Rozprawy doktorskie na temat „Pulmonary disease”
Kliknij ten link, aby zobaczyć inne rodzaje publikacji na ten temat: Pulmonary disease.
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 50 najlepszych rozpraw doktorskich naukowych na temat „Pulmonary disease”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
1
McAllister, David Anthony. "Chronic obstructive pulmonary disease, pulmonary function and cardiovascular disease". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5615.
Pełny tekst źródłaStreszczenie:
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.
2
Chang, Betty. "Pulmonary disease in scleroderma combined interstitial lung disease and pulmonary hypertenson and predictors of pulmonary hypertension /". Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3068129.
Pełny tekst źródła
3
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.
Pełny tekst źródłaStreszczenie:
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.
Pełny tekst źródłaStreszczenie:
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/.
Pełny tekst źródłaStreszczenie:
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.
6
Marante, Tânia Alves. "The impact of chronic obstructive pulmonary disease on iNKT lymphocytes". Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/17144.
Pełny tekst źródłaStreszczenie:
Mestrado em Biomedicina MolecularA doença pulmonar obstrutiva crónica (DPOC) é uma das doenças inflamatórias mais comuns das vias aéreas e uma das principais causas de morbidade e mortalidade em todo o mundo. A doença é caracterizada por uma limitação persistente do fluxo aéreo, geralmente progressiva. As respostas inflamatórias crónicas e imunes desempenham papéis fundamentais no desenvolvimento e progressão da DPOC. A inflamação é uma resposta protetora normal, mas na DPOC esta inflamação é amplificada. Várias células inflamatórias, seus mediadores e enzimas participam na resposta inflamatória na DPOC. A reabilitação respiratória é um componente fundamental da gestão da doença pulmonar obstrutiva crónica. Ela é projetada para melhorar a condição física e psicológica de pessoas com doenças respiratórias crónicas e para promover a adesão a longo prazo do comportamento que melhora a saúde. O objetivo principal deste trabalho foi contribuir para a compreensão do papel das células iNKT na patologia da DPOC. Além disso, também pretendemos explorar o efeito da reabilitação respiratória nas células iNKT em pacientes com DPOC. Análises clínicas e imunológicas foram feitas em pacientes com DPOC (n=7), pacientes com DPOC que realizaram reabilitação respiratória (n=4) e controlos saudáveis com idade e género idêntico aos doentes (n=14). Os participantes foram estudados duas vezes, com um intervalo de 12 semanas. Foram estudados os seguintes parâmetros clínicos: índice de massa corporal, percentagem de massa gorda, função pulmonar, força dos músculos respiratórios, força muscular isométrica, teste das cinco repetições sentar-levantar, teste de avaliação da DPOC e questionário da dispneia. As células iNKT foram estudadas em termos de percentagem, fenótipo, citotoxicidade e produção de citocinas. Não foi observada nenhuma alteração na percentagem de células iNKT, seus subconjuntos e produção de citocinas no sangue periférico de pacientes com DPOC em comparação com os controlos. Os nossos resultados sugeriram que as células iNKT de pacientes com DPOC podem ter uma diminuição na ativação precoce pela redução da expressão do CD69. Foi também sugerida uma redução na capacidade citotóxica em doentes. A reabilitação respiratória não pareceu afetar a redução da expressão do CD69, mas pareceu contribuir para o aumento da citotoxicidade das células iNKT e desempenhar um papel na melhoria do defeito citotóxico. Este é o primeiro estudo que conduziu uma extensa análise de correlações entre variáveis clínicas para a DPOC e variáveis imunológicas. Os resultados das nossas correlações indicaram que algumas células podem estar associadas a uma melhoria no estado de saúde do paciente e outras com o agravamento da DPOC. Este foi um estudo exploratório, e mais investigações sobre este tema são necessárias para fortalecer as conclusões.
Chronic obstructive pulmonary disease (COPD) is one of the most common inflammatory diseases of the airways and a leading cause of morbidity and mortality worldwide. The disease is characterized by a persistent airflow limitation, generally progressive. Chronic inflammatory and immune responses play key roles in the development and progression of COPD. The inflammation is a normal protective response, but in COPD this inflammation is amplified. Several inflammatory cells, their mediators and enzymes participate in the inflammatory response in COPD. Pulmonary rehabilitation is a core component of chronic obstructive pulmonary disease management. It is designed to improve the physical and psychological condition of people with chronic respiratory disease and to promote the long-term adherence of health-enhancing behavior. The main aim of this work was to contribute for understanding the role of iNKT cells in COPD pathology. In addition we also aimed to explore the effect of pulmonary rehabilitation on the iNKT cells in patients with COPD. Clinical and immunological analysis were done in patients with COPD (n=7), patients with COPD performing pulmonary rehabilitation (n=4) and age- and gender-matched healthy controls (n=14). Participants were studied twice, with an interval of 12 weeks. The following clinical parameters were studied: body mass index, body fat percentage, pulmonary function, respiratory muscle strength, quadriceps muscle strength, five time seat to stand, COPD assessment test and modified medical research council. The iNKT cells were studied in terms of percentage, phenotype, cytotoxicity and cytokine production. No alteration in percentage of iNKT cells, their subsets and cytokine production were observed in the peripheral blood of patients with COPD in comparison with controls. Our results suggested that iNKT cells from patients with COPD might have a decrease in early activation by reduction of CD69 expression. A reduction in cytotoxic capacity in patients was also suggested. Pulmonary rehabilitation did not seem to affect the reduction of CD69 expression, but seemed to contribute to the increase in iNKT cell cytotoxicity and might have a role in improving the cytotoxic defect. This is the first study that conducted an extensive correlation analysis between clinical variables for COPD and immunological variables. Findings from our correlations indicated that some cells might be associated with an improvement in the health condition of the patient, and others with the worsening of COPD. This was an exploratory study, and further research on this topic is warranted to strengthen conclusions.
7
Murphy, Nicola. "Chronic obstructive pulmonary disease and anxiety". Thesis, Coventry University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368862.
Pełny tekst źródła
8
Shafi, N. T. "Pulmonary involvement in Anderson Fabry Disease". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1414900/.
Pełny tekst źródłaStreszczenie:
Aim: To investigate the clinical, physiological, radiological and pathological changes which occur in the lungs in Anderson Fabry Disease (AFD) Methods: In this study we have used lung function testing, high resolution CT scanning and induced sputum examination to investigate the lung. We have measured sputum enzyme activity using fluorometric assays, cell populations using flow cytometry and cytokines using enzyme linked immunosorbent assays. We have compared investigation findings from AFD subjects with those from patient’s with airways disease in the form of chronic obstructive pulmonary disease (COPD) and healthy controls Results: We have shown that respiratory symptoms are common, and airway involvement is widespread though mild in AFD. Pulmonary involvement is more common in males, in subjects with worse overall disease as measured by Mainz Severity Score Index, and is independent of smoking. No significant radiological changes were evident on CT chest imaging in AFD. We have presented novel data on α-galactosidase A activity from lung derived samples, which demonstrate low sputum enzyme activity in AFD males compared to controls and AFD females, and consistently higher enzyme activity in sputum derived leucocytes compared to those derived from peripheral blood. We did not find any detectable differences in blood or sputum α-galactosidase A activity in subjects on enzyme replacement therapy. Cell populations from induced sputum in AFD subjects demonstrated a predominance of monocytes/macrophages, similar to the COPD subjects, and there was the suggestion of an increased T cell population in AFD subjects with airway obstruction compared to those without. Elevated concentrations of sputum IL-8 were seen in the sputum of AFD subjects compared to controls. Conclusion: There is demonstrable and clinically relevant involvement of the lungs in AFD, which appears to occur as a result of deficient α-galactosidase A in the lungs and subsequent inflammatory processes.
9
Raeside, David Alexander. "Ambulatory pulmonary artery pressure monitoring in pulmonary vascular disease in man". Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398763.
Pełny tekst źródła
10
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.
Pełny tekst źródła
11
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.
Pełny tekst źródła
12
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.
Pełny tekst źródłaStreszczenie:
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.
13
Nicholson, Andrew Gordon. "Pulmonary lymphoproliferative disorders". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320619.
Pełny tekst źródła
14
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.
Pełny tekst źródła
15
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.
Pełny tekst źródła
16
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.
Pełny tekst źródła
17
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.
Pełny tekst źródła
18
Revill, Susan M. "Endurance exercise in chronic obstructive pulmonary disease". Thesis, Loughborough University, 1997. https://dspace.lboro.ac.uk/2134/15388.
Pełny tekst źródła
19
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.
Pełny tekst źródła
20
Donaldson, Anna. "Circulating microRNA in Chronic Obstructive Pulmonary Disease". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24776.
Pełny tekst źródłaStreszczenie:
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.
21
Darrah, Rebecca J. "Genetic Modifiers of Cystic Fibrosis Pulmonary Disease". Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270133199.
Pełny tekst źródła
22
Taylor, Abigail Elizabeth. "Macrophage phagocytosis in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/7374.
Pełny tekst źródłaStreszczenie:
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.
23
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.
Pełny tekst źródła
24
Noell, Guillaume. "Multi-Level Integrated Analysis of Chronic Obstructive Pulmonary Disease (COPD) heterogeneity". Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667980.
Pełny tekst źródłaStreszczenie:
Non-Communicable Diseases (NCDs), including cancer, cardiovascular (heart diseases or stroke), respiratory (COPD or asthma) and metabolic diseases (diabetes) are chronic conditions that represent a major global health problem of the 21st century. All of them, however, are the end-result of a complex set of gene-environment interactions that develop over years and often lead to several NCDs co-existing in the same individual (multi-morbidity).
Multi-level integrated analysis has the potential to uncover the heterogeneity of NCDs by conceptualizing them as emergent properties of a complex, non-linear, dynamic and multilevel biological system, or network of biological and environmental interactions.
Chronic Obstructive Pulmonary Disease (COPD) is a NCD of increasing prevalence worldwide that is projected to be by 2020 the third leading cause of death worldwide. It is currently viewed as a broad diagnostic term that encompass a continuum of subtypes each characterized by distinct functional or pathobiological mechanisms (endotypes) and is characterized by persistent respiratory symptoms and airflow limitation.
The underlying hypothesis of this PhD Thesis is that multi-level integrated analysis can help us understand highly heterogeneous respiratory diseases such as COPD. Specifically, the following two aspects of COPD heterogeneity will be addressed:
1) Exacerbations of COPD (ECOPD): ECOPD are episodes of worsening of the symptoms whose pathogenesis and biology are not entirely understood. They are heterogeneous events of non-specific diagnosis. Biomarkers analysis and networks medicine were used to uncover novel pathobiological information from the comparison of the multi-level (i.e., clinical, physiological, biological, imaging and microbiological) correlation networks determined during ECOPD and clinical recover. We concluded that ECOPD are characterised by disruption of network homeokinesis that exists during convalescence and can be identified objectively by using a panel of three biomarkers (dyspnoea, circulating neutrophils and CRP levels) frequently determined in clinical practice.
2) Early low lung function and health in later life: In 2015 Lange P. et al. showed that low peak lung function in early adulthood is associated with the diagnosis of COPD later in life. We assessed in three general population cohorts the prevalence of low peak lung function and its association with other clinical or biological parameters - specifically respiratory, cardiovascular, and metabolic abnormalities – as well as incidence of comorbid diseases during follow-up. We concluded that low peak lung function in early adulthood is common in the general population and could identify a group of individuals at risk of early (cardiovascular, metabolic and systemic) comorbidities and premature death.
25
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.
Pełny tekst źródła
26
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.
Pełny tekst źródła
27
Puhan, Milo Alan. "Patient-oriented research in chronic obstructive pulmonary disease /". Zürich, 2005. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253399.
Pełny tekst źródła
28
Roberts, Della Kim. "The family experience with chronic obstructive pulmonary disease". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24422.
Pełny tekst źródłaStreszczenie:
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
29
Thomas, Catherine. "Defective innate immunity in chronic obstructive pulmonary disease". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/40171.
Pełny tekst źródłaStreszczenie:
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.
30
Camp, Patricia. "Sex and gender in chronic obstructive pulmonary disease". Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1410.
Pełny tekst źródłaStreszczenie:
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.
31
Sze, Marc Alexander. "The lung microbiome in chronic obstructive pulmonary disease". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/36343.
Pełny tekst źródłaStreszczenie:
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).
32
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.
Pełny tekst źródła
33
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.
Pełny tekst źródłaStreszczenie:
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.
34
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.
Pełny tekst źródła
35
Eltboli, Osama M. I. "Eosinophilic airways inflammation in Chronic Obstructive Pulmonary Disease". Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32546.
Pełny tekst źródłaStreszczenie:
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.
36
Hobbs, Brian. "Exome Array Analysis of Chronic Obstructive Pulmonary Disease". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:22837731.
Pełny tekst źródłaStreszczenie:
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.
37
Alhaddad, Maath. "Cardiopulmonary manifestations in chronic obstructive pulmonary disease (COPD)". Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/30008/.
Pełny tekst źródłaStreszczenie:
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.
38
Bevan-Smith, Elaine. "Motivation in pulmonary rehabilitation". Thesis, Coventry University, 2008. http://curve.coventry.ac.uk/open/items/10ee3dc6-2fee-4897-8dde-eb7be1b686e6/1.
Pełny tekst źródłaStreszczenie:
Pulmonary rehabilitation is a highly evidenced intervention used in the management of patients with chronic obstructive pulmonary disease. Both patients and healthcare professionals have anecdotally acknowledged motivation as a key element in a programme. It has been suggested by some authors that motivation should be a prerequisite to entry, yet there is no evidence to support this suggestion. The purpose of this study therefore, was to provide some theory about the role of motivation in pulmonary rehabilitation and to produce a measurement instrument to enable further quantitative study. Methods A qualitative, exploratory investigation using focus groups and face-to-face interviews with patients undergoing a pulmonary rehabilitation programme was undertaken to generate data around factors influencing motivation. Results were used to develop a 43 item self-report questionnaire. The questionnaire was administered to 77 patients before and after a pulmonary rehabilitation programme along with other health status measures. The questionnaire was tested for reliability and validity. Item reduction was performed using factor analysis. Results Motivation within the context of a PR programme was shown to consist of a number of psychological, social and circumstantial variables that fell into 3 broad dimensions: Essential motivation, external motivation and functional outcome. A key finding was that attending pulmonary rehabilitation had an enormous positive influence on the patients’ essential motivation. The questionnaire was reduced to 21 items and principal components analysis demonstrated 9 factors within the questionnaire. These were function, self-efficacy, effort, optimism, tenacity, self worth, isolation, ability and achievement. The questionnaire was named the Malvern pulmonary rehabilitation motivation questionnaire (MPMQ) for identification. The MPMQ was shown to be reliable with internal consistency, reproducibility on test-retest and sensitivity to change. Correlations were found between the MPMQ and health related quality of life, anxiety and depression, breathlessness, exercise capacity and hospital admissions during the previous 12 months. Motivation score was significantly lower in patients who dropped out of the programme and was significantly higher at the end than the start of a programme. Conclusion The MPMQ has been shown to be a reliable tool with sound evidence of validity that can be used to objectively assess patients’ motivation within the context of a pulmonary rehabilitation programme. These findings need to be supported with further evidence for the validity and reliability of the questionnaire. Further investigation of the association of MPMQ score and adherence in pulmonary rehabilitation is needed along with further exploration of the determinants of motivation. This would enable specialist staff to identify patients who are likely to have adherence problems and channel efforts into effective cognitive-behavioural interventions in the ongoing effort to establish the optimum pulmonary rehabilitation programme.
39
Allwood, Brian William. "Tuberculosis-associated obstructive pulmonary disease: a clinical, radiological and pathophysiological study of the contribution of previous pulmonary tuberculosis in a community-based study of chronic obstructive pulmonary disease". Doctoral thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/12715.
Pełny tekst źródłaStreszczenie:
Includes bibliographical references.Epidemiological studies in populations with a high burden of pulmonary tuberculosis (PTB), including the Burden of Obstructive Lung Disease (BOLD) survey performed in Cape Town, South Africa in 2005, have suggested an association between PTB and the development of chronic airflow obstruction (CAO). The nature of this association and mechanisms responsible for CAO has not been previously studied, but likely includes: airway narrowing (from bronchiolitis, bronchiectasis or persistent low-grade inflammation associated with healed PTB); and reduced lung elastic recoil from coexistent emphysema. The present study investigated the structure and function of the lung in subjects with tuberculosis-associated obstructive pulmonary disease (TOPD) identified in BOLD 2005, and aspects of its natural history and response to treatment. It also examined the diagnostic performance of the standardised and internationally accepted BOLD method for estimating the prevalence of COPD in community-based surveys, with specific reference to misdiagnosis that might lead to overestimates of prevalence.
40
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.
Pełny tekst źródłaStreszczenie:
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.
41
Batlle, Garcia Jordi de. "Measure and effect of diet in chronic obstructive pulmonary disease". Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/52896.
Pełny tekst źródłaStreszczenie:
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.
42
Terada, Kunihiko. "Impact of gastro-oesophageal reflux disease, symptoms on chronic obstructive pulmonary disease exacerbation". Kyoto University, 2009. http://hdl.handle.net/2433/124263.
Pełny tekst źródła
43
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.
Pełny tekst źródłaStreszczenie:
Thesis (M.S.)--Worcester Polytechnic Institute.Keywords: latent class model; Poisson regression model; Metropolis-Hastings sampler; order restriction; disease mapping. Includes bibliographical references.
44
Domenech, Pena Arnau. "Dynamics of Streptococcus pneumoniae in patients with Chronic Obstructive Pulmonary Disease". Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/134277.
Pełny tekst źródłaStreszczenie:
It is estimated that within a few years chronic obstructive pulmonary disease (COPD) will be the third leading cause of death worldwide. The morbidity and mortality associated with COPD are due, in part to acute exacerbation episodes (AECOPD), mainly caused by microbial pathogens such as Haemophilus influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa. Moreover, COPD is the main underlying disease associated with pneumococcal pneumonia episodes.
This thesis describes four studies performed to gain insights into the role of pneumococci and their closely-related species S. pseudopneumoniae in causing acute exacerbation and pneumonia episodes in COPD patients.
In the first study, a total of 188 sputum samples were obtained from AECOPD episodes occurring in severe COPD patients during a 1-year period. Samples were quantitatively cultured; of them, S. pneumoniae was isolated in 31 (16.5%) episodes and S. pseudopneumoniae in 9 (4.8%) episodes. S. pneumoniae was the third most frequent cause after Pseudomonas aeruginosa (28.8%) and Haemophilus influenzae (19.7%).
There are major differences in the invasiveness potential of pneumococci, depending on their serotype and genotype. Indeed, in our second study (from 2001 to 2008) we found an association of certain serotypes, and their related genotypes, with different pneumococcal infections. Serotypes 4 (ST2474), 5 (Colombia5-ST289) and 8 (Netherlands8-ST53) were associated with bacteraemic pneumonia, serotypes 1 (Sweden1-ST306) and 3 (Netherlands3-ST180 and ST2603) with bacteraemic and non-bacteraemic pneumonia, and serotypes 16F (ST3016F), 11A and non-typeable pneumococci with AECOPD episodes (P<0.05). Finally, in our experience, serotype 3 pneumococcus was the most frequent cause of pneumonia and acute exacerbations in COPD patients.
Moreover, the implementation of pneumococcal conjugate vaccine PCV7 for children in 2001 in Spain has been shown to be highly effective in reducing invasive pneumococcal disease in children, and in adults as well due to the phenomenon of herd protection. This effect was also observed among pneumococci causing acute exacerbations in adults: PCV7 serotypes decreased from 39.4% in the 2001-04 period to 11.2% in the 2009-12 period. In parallel, the prevalence of multi-drug resistant serotypes 15A and 6C has dramatically increased in recent years. For this reason, although the resistance rates of β-lactams decreased over time, macrolides and multi-drug resistance remained stable throughout the study period.
The presence of bacteria colonizing the lower airways of most severe COPD patients results in bronchial epithelial injury and increases morbidity among these patients. In the third study (1995-2010 period), it was found that a third of recurrent pneumococcal acute exacerbations were relapses (caused by a pre-existing strain), mainly associated with serotypes 9V and 19F (P<0.02). This suggests an important role for capsular type in pneumococcal persistence. In view of these results, we analysed the impact of antimicrobial consumption in the development of pneumococcal resistance to β-lactams and fluoroquinolones in 13 patients with a long-time persistence of pneumococci (average time: 582 days, SD ±362). Changes in quinolone-resistant determining regions (QRDR) involved in fluoroquinolone resistance were frequently observed in persistent strains after fluoroquinolone treatment; however, the penicillin-binding protein (PBP) sequences were stable over time, even though all but two patients received multiple courses of β-lactam treatment. These results suggest that an optimal combination of pbp genes is maintained to compensate for the fitness cost imposed by additional changes in these genes.
Despite the genetic stability of these persistent strains, S. pneumoniae is naturally transformable and is able to acquire exogenous DNA, resulting in a dynamic and complex epidemiology of pneumococcal diseases. This genetic diversity was also observed among the 36 S. pseudopneumoniae strains analysed.
Altogether, our studies can help to improve the understanding of the dynamics of S. pneumoniae and S. pseudopneumoniae populations causing disease in COPD patients.En aquesta tesis, es van dur a terme quatre estudis amb l’objectiu d’aprofundir en el paper de S. pneumoniae com a causant d’exacerbacions agudes i pneumònia en pacients amb MPOC. En el primer estudi, es van sembrar quantitativament un total de 188 mostres d’esput obtingudes durant episodis d’EAMPOC en pacients amb MPOC avançat, durant un any d’estudi (febrer 2010 - febrer 2011). S. pneumoniae es va aïllar en 31 (16.5%) episodis i fou la tercera causa d’exacerbació, després de Pseudomonas aeruginosa (28.8%) i Haemophilus influenzae (19.7%). En el segon estudi es va trobar una diferent associació d’alguns serotipus i del seus genotipus relacionats, en pacients amb MPOC amb diferents infeccions pneumocòcciques (període 2001-2008). El serotipus 3 va ser la causa més freqüent de pneumònia i d’EAMPOC, però els serotipus 4 (ST2474), 5 (Colombia5-ST289) i 8 (Netherlands8-ST53) es varen associar amb pneumònia bacterièmica; serotipus 1 (Sweden1-ST306) i 3 (Netherlands3-ST180 i ST2603) es varen associar amb pneumònia tant bacterièmica com no bacterièmica; mentre serotipus 16F (ST3016F), 11A i els pneumococs no-tipificables es varen associar amb EAMPOC (P<0.05). Degut a la implementació de la vacuna conjugada PCV7, els serotipus inclosos en la vacuna han disminuït del 39.4% en el període 2001-2004 a 11.2% en el període 2008-2012. Paral•lelament a aquest descens, els serotipus 15A i 6C han augmentat dramàticament en els últims anys. Per aquesta raó, la multiresistència s’ha mantingut estable durant tot el període d’estudi. En el tercer estudi (1995-2010), es va observar que un terç dels episodis d’EAMPOC recurrents, varen ser causats per una soca preexistent, principalment serotipus 9V i 19F (P<0.05), considerant-se recaigudes. Aquest fet suggereix un paper important del tipus capsular en la persistència. Finalment, es va analitzar l’impacte del consum d’antimicrobians en el desenvolupament de resistència en 13 pacients colonitzats per pneumococc (temps mitjà: 582 dies, DS ±362). Es van observar canvis en les QRDRs de les soques d’aquells pacients que van rebre tractament amb fluoroquinolones. En canvi, les PBPs de les soques persistents van romandre estables tot i els múltiples tractaments amb β-lactàmics que van rebre els pacients. En total, els estudis presentats han millorat el coneixement de la dinàmica de les poblacions de S. pneumoniae i S. pseudopneumoniae en pacients amb MPOC.
45
Meshe, Oluwasomi F. "Physical activity, health status and hospital admission in chronic obstructive pulmonary disease following pulmonary rehabilitation". Thesis, Anglia Ruskin University, 2018. http://arro.anglia.ac.uk/703781/.
Pełny tekst źródłaStreszczenie:
Background: Despite the several benefits of post-rehabilitation Community-based Exercise Programmes (CEPs) to people with COPD, it is unclear whether these patients objectively improve their levels of daily physical activity (PA) and whether this is associated with improvement in other clinical outcomes. Methods: A mixed-methods sequential explanatory study design was applied. Daily PA (accelerometers, model AM300), health status (Saint George’s Respiratory Questionnaire, SGRQ), exercise capacity (6MWD testing), pulmonary functional, FEV1 (spirometry) and number of hospital admission (self-reporting) were measured at time points 1 (start of study) and 2 (after 3 months) of a CEP in 26 participants with COPD (mean [±SD] age, 73±7 years; FEV1, 64±19% predicted). Participants’ views of the benefits, barriers and enablers of participation were also explored. Results: Levels of daily PA improved moderately (42 minutes/day on moderate-intensity PA) but not significantly. Health status, 6MWD and FEV1 improved while hospital admission reduced significantly after 3 months (all p< 0.05). Daily PA correlated positively with 6MWD (r = 0.40, p=0.046) and negatively with health status (r= -0.52, p=0.006) and number of hospital admission (r= -0.394, p<0.05). Changes in levels of daily PA correlated positively with changes in 6MWD (r= 0.31, p= 0.048) and negatively with changes in health status (r= -0.65, p= 0.0001). Only health status significantly predicted levels of daily PA (Beta= -0.47, t= -2.85, p=0.009, R2adjusted= 0.38). These results were enabled by six factors; ease of access to PA intervention, convenient programme components, being retired, feeling safe, social support and seasons. Four barriers to activity participation were identified; poor physical health, family commitments, transport difficulties and other commitments. Conclusion: Moderate improvement in levels of daily PA produced by a CEP is associated with improvements in clinical outcomes in people with COPD. Strengthening enablers of adherence to the programme is important to achieving the goals of COPD management.
46
Curtis, Katrina Jane. "Augmenting pulmonary rehabilitation in chronic obstructive pulmonary disease : studies of ACE-inhibition and nitrate supplementation". Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/44728.
Pełny tekst źródłaStreszczenie:
This thesis addresses two approaches to enhancing exercise capacity in chronic obstructive pulmonary disease (COPD). The first is by manipulation of the renin-angiotensin system through angiotensin-converting enzyme (ACE) inhibition to establish if this can augment the response to pulmonary rehabilitation. The second is nitrate supplementation, assessed for its effects on endurance exercise parameters. In a cross-sectional study of 78 patients with at least moderate severity COPD I found no association between ACE genotype and exercise parameters during incremental cycle ergometry, in contrast to previous work from a Chinese group. The role of the renin-angiotensin pathway in skeletal muscle impairment in COPD is likely to be highly complex, and there are both potential beneficial and adverse effects of angiotensin II, and potentially conflicting effects on strength and endurance exercise capacity. The absence of differences in a cross-sectional study do not preclude the possibility that the ACE genotype may influence the response to both training and detraining through physical inactivity, and this remains an area of possible future research. I went on to test the effect of the ACE-inhibitor enalapril on the response to pulmonary rehabilitation, focussing on the change in peak exercise capacity. I undertook a double-blind randomised controlled trial of 80 COPD patients with at least moderate airflow obstruction referred for pulmonary rehabilitation. There was evidence of adequate suppression of ACE activity through both the suppression of serum ACE levels and alteration in blood pressure parameters in the enalapril treated arm. Contrary to expectations the peak power achieved on incremental cycle ergometry increased more in the placebo arm of the study than the ACE-inhibitor treated arm. No significant differences were noted in computed tomography measures of muscle bulk, quadriceps strength or health-related quality of life. Thus, in subjects without a pre-existing clinical indication for ACE-inhibition, use of the ACE-inhibitor enalapril reduced the response to exercise training in COPD. I also conducted a pilot study to investigate the role of acute nitrate supplementation on endurance exercise characteristics and oxygen consumption during endurance exercise in COPD. I recruited 25 subjects into a double-blind, placebo-controlled, single-dose cross-over study. Nitrate supplementation, in the form of beetroot juice at a dose of 12.9 mmoles, significantly lowered resting diastolic blood pressure and isotime pulmonary oxygen consumption. This did not translate into an improvement in endurance time. This preliminary work will provide the basis for further studies, including the potential role of nitrate supplementation in enhancing the response to pulmonary rehabilitation and the role of nitrate supplementation on exercise capacity in individuals with exercise induced hypoxaemia.
47
Meshe, Oluwasomi F. "Physical activity, health status and hospital admission in chronic obstructive pulmonary disease following pulmonary rehabilitation". Thesis, Anglia Ruskin University, 2018. https://arro.anglia.ac.uk/id/eprint/703781/1/Meshe_2018.pdf.
Pełny tekst źródłaStreszczenie:
Background: Despite the several benefits of post-rehabilitation Community-based Exercise Programmes (CEPs) to people with COPD, it is unclear whether these patients objectively improve their levels of daily physical activity (PA) and whether this is associated with improvement in other clinical outcomes. Methods: A mixed-methods sequential explanatory study design was applied. Daily PA (accelerometers, model AM300), health status (Saint George’s Respiratory Questionnaire, SGRQ), exercise capacity (6MWD testing), pulmonary functional, FEV1 (spirometry) and number of hospital admission (self-reporting) were measured at time points 1 (start of study) and 2 (after 3 months) of a CEP in 26 participants with COPD (mean [±SD] age, 73±7 years; FEV1, 64±19% predicted). Participants’ views of the benefits, barriers and enablers of participation were also explored. Results: Levels of daily PA improved moderately (42 minutes/day on moderate-intensity PA) but not significantly. Health status, 6MWD and FEV1 improved while hospital admission reduced significantly after 3 months (all p< 0.05). Daily PA correlated positively with 6MWD (r = 0.40, p=0.046) and negatively with health status (r= -0.52, p=0.006) and number of hospital admission (r= -0.394, p<0.05). Changes in levels of daily PA correlated positively with changes in 6MWD (r= 0.31, p= 0.048) and negatively with changes in health status (r= -0.65, p= 0.0001). Only health status significantly predicted levels of daily PA (Beta= -0.47, t= -2.85, p=0.009, R2adjusted= 0.38). These results were enabled by six factors; ease of access to PA intervention, convenient programme components, being retired, feeling safe, social support and seasons. Four barriers to activity participation were identified; poor physical health, family commitments, transport difficulties and other commitments. Conclusion: Moderate improvement in levels of daily PA produced by a CEP is associated with improvements in clinical outcomes in people with COPD. Strengthening enablers of adherence to the programme is important to achieving the goals of COPD management.
48
Koreny, Maria 1972. "Determinants of physical activity behaviour in patients with chronic obstructive pulmonary disease". Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/671432.
Pełny tekst źródłaStreszczenie:
Background: Although physical activity is key to improve prognosis in patients with chronic obstructive pulmonary disease (COPD), information to tailor interventions individually is still required. This thesis aims to understand physical activity progression and explore its determinants in COPD patients.
Methods: We used baseline and 12-month data from 643 COPD patients with stable mild-to very severe disease from two European multicenter studies. We assessed: physical activity (Dynaport MoveMonitor), physical activity experience (Clinical visit-PROactive physical activity in COPD [C-PPAC]), functional exercise capacity (6-minutes walk distance [6MWD]), as well as sociodemographic, interpersonal, environmental, clinical and psychological variables.
Results: (1) The natural progression in physical activity over time was heterogeneous and three distinct patterns could be identified: Inactive, Active Improvers and Active Decliners. While Inactive patients related to worse scores for clinical COPD characteristics, Active Improvers and Decliners could not be predicted at baseline; (2) Higher population density and long-term NO2 exposure were associated with lower physical activity, while a steeper slope of the terrain related to better exercise capacity; (3) twelve-month completion of a behavioral physical activity intervention was determined by previous physical activity habits as well as interpersonal and environmental facilitators, while response to the intervention was related to diverse factors associated with motivation to change to an active lifestyle.
Conclusions: This thesis shows that the natural progression of physical activity in COPD patients is heterogeneous and highlights that environmental, interpersonal and psychological factors are important determinants of physical activity behaviour in COPD patients, beyond clinical factors.Antecedentes: Aunque la actividad física es clave para mejorar el pronóstico en pacientes con enfermedad pulmonar obstructiva crónica (EPOC), todavía no se dispone de información que permita adaptar las intervenciones de manera individualizada. El objetivo de la presente tesis es comprender la progresión de la actividad física y explorar sus determinantes en pacientes con EPOC. Métodos: Utilizamos datos basales y de seguimiento (12 meses) de 643 pacientes con EPOC estable de estadio leve a muy grave, procedentes de dos estudios europeos multicéntricos. Evaluamos: actividad física (Dynaport MoveMonitor), experiencia de actividad física (Clinical visit-PROactive physical activity in COPD [C-PPAC]), capacidad funcional de ejercicio (distancia caminada en la prueba de la marcha de 6 minutos [6MWD]) y variables sociodemográficas, interpersonales, ambientales, clínicas y psicológicas. Resultados: (1) La progresión natural de la actividad física a lo largo del tiempo fue heterogénea y se pudieron identificar tres patrones distintos: inactivo, activo que aumenta y activo que reduce. Mientras que el patrón de pacientes inactivo se relacionaba con peores características clínicas de la EPOC, no se pudo predecir la evolución de los activos a aumentar o reducir; (2) la mayor densidad de población y la exposición a largo plazo al NO2 se asociaron desfavorablemente con la actividad física, mientras que una mayor pendiente del terreno se relacionó con una mejor capacidad de ejercicio; (3) la compleción a los 12 meses con una intervención de actividad física conductual estuvo determinada por los hábitos de actividad física previos, así como por facilitadores interpersonales y ambientales, mientras que la respuesta a la intervención se relacionó con diversos factores asociados a la motivación para cambiar a un estilo de vida activo. Conclusiones: Esta tesis muestra que la progresión natural de la actividad física en los pacientes con EPOC es heterogénea y destaca que los factores ambientales, interpersonales y psicológicos son importantes determinantes de la actividad física en los pacientes con EPOC, más allá de los factores clínicos. Resum Antecedents: Malgrat el paper clau de l’activitat física per millorar el pronòstic en pacients amb malaltia pulmonar obstructiva crònica (MPOC), encara no disposem d’informació que permeti individualitzar les intervencions. L’objectiu d’aquesta tesi és entendre la progressió de l’activitat física i explorar-ne els determinants en pacients amb MPOC.
49
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.
Pełny tekst źródłaStreszczenie:
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
50
McPherson, E. A. "Equine chronic obstructive pulmonary disease (COPD) : publications 1974-1985". Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/28607.
Pełny tekst źródła