive Pulmonary Disease". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:22837731.
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Background: Chronic obstructive pulmonary disease (COPD) susceptibility is in part related to genetic variants. Most genetic studies have focused on common variation, but rare coding variants are known to affect COPD susceptibility. We hypothesized that an exome array analysis would identify single non-synonymous variants and gene-based aggregates of non-synonymous variants associated with COPD.
Methods: We used the Illumina HumanExome array to genotype individuals in six COPD cohorts: Caucasian subjects from the family-based Boston Early-Onset COPD Study (BEOCOPD) and International COPD Genetics Network (ICGN), and the case-control COPDGene (non-Hispanic whites and African-Americans) and Transcontinental COPD Genetics Study (Poland and Korea). Cases were defined as GOLD Grade 2 and above COPD. Controls had normal lung function; the vast majority were current or former smokers. We tested single non-synonymous, stop and splice variants with a minor allele frequency (MAF) of > 0.5% in an additive model using logistic regression and combined results in a fixed-effects meta-analysis. Our gene-based testing was performed on non-synonymous, stop, and splice variants with MAF < 5% and used SKAT-O with meta-analysis in the MetaSKAT software in R. We performed meta-analyses for all subjects and separately by ethnicity. We adjusted all analyses for age, sex, pack-years of smoking, and ancestry-related principal components. Exome-wide significance was determined to be 2.3x10-6 for single variant testing and 4.1x10-6 for gene-based testing.
Results: Across the six cohorts, we included 5971 controls and 6054 cases in our analysis. We identified an exome-wide significant non-synonymous variant rs16969968 (p=1.4x10-13) in CHRNA5 at a locus previously described in association with COPD susceptibility and nicotine addiction. No additional variants or genes met exome-wide significance. Additional top association results included variants in MMP3, AGER, and SERPINA1. A non-synonymous variant in IL27 (p=5.6x10-6) was just below the level of exome-wide significance. In gene-based testing, the top gene was CYB5RL with p=3.9x10-5. We also identified several non-synonymous SNPs at previously described GWAS loci for COPD or lung function, including GPR126, RIN3, MECOM, and TNS1.
Conclusions: We have performed an exome array analysis for COPD in multiple populations. Although no novel variants or genes were identified at exome-wide significance, our analysis confirms associations at previously discovered loci and identifies coding variants for potential future study. Additionally, we identified a variant in IL27 just below the significance threshold as a potential candidate for COPD pathogenesis.
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Alhaddad, Maath. "Cardiopulmonary manifestations in chronic obstructive pulmonary disease (COPD)". Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/30008/.
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Rationale Chronic obstructive pulmonary disease (COPD) is a progressive lung condition with extrapulmonary manifestations- cardiovascular diseases (CVD), impaired physical function, activity and increased frailty. Integrating measures of function into community assessments is hindered by the space and time required. The association of function, activity and CVD has not been extensively investigated in COPD. Objectives Explore the potential utility of Time Up and Go (TUG) as a measure of physical function in COPD Assess association of non-invasive measures of haemodynamics to physical function and self-reported activity Explore ambulatory haemodynamics in COPD and controls Methods Subjects with COPD (n=119) and controls (n=58) were recruited. Ethical and governance approvals were obtained. A medical history including falls, spirometry, peripheral and central haemodynamics, self-reported physical activity questionnaires and functional assessments (TUG and six-minute walk distance (6MWD)) were obtained from all subjects. Ambulatory 24-hour haemodynamics including aortic pulse wave velocity (aPWV) and blood pressure were measured in patients (n=20) and controls (n=19). Results TUG mean(SD) was increased in patients 11.9(3.7)s compared to controls 9.5(1.8)s, p < 0.001. In patients, fallers had longer TUG than non-fallers (p=0.02) and a cut-off time of 12s had the highest sensitivity and specificity to detect fallers and non-fallers. Aortic stiffness was not associated to physical function or physical activity, p > 0.05. In the pilot study, significant nocturnal dip in aPWV was seen in controls, p < 0.01, but not in patients, p=0.07. Conclusion TUG could be a useful measure of function and possibly be incorporated into COPD assessment, particularly where time and space are limited. Finally, ambulatory haemodynamic machine, the Mobil-O-Graph, is feasible and offers opportunity to assess 24-hour haemodynamics profile including aPWV as opposed to a one-off measurement.
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Bestall, Janine Caroline. "Outcome of pulmonary rehabilitation in patients with severe chronic obstructive pulmonary disease". Thesis, Queen Mary, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322237.
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Brazil, Timothy John. "Pulmonary neutrophil recruitment, activation and clearance in equine chronic obstructive pulmonary disease". Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/29982.
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The functional status of neutrophils within both the circulating granulocyte pool and the airways of horses with COPD remains largely unexplored. Likewise, little is known of the kinetics of pulmonary neutrophil recruitment and clearance during and after an acute episode of COPD or indeed the subsequent fate of these cells. I have demonstrated in vitro that isolated peripheral blood neutrophils may be primed by exposure to inflammatory mediators such as lipopolysaccharide, platelet activating factor and tumour necrosis factor-a. This results in enhanced respiratory burst activity upon subsequent exposure to secretagogue stumuli. Indeed, priming was found to be a necessary step in the induction of functional coupling of receptors for the bacterial peptide fMLP in equine neutrophils. I have also demonstrated that purified peripheral blood neutrophils undergo apoptosis constitutively when aged in vitro and that the rate of apoptosis can be modulated by exposure to a range of pro-inflammatory mediators. In order models of neutrophilic inflammation, cells that have undergone apoptosis have been shown to be recognized by phagocytes such as inflammatory macrophages, engulfed and degraded without inducing an inflammatory response. Acute COPD was induced in susceptible horses by exposure to a 5 h hay/straw challenge. The kinetics and function of airspace neutrophils harvested by bronchoalveolar lavage and peripheral blood neutrophils was monitored sequentially for 14 days after challenge. Hay/straw challenge primed both peripheral blood and airspace neutrophils for an enhanced secretagogue-induced respiratory burst. Significant degranulation of neutrophils occurred within the airspaces as evidenced by a marked increase in neutrophil elastase in bronchoalveolar lavage fluid. As the pulmonary inflammation resolved, airspace neutrophils underwent apoptosis and were phagocytosed by alveolar macrophages in vivo. This work demonstrates significant upregulation of neutrophil function in horses with COPD and provides evidence of a pivotal role for neutrophil apoptosis in the resolution of the pulmonary neutrophil burden in this disease.
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Biondini, Davide. "From cigarette smoking to Chronic Obstructive Pulmonary Disease or Idiopathic Pulmonary Fibrosis. Why?" Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3423181.
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Chronic Obstructive Pulmonary Disease (COPD) and Idiopathic Pulmonary Fibrosis (IPF) are two chronic lung diseases with distinct clinical, pathological and epidemiologic features. In both disorders cigarette smoking represents a major risk factor; indeed, it causes a repetitive alveolar damage that elicit inflammatory response and may enhance the establishment of the disease. During my PhD, we investigated the role of innate and adaptive immune response in COPD and IPF, and how it may be related to different clinical outcomes.
In COPD, the role of inflammation is consolidated; alveolar macrophages (AM), which are one of the main actors of innate immune response, were firstly recognized to play a key role in the pathogenesis of the disease, by releasing protease that damage lung parenchyma. In our studies, we investigated how AM may be involved in the development of COPD with alternative mechanisms; for example, we analyzed AM polarization, classic (M1) and alternative (M2), in lung tissue and how it may be influenced by smoking and disease severity. The model of COPD as a disease caused only by an antiprotease-protease imbalance has been overtaken; indeed, not all subjects with α1-Antitrypsin (AAT) deficiency (AATD) develop disease, meaning that other immune regulatory factors are involved. In fact, we investigated α1AT polymerization in AM as a pro-inflammatory trigger, due to its abnormal accumulation in AM endoplasmatic reticulum. Moreover, we performed a genome wide analysis in siblings with AATD, with extreme phenotypes of the disease (emphysema/no emphysema), searching for genes variants that may modulate or promote inflammatory response, possibly explain these opposite manifestations.
Since the study of biomarkers is becoming of great interest in the field, we focused our research on adaptive immune cells in the blood, examining blood eosinophils (BE) and lymphocytes (BL), to investigate whether they can be predictor of clinical outcomes, and if they reflect what is happening in the lung. In addition, we have started to unravel the possible role of the peripheral BL in the development or prevention of cancer. Then we moved from peripheral blood to the lung tissue, examining how lymphocyte and eosinophil counts in the lung may change after the introduction of an anti-inflammatory treatment with Roflumilast, adding some clues on its mechanisms of action. Indeed, the study of lung infiltrate is mandatory to better understand the pathogenesis of the disease, and we are currently developing new techniques to deeply analyze the immune cells in COPD lung, and the presence of markers of immunomodulation.
In IPF, the role of inflammation is more debated than COPD. Our idea that an inflammatory reaction could be an important part of IPF has lead us to investigate the possible role of innate and adaptive immune response in the pathogenesis of the disease, not only in explanted lungs of end-stage IPF, but also in the surgical lung biopsies of patients with mild disease. The pathological evidences we found were then correlated to clinical outcomes, as disease progression, to study if they may account for the variability in lung function decline. Moreover, we also explored whether different lung tissue inflammatory profiles may impact on the response to Pirfenidone treatment, which exerts also an anti-inflammatory effect. Finally, we investigated HRCT as a possible non-invasive predictor of disease behavior and treatment response in IPF.
The results of the studies we have conducted so far, highlights how inflammatory response, and especially the immune regulation, is pivotal in COPD and IPF, adding novel findings to previous knowledge in the areas of innate and adaptive inflammation, and putting the basis for future research in these smoking-induced diseases.
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Chen, Roy Yu-Wei. "Biomarkers for acute exacerbation of chronic obstructive pulmonary disease". Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/57759.
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Rationale: There are currently no generally accepted and validated blood tests available for diagnosing acute exacerbations of chronic obstructive pulmonary disease (AECOPD). There is an urgent need of biomarkers that can guide therapeutic management in AECOPD. Based on literature review, systemic inflammation and mild cardiac dysfunction are often associated with AECOPD. We hypothesized that certain protein markers can indeed be useful in tracking and diagnosing AECOPD progression.
Methods: The study cohort consisted of 368 patients recruited in the chronic obstructive pulmonary disease (COPD) Rapid Transition Program who were hospitalized with a primary diagnosis of AECOPD, and 76 stable COPD patients who served as controls. We first determined the relationship of AECOPD of C-reactive protein (CRP) and the N-terminal of the prohormone brain natriuretic peptide (NT-proBNP). We then performed a discriminatory analysis using receiver-operating characteristics (ROC) curve in a logistic regression model. We compared the area under the curve (AUC) of 4 different combinations of CRP and NT-proBNP models. Lastly, we examined several potential biomarkers that were implicated in AECOPD.
Results: The demographic data of the cohort and the controls were well matched, with an average age of 68 versus 65 years old, 64% versus 77% male, and a forced expiratory volume in 1 second (FEV1) % predicted of 52% versus 58%. The CRP and NT-proBNP levels at exacerbation onset were found to be the highest and progressively decreased over time. Of the 4 models of ROC curves, the leave-one-out cross-validated model including both CRP and NT-proBNP had an AUC of 0.80. This model replicated well in an external LEUKO dataset. On the ii
other hand, D-Dimer, pulmonary and activation-regulated chemokine (PARC) and troponin I, showed minimal or no temporal changes during hospitalization and were no different than those with stable COPD.
Conclusions: In summary, this thesis demonstrated that biomarkers such as CRP and NT-proBNP are significantly elevated during AECOPD and decreased with recovery. Secondly, a combination of CRP and NT-proBNP could discriminate patients who were hospitalized for their AECOPD from stable patients. Together, these two biomarkers show promise in diagnosing and tracking AECOPD.Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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McPherson, E. A. "Equine chronic obstructive pulmonary disease (COPD) : publications 1974-1985". Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/28607.
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Schleifer, Taylor Jacqueline. "Exploring the social construction of chronic obstructive pulmonary disease". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ54197.pdf.
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Toma, Tudor Paul. "Endoscopic lung volume reduction in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428589.
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Saha, Shironjit K. "Inflammatory profiles in chronic obstructive pulmonary disease and asthma". Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/8206.
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Historically, asthma and chronic obstructive pulmonary disease (COPD) represent polar ends of the spectrum of airways disease defined in part by distinctive profiles of airway inflammation; in practice, overlap can exist between asthma and COPD. This thesis examined the pattern of inflammatory cell infiltration and cytokine expression within the bronchus in COPD and asthma with further study of moderate-severe asthma. In addition using sputum, cytokine expression was further assessed in COPD and asthma and its relation to severity. Based on previous studies, this thesis examined the expression of specifically Interleukin (IL)-13 and Granulocyte Macrophage Colony Stimulating Factor (GMCSF). We demonstrated mast cell myositis in moderate and severe asthma which reflected increased disease symptoms. Preferential localization of inflammatory cells to airway smooth muscle (ASM) was absent in COPD. CD3+ T-cells infiltration of large airway glands was increased in COPD which may influence mucus hyper-secretion. We demonstrated IL-13 overexpression within the submucosa in moderate-severe asthma with specific increase in the ASM in severe disease. IL-13 expression was related to eosinophilic inflammation. In sputum, IL-13 protein was increased in mild and severe asthma reflecting IL-13 expression in ASM. There was a general absence of bronchus and sputum IL-13 in COPD. Sputum GMCSF was increased in moderate-severe asthma and mild-severe COPD. Parallel upregulation of GMCSF and associated receptor (GMCSFr) expression in the submucosa and ASM was present in severe asthma. GMCSF/GMCSFr expression did not exhibit preferential expression in the large airway of COPD. Our findings suggest inflammatory cell infiltration of the airway structures is present in asthma and COPD which may influence the phenotype. In addition IL-13 is important in severe asthma whilst GMCSF is expressed in asthma and COPD across a range of severity, but to a greater degree in severe asthma.
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Moore, Alastair. "Physiological approaches to hyperinflation in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505304.
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Chronic Obstructive Pulmonary Disease (COPD) is one of the leading causes of mortality and morbidity worldwide. The purpose of this thesis was to explore the role of hyperinflation in COPD by investigating its effect on mortality, and then having established that hyperinflation is a predictor of mortality in COPD, to then explore how it has an effect on the mechanics of the diaphragm at a sub-cellular level.
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Rickards, Karen Jane. "Neutrophil phosphodiesterase inhibition in equine chronic obstructive pulmonary disease". Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251618.
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Stockley, James. "Neutrophil migration and inflammation in chronic obstructive pulmonary disease". Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5999/.
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COPD is a leading cause of morbidity and mortality worldwide and it is believed that the neutrophil is key to the pathology. Evidence to date suggests that neutrophils migrate less accurately in patients with COPD, although the precise mechanisms by which this occurs have not been defined. We have shown that COPD neutrophils migrate faster (chemokinesis) but less accurately (chemotaxis) in various chemokine gradients. It appears to be an intrinsic cell defect, as incubation of healthy neutrophils in COPD plasma did not alter migratory dynamics. This phenomenon does not occur in other respiratory diseases and is unrelated to age, disease severity, smoking status or the presence of emphysema. Furthermore, there were no differences in markers of neutrophil activation or maturity, although degranulation markers were higher in COPD. Expression of certain chemokine receptors was lower on quiescent COPD neutrophils, but these differences were abolished after stimulation. Receptors localised to the leading edge effectively in COPD neutrophils and there were no differences in receptor shedding. PI3K phosphorylation was increased in COPD and inhibition of γ and δ isoforms improved chemotaxis. Neither Akt phosphorylation nor intracellular calcium signalling was altered. Simvastatin also improved chemotaxis of COPD neutrophils but CXCR1/2 inhibitors did not.
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Heneghan, Nicola R. "Chronic obstructive pulmonary disease and cervico-thoracic musculoskeletal dysfunction". Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/4779/.
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Conservative non-pharmacological evidence-based management options for Chronic Obstructive Pulmonary Disease (COPD) primarily focus on developing physiological capacity. With co-morbidities, including those of the musculoskeletal system, contributing to the overall disease severity, further research was needed. This thesis presents a critical review of musculoskeletal management approaches used in COPD, which concluded there is insufficient evidence for using musculoskeletal interventions in COPD management. With a paucity of literature exploring chest wall flexibility and clinical guidelines advocating research into thoracic mobility exercises in COPD, a focus on thoracic spine motion analysis was taken. Soft tissue artefact (STA) threatens the validity of existing in vivo measurement techniques. Having measured and reported unacceptable levels of STA, an alternative approach was developed and tested for reliability as part of this thesis. This technique, along with other measures, was subsequently used to evaluate cervico-thoracic musculoskeletal changes and their relationship with pulmonary function in COPD. In summary, subjects with COPD had reduced spinal motion, altered posture and increased muscle sensitivity compared to controls. Reduced spinal motion and altered neck posture were associated with reduced pulmonary function and having diagnosed COPD. Results from this thesis provide evidence to support inception of a clinical trial of flexibility exercises in COPD.
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Walton, Georgia May. "Neutrophil migration and phagocytosis in chronic obstructive pulmonary disease". Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8647/.
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COPD is a leading cause of morbidity and mortality. A wealth of data supports a role of the neutrophil in disease pathogenesis. Despite abundance of neutrophils in airway secretions, patients suffer recurrent respiratory infections and colonisation suggesting immune dysfunction. This thesis describes impaired migratory function of neutrophils from patients with COPD, but not Alpha-1 Anti-Trypsin Deficiency (AATD) where similar inflammation is present. This is a feature of all COPD disease phenotypes and may constitute an early disease alteration to cell function, or a factor that predisposes patients to disease development. Aberrant migration may result in increased collateral tissue damage and delayed neutrophil arrival at sites of infection. Defective neutrophil migration in COPD can be improved by selective inhibition of PI3Kinase-γ and –δ, which may offer a strategy to reduce bystander tissue damage and improve bacterial clearance. The intrinsic ability of neutrophils to carry out effective phagocytosis in COPD and AATD does not appear reduced. However, in some patients, impaired serum opsonisation of bacteria reduced effective bacterial clearance by phagocytosis. Defective opsonisation may therefore make patients more vulnerable to bacterial colonisation and infection, and associated disease progression.
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Wainwright, Megan Julie. "Breathing and breathlessness : chronic obstructive pulmonary disease in Uruguay". Thesis, Durham University, 2013. http://etheses.dur.ac.uk/7270/.
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An increasingly common part of being human is living with chronic health problems for which management over time, and not cure, is the goal of medical treatment. One such chronic condition is chronic obstructive pulmonary disease (COPD), a lung disease caused by breathing-in smoke, dusts and chemicals, including tobacco smoke. This ethnographic study set out to explore how COPD is lived with and cared for in Uruguay, where rates of COPD are amongst the highest in South America and where most cases go undiagnosed. The aims of the research were to explore the following questions: a) what does it feel like to be breathless and how is COPD experienced within family and healthcare relationships? b) how is the lived-experience of COPD shaped by cultural, social, economic and political contexts? And, c) what are some of the challenges and opportunities for preventing and treating COPD? The objective of this ethnography is to contribute a unique case study to the anthropological literature on chronic illness both in terms of the disease under investigation and the cultural context. The thesis responds to a call in the literature for more sophisticated phenomenological approaches. By incorporating a multitude of field methods into ethnographic fieldwork I combine a sensorial medical anthropology approach and a political-economy of health perspective. The ethnography begins with a cultural and sensorial analysis of breathing and breathlessness in Uruguay in order to situate the expressions of this disease across a diverse group of participants. I argue that the experience of COPD is shaped by healthcare systems and inequalities and highlight two healthcare contexts where space is made for people to socially interpret sensations in the body. The thesis culminates in the critical assessment of public health goals and makes recommendations for improving COPD prevention and care in Uruguay.
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Haldar, Kairabi Sadhu. "Profiling of bacterial communities in chronic obstructive pulmonary disease". Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32292.
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Introduction: It is hypothesized that bacteria are important in the pathogenesis of COPD and exacerbations. Most bacteriological research in COPD has utilised culture based methods. Novel molecular approaches enable detailed evaluation of the airway microbiome that may better inform the role of bacteria in COPD. This project aimed to characterise the microbial community in COPD at stable state and during acute exacerbations through assessment of serial sputa at stable (S), exacerbation (E), follow up (F) and recovery (R) visits. Methods: Sputum from 145 clinical trial COPD patients was collected at multiple stable visits and at each exacerbation (E, F and R visit) over 12 months. Real-time quantitative PCR (qPCR) was performed on sputum DNA using universal 16S gene primers and specific gene targets to quantify total bacterial load and the specific pathogens H. influenzae, S. pneumoniae, M. catarrhalis and S. aureus. In a subgroup of 30 exacerbating patients, 454 high-throughput pyrosequencing of 16S rDNA amplicons was performed at each of the 4 visits. Results: There was no significant difference in total bacterial load or any specific pathogen between longitudinal stable and exacerbation samples. 454 pyrosequencing identified Proteobacteria and Firmicutes to be the dominant groups contributing >80% of the sequence reads at phylum level. Haemophilus, Moraxella and Streptococcus were the dominant groups at genus level. No significant within-subject change in the microbial community was observed across visits. Cluster analysis, based on the ratio of Proteobacteria to Firmicutes (P:F) characterised three subgroups. The high P:F subgroup was characterised by a significant increase in P:F from S to E visits, associated with raised blood CRP and sputum IL-1β levels, suggesting a role for bacteria in exacerbation pathogenesis for this subgroup. Conclusions: Molecular profiling identifies heterogeneity in the airway microbiome of COPD patients, with a role for bacteria suggested in a subgroup.
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Correll, Amanda Leigh. "Strength training in patients with chronic obstructive pulmonary disease". Winston-Salem, NC : Wake Forest University, 2009. http://dspace.zsr.wfu.edu/jspui/handle/10339/42574.
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Thesis (M.S.)--Wake Forest University. Dept. of Health and Exercise Science, 2009.Title from electronic thesis title page. Thesis advisor: Michael J. Berry. Includes bibliographical references (p. 49-54).
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Jones, Sharon Scardina. "Evaluating a Discharge Bundle for Chronic Obstructive Pulmonary Disease". ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/4861.
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Acute exacerbation of chronic obstructive pulmonary disease (COPD) is one of the leading causes of hospital readmissions within 30 days. Frequent readmissions negatively affect hospital reimbursements and patient outcomes. Creative strategies, such as COPD care bundles, have been shown to reduce readmission rates according to existing studies. A COPD discharge bundle was developed and implemented at 1 community hospital in response to an identified problem with COPD readmissions. Evaluation of this quality improvement initiative was the purpose of this project study. The practice-focused question was: Have 30-day readmission rates changed following the implementation of a COPD discharge bundle prior to transitioning from hospital to home? The framework selected for this project was the model for improvement. Sources of evidence included existing hospital data to evaluate the change in readmissions. The chi-square test of independence was used to assess the difference in frequency of 30-day readmissions. Pre and post-bundle implementation comparisons of readmission rates showed a decrease for 3 out of the 4 groups compared; these results were not statistically significant. Analysis of the post-bundle intervention groups revealed lower 30-day readmissions for individuals who were bundle compliant versus noncompliant and for those who spoke with a pharmacist within 48 hours of discharge opposed to those who did not; these results were statistically significant. Continued use of the bundle and maintaining the role of the pharmacist was recommended. Reduction of readmissions within 30-days has positive social implications for hospitals through financial gains and for the COPD population by improving overall health outcomes.
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Akiki, Zeina. "Biological Markers For Chronic Obstructive Pulmonary Disease And Asthma". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS081/document.
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L’étude des marqueurs biologiques dans la broncho-pneumopathie chronique obstructive (BPCO) et l'asthme, deux maladies respiratoires chroniques affectant des millions de personnes dans le monde, pourrait améliorer leur diagnostic, leur traitement et leur prévention.Cette thèse comprend deux parties. La première visait à évaluer l'association entre un marqueur spécifique des poumons, la protéine surfactant D (SP-D) sérique, et la BPCO, et à trouver un seuil de SP-D capable de discriminer les patients BPCO des témoins. Elle a été réalisée dans le cadre d’une étude cas-témoin au Liban incluant des patients BPCO (n=90), des asthmatiques (n=124) et des témoins (n=180). La deuxième partie visait à évaluer les associations chez les adultes des marqueurs de l’inflammation systémique (protéine C-réactive ultra-sensible, hs-CRP (n=252), et des cytokines (n=283)) et des marqueurs de dommages dus au stress oxydant (8-isoprostanes 8-IsoPs (n=258) du condensat de l’air exhalé) avec les phénotypes de l’asthme.Elle a été réalisée dans le cadre de l'étude épidémiologique longitudinale Française des facteurs génétiques et environnementaux de l'asthme (EGEA).Les résultats ont montré que les niveaux de SP-D sériques étaient associés positivement avec la BPCO et des seuils des niveaux de SP-D chez ces patients ont été identifiés avec d'excellentes valeurs discriminantes. Dans EGEA, aucune association n'a été trouvée entre les niveaux de hs-CRP sériques et le contrôle de l’asthme. Des profils de cytokines sériques (identifiés par analyse en composante principale) avec des niveaux élevés d’interleukine(IL)-1Ra et d’IL-10 ont été associés avec moins de crises d'asthme et un risque plus faible d'un mauvais contrôle de l'asthme sept ans plus tard. Les résultats des analyses préliminaires sur les associations entre les niveaux de 8-IsoPs et les phénotypes de l'asthme sont également présentés.Globalement, ces résultats ont montré l'utilité d'étudier les marqueurs biologiques en lien avec la BPCO et l'asthmeStudying the biological markers in chronic obstructive pulmonary disease (COPD) and asthma, two chronic respiratory diseases affecting millions of individuals around the world, could improve their diagnosis, their treatment and their prevention.This thesis includes two parts. The first aimed to assess the association between a lung-specific biomarker, serum Surfactant Protein D (SP-D), and COPD, and to find cut-off points able to discriminate COPD patients from controls using SP-D levels. It was performed in a case-control study in Lebanon including COPD (n=90) and asthma patients (n=124) and controls (n=180). The second part aimed to assess the cross-sectional and longitudinal associations in adults for systemic inflammatory biomarkers (high sensitivity C reactive protein hs-CRP (n=252) and cytokines (n=283) as well as biomarkers of damage due to oxidative stress (8-Isoprostanes 8-IsoPs (n=258) from the exhaled breath condensate) and asthma outcomes.It was performed in the French longitudinal epidemiological study on the genetics and environmental factors of asthma (EGEA).Results showed that serum SP-D levels were positively associated with COPD and thresholds for SP-D levels in these patients were identified with excellent discriminant values. In EGEA, no association was found between serum hs-CRP levels and asthma control. Serum cytokine profiles (identified by principal component analysis) with high levels of interleukin (IL)-1Ra and IL-10 were associated with less asthma attacks and lower risk of poor asthma control in adults seven years later. The results of the preliminary analyses on the associations between the levels of 8-IsoPs and asthma outcomes are also presented.Overall, these results have shown the usefulness of studying the biological markers related to COPD and asthma
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Shuper, V. A. "Clinical features of chronic obstructive pulmonary disease combined with ischemic heart disease". Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17112.
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Soicher, Judith Eileen. "A longitudinal study of physical activity behaviour in chronic disease: the example of chronic obstructive pulmonary disease". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32532.
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In chronically ill adults, involvement in physical activity is associated with reduced mortality and better quality of life. In chronic obstructive pulmonary disease (COPD), exercise training within a pulmonary rehabilitation program leads to improvements in dyspnea, exercise capacity and quality of life measured immediately after the program. These gains diminish within 6-18 months of program completion, in part due to patients' difficulty in sustaining physical activity behaviour. The global objective of this thesis was to examine behavioural and disease-related aspects of physical activity over 1 year among individuals with COPD. A longitudinal behavioural study was embedded within a randomized multicentre trial comparing the effectiveness of home-based versus hospital-based outpatient pulmonary rehabilitation. The first study of this thesis assessed behavioural aspects of exercise before and after a 3-month rehabilitation program. Exercise habits, self-efficacy for exercise and barriers to exercise improved significantly following rehabilitation. In cross-sectional path analysis, past exercise habits and greater exercise capacity had a positive effect on self-efficacy for endurance exercise (measured pre-rehabilitation), while external barriers, depression and female sex had a negative effect. In the second study, logistic longitudinal modelling showed that adherence to exercise (at least 3 days per week for endurance exercise and at least 2 days per week for strength exercise) declined progressively between 4 and 12 months after rehabilitation start. Adherence to endurance exercise was higher during spring/summer, and if individuals had exercised prior to rehabiliL'activité physique est associée à un taux de mortalité réduit et à l'amélioration de la qualité de vie chez les adultes atteints de maladies chroniques. L'entraînement physique chez les sujets atteints de la maladie pulmonaire obstructive chronique (MPOC) dans le cadre d'un programme de réadaptation pulmonaire entraîne l'amélioration de la dyspnée, de la capacité d'exercice et de la qualité de vie. Cependant, ces améliorations diminuent dans les 6 à 18 mois suivant la fin du programme du, en partie, aux difficultés de maintenir l'activité physique. L'objectif général de cette thèse était d'examiner pendant un an les aspects comportementaux et médicaux (reliés à la maladie) de l'activité physique chez les individus atteints d'une MPOC. Une étude longitudinale fut incorporée à un essai multicentrique randomisé comparant l'efficacité de la réadaptation pulmonaire à domicile à celle en clinique externe. La première étude de cette thèse a évalué l'aspect comportemental de l'exercice avant et après le programme de réadaptation qui était d'une durée de 3 mois. Les habitudes d'exercices, l'auto-efficacité et les barrières à l'exercice se sont améliorées de façon significative suivant la réadaptation. Il a été démontré que les habitudes passées relatives à l'exercice et la capacité à l'exercice ont un effet positif sur l'auto-efficacité en exercice d'endurance (mesurée avant la réadaptation) tandis que les barrières externes, la dépression et le sexe féminin ont un effet négatif. Pour la seconde étude, le modèle logistique longitudinal a démontré que l'adhésion à l'exercice (exercices en endurance au moins 3 jours par se
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Theander, Kersti. "Fatigue, functional status, health and pulmonary rehabilitation in patients with chronic obstructive pulmonary disease". Doctoral thesis, Linköping : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-8268.
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Terada, Kunihiko. "Impact of gastro-oesophageal reflux disease, symptoms on chronic obstructive pulmonary disease exacerbation". Kyoto University, 2009. http://hdl.handle.net/2433/124263.
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Liu, Jie. "Novel Bayesian Methods for Disease Mapping: An Application to Chronic Obstructive Pulmonary Disease". Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0501102-110350.
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Thesis (M.S.)--Worcester Polytechnic Institute.Keywords: latent class model; Poisson regression model; Metropolis-Hastings sampler; order restriction; disease mapping. Includes bibliographical references.
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Batlle, Garcia Jordi de 1981. "Measure and effect of diet in chronic obstructive pulmonary disease". Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/52896.
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Background and objectives: Recent research has shown an
association between a healthy diet and reduced chronic obstructive
pulmonary disease (COPD) incidence. However, the potential role
of diet in COPD prognosis is unknown. This thesis aimed to
describe the characteristics of diet in COPD patients and to
estimate its association with the disease evolution, in terms of
pathophysiological impairment and hospitalizations. A secondary
objective was to study the role of diet in asthma, as a COPDrelated
phenotype.
Methods: A dietary ancillary protocol was included in a well
phenotyped cohort of 342 COPD patients recruited during their first
admission for a COPD exacerbation in Spain. Dietary data of the
last 2 years was assessed using a validated food frequency
questionnaire (122 items). Levels of oxidative stress and
inflammatory markers were measured in serum. Hospital
admissions during follow-up were obtained from national datasets.
Additionally, data from the International Study of Asthma and
Allergies in Childhood (ISAAC) in Mexico was used to assess the
effect of diet in childhood asthma.
Results: (i) COPD patients report an adequate intake of the main
food groups and macro- and micro-nutrients according to local
recommendations, excepting vitamin D; (ii) vitamin E and olive oil
intakes are associated with reduced oxidative stress in COPD
active smokers; (iii) intake of _3 and _6 fatty acids is related to the
levels of serum inflammatory markers; (iv) cured meat intake
increases the risk of COPD admission during follow-up; and (v)
children adherence to a Mediterranean dietary pattern relates to
reduced childhood asthma prevalence.
Conclusions: Dietary habits may modify COPD prognosis and
childhood asthma. Therefore, advice on healthy diet should be
considered in chronic respiratory diseases guidelines.Antecedents i objectius: Estudis recents mostren associacions entre una dieta sana i reduccions en la incidència de malaltia pulmonar obstructiva crònica (MPOC). Tanmateix, el possible rol de la dieta en l'evolució de l'MPOC és desconegut. L'objectiu d'aquesta tesi és descriure les característiques de la dieta en pacients amb MPOC i estimar-ne l’associació amb l'evolució de la malaltia en termes d’alteracions fisiopatològiques i hospitalitzacions. Com a objectiu secundari, també es vol estudiar el paper de la dieta en l'asma, com a malaltia estretament relacionada amb l'MPOC. Mètodes: Es va aniuar un protocol d’epidemiologia nutricional en una cohort de 342 malalts d’MPOC, ben fenotipats, reclutats a Espanya durant la seva primera hospitalització per agudització de l'MPOC. Es va administrar un qüestionari de freqüència de consum d'aliments (122 ítems) preguntant per la dieta dels darrers 2 anys. Es van mesurar en sèrum els nivells de marcadors d'estrès oxidatiu i d'inflamació. Les hospitalitzacions durant el temps de seguiment s’obtingueren a partir de registres nacionals. Per últim, s'utilitzaren dades de l'International Study of Asthma and Allergy in Childhood (ISAAC) a Mèxic per a estimar l'efecte de la dieta en l'asma infantil. Resultats: (i) El consum d'aliments i macro- i micro-nutrients fou considerat adient respecte a les recomanacions locals, exceptuant la vitamina D; (ii) la ingesta de vitamina E i oli d’oliva s’associà a menors nivells d’estrès oxidatiu en pacients fumadors actius; (iii) els nivells de ingesta d'àcids grassos _3 i _6 es va relacionar amb els nivells d’inflamació sistèmica; (iv) la ingesta d’embotits i carns curades va incrementar el risc d'hospitalització per MPOC durant el seguiment; i (v) l’adherència a un patró mediterrani d'alimentació s’associà a menor prevalença d'asma infantil. Conclusions: Els hàbits alimentaris poden modificar l'evolució de l'MPOC i el desenvolupament d'asma infantil. Per tant, s’hauria de considerar l’inclusió de consells alimentaris en les guies clíniques per a malalties respiratòries cròniques.