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1
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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2
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
3
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).
4
Dhillon, Satvir Singh. "Physical activity measurement strategies in advanced chronic lung disease." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50830.
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Background: Physical activity may reduce mortality risk in advanced chronic lung disease by optimizing functional capacity, which is a major prognostic indicator in lung transplantation candidates. There is uncertainty as to the optimal method to measure physical activity in this patient population. We assessed different commercially-available physical activity measurement techniques (flex heart rate monitoring (FHR); pedometry; tri-axial accelerometry; and multi-sensor technology) by investigating their agreement with indirect calorimetry (IC) in adult lung disease patients (chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), and cystic fibrosis (CF)) with advanced pulmonary impairment.
Methods: This is a cross-sectional method comparison study conducted on two separate days. We recruited consecutive COPD, ILD, and CF patients with physician diagnosis of advanced pulmonary impairment. On day one, participants performed cardiopulmonary exercise testing until exhaustion with measurements of oxygen uptake (VO₂) and heart rate (HR) collected. On day two, subjects had their VO₂ and HR measured during standardized resting and sub-maximal activity. Simultaneous VO₂ and HR measures from both days were used to develop individual regressions for FHR-derived energy expenditure (EE). We then simultaneously measured each subject’s EE using a variety of index measures of physical activity and IC during standardized “free-living” type activities and varying intensities of sub-maximal cycle exercise.
Results: In a sample of eight participants (CF, n=5; COPD, n=2; ILD, n=1), Flex HR methods using submaximal (FMSUB) and CPET-derived (FMCPX) calibrations showed the best agreement and interchangeability with IC during free-living and cycling activities compared to the SenseWear (SW) and ActiCal (AC) devices as evidenced by lower mean differences with IC and widths of limit of agreement (LOA) + 95% confidence interval (CI). For the secondary index methods assessed, the Tractivity and DigiWalker devices significantly over and underestimated IC EE respectively (p<0.05), whereas the Dynaport device did not differ from IC (p>0.05) over the entire protocol.
Conclusion: Our study found that the Flex HR method for EE estimation had the lowest bias and variability during free-living activities and exercise. EE estimation using Flex HR methods may be potentially useful clinical tools to ensure metabolic energy balance and activity monitoring in advanced lung disease groups.Medicine, Faculty of
Graduate
5
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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6
Sweet, D. G. "Studies on the pathogenesis of neonatal chronic lung disease." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395367.
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Kotecha, Sailesh. "The role of cytokines in chronic lung disease of prematurity." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244032.
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Soler, Artigas María. "Genetic epidemiology of lung function and chronic obstructive pulmonary disease." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/31980.
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Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. Lung function measures obtained through spirometry play a key role in the diagnosis of COPD. Both COPD and lung function are affected by genetic factors, and identifying genetic variants that have an effect on lung function or COPD risk has the potential to lead to improved treatment and prevention of COPD. This thesis is structured in five chapters, an introductory, a concluding chapter and three main chapters which present different approaches that aim to bring insights into the genetics of COPD and lung function. Chapter 2 tests the association with COPD risk of genetic variants previously associated with lung function, and tests their combined effect on lung function and COPD risk, in order to explore the role of risk prediction. Chapter 3 aims to identify new genetic variants associated with lung function and tests the association of genetic variants genome-wide. Chapter 4 focuses on the analysis of low frequency variants using different approaches and methodologies, and includes two studies. One study assesses associations of low frequency variants genome-wide, and the other focuses on genetic regions associated with lung function, in order to improve the localization of association signals that often comprise broad regions and several genes. These studies overall have identified 16 new genetic variants associated with lung function, have shown the association with COPD of 4 genetic variants previously associated with lung function, and present suggestive evidence of association with COPD for low frequency variants within regions associated with lung function.
9
Brandén, Eva. "Chronic infection with Chlamydia pneumoniae in COPD and lung cancer." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-344-2/.
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Steele, Bonnie Gail. "Dimensions of dyspnea in chronic obstructive pulmonary disease : a nociceptive model /." Thesis, Connect to this title online; UW restricted, 1991. http://hdl.handle.net/1773/7347.
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Ramis, Cabrer Daniel 1993. "From chronic obstructive pulmonary disease to lung cancer : an immunologic approach." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/667310.
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Se ha establecido que un subconjunto de pacientes con cáncer debuta con
infiltrados inmunes que se organizan en agregados en el nicho tumoral y
sus alrededores. Estas estructuras linfoides se desarrollan en respuesta a
estímulos inflamatorios a través de un proceso estrechamente regulado.
Además de su valor pronóstico, las TLSs pueden representar una nueva
vía para las estrategias terapéuticas, pero actualmente se encuentra en
etapas iniciales. En contraste con el papel en la activación inmune de las
TLSs, en ciertos tumores, su efecto puede apuntar hacia la progresión
tumoral como consecuencia de las condiciones altamente
inmunosupresoras mediadas por las células malignas presentes en el
nicho tumoral. Los datos preliminares proporcionados por la siguiente
investigación sugieren que los pacientes con cáncer de pulmón podrían
presentar un perfil inmunitario diferencial respecto a estos mismos que
además subyacen EPOC. Este hecho podría presentar un impacto
potencial en el pronóstico y la terapia de estos pacientes. Por otra parte,
resultados procedentes de la actual investigación también revelan que
ciertos marcadores cruciales presentes en diferentes vías de señalización
involucradas con el estrés oxidativo, la apoptosis y la autofagia podría
sobre expresarse en respuesta a la administración de
inmunomoduladores. Estos datos ponen de manifiesto el interés de
mecanismos adicionales relacionados con la inmunidad que podrían ser
manipulados para asistir a la inmunidad contra el cáncer.It is well established that a subset of cancer patients debuts with immune infiltrates, which organize into aggregates in the tumor niche and its vicinity. These lymphoid structures develop in response to inflammatory stimuli through a tightly regulated process. Besides the prognostic value of TLSs, they also may represent a novel avenue for therapeutic strategies, but it is currently still in its early stages. In contrast with the immune activator role of TLSs, in certain cancers, its effect may point towards tumor progression as a consequence of highly tumor-mediated immunosuppressive conditions present in the tumor niche. Preliminary data provided by the current investigation suggests that a differential immune profile may be present between LC patients and LC patients underlying COPD. This fact could present a potential impact in the prognosis and therapy of these patients. Moreover, crucial markers targeting different signaling pathways involved with oxidative stress, apoptosis, and autophagy were found to be overexpressed in response to immunomodulators administration in the current thesis. These data puts into manifest the interest of additional immunity-related mechanisms that could be targeted in order to assist immunity against cancer.
12
Urs, Rhea Caroline. "Characterising Biomarkers of Chronic Lung Disease in Survivors of Preterm Birth." Thesis, Curtin University, 2021. http://hdl.handle.net/20.500.11937/88817.
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This research found preterm-born children displayed poor respiratory outcomes, with evidence of increased neutrophilic inflammation and oxidative stress, rather than the eosinophilic profile associated with “typical” childhood asthma. Additionally, metabolomic analysis showed preterm-born individuals have an altered metabolome from those born at term. Together this research provides insight into the contributors of chronic lung disease providing opportunities for early intervention and better lifelong respiratory outcomes in survivors of preterm birth.
13
Lithopoulos, Marissa Athena. "Mesenchymal Stromal Cells to Treat Lung and Brain Injury in Neonatal Models of Chronic Lung Disease." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42124.
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Bhunthurat, Anurak. "The Vitamin B-6 Status of Patients with Chronic Obstructive Pulmonary Disease." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc500541/.
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The problem of this study is to determine the vitamin B-6 status of patients who have chronic obstructive pulmonary disease (COPD). Erythrocyte aspartate transaminase assay was the method for measuring vitamin B-6 status. The vitamin B-6 status was examined in thirty subjects (ten COPD subjects and twenty control subjects). An unpaired t-test was used to compare the vitamin B-6 status of the COPD group versus the control group. Four determinants (percentage stimulation, ratio of basal to stimulated activity, basal activity, and stimulated activity) were used to determine vitamin B-6 status in both groups of subjects. Percentage stimulation and ratio of basal to stimulated activity were not significantly different (control group versus COPD group) at the .05 level. However, two of ten COPD subjects had values for percentage stimulation that were two standard deviations above the mean, indicating a poor B-6 status. In contrast, basal activity and stimulated activity of erythrocyte aspartate transaminase were found to be significantly lower at the .05 level in the COPD group than the control group. Therefore, the COPD subjects as a group had some biochemical characteristics of a lower level of vitamin B-6 than the controls.
15
Lehtonen, S. (Siri). "Localization and regulation of peroxiredoxins in human lung and lung diseases." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514277651.
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Abstract
Reactive oxygen species (ROS) can cause severe damage to cells and organs but they are also important mediators of inflammatory responses and cellular signalling. Due to the significant role of ROS, the cells have evolved a broad antioxidative system to regulate the concentration of these species. Peroxiredoxins (Prxs) are enzymes that participate in the regulation of the cellular redox-homeostasis by detoxifying hydrogen peroxide. Prxs are not classified as conventional antioxidant enzymes and their physiological role, whether protective or regulatory, is still unclear.
The aim of this project was to study the localization and regulation of Prxs in normal human lung and also their role in selected lung disorders (pulmonary sarcoidosis, pleural mesothelioma, lung carcinomas and chronic obstructive disorder, COPD). Additionally the expression of thioredoxin (Trx) and thioredoxin reductase (TrxR) was analysed in the lung of smokers and COPD patients. These enzymes are important reductants in cell and Prxs are one of their targets. Lung is an important organ in the field of ROS and antioxidant research since it is especially vulnerable to exogenous oxidative stress caused by pollutants, cigarette smoke and also by high oxygen pressure.
The results showed that all six human Prxs were expressed in healthy human lung but in a cell-specific manner. The most prominent expression was detected in the epithelium and in macrophages, the cells most prone to oxidative stress. There were also differences in subcellular locations of Prxs.
The expression of Prxs in non-malignant lung diseases (pulmonary sarcoidosis and COPD) and in smoker's lung was very similar with that in normal lung. Higher expression of Prx V and VI was detected in a subpopulation of macrophages sampled from COPD patients' lung. In contrast, Trx expression was induced in the bronchial epithelium of smoker's lung.
Differences in the expression compared to normal lung were seen in lung malignancies (pleural mesothelioma and lung carcinomas). Interestingly, different Prxs were highly expressed in different types of carcinomas. In pleural mesothelioma, all Prxs except Prx IV were highly expressed when compared to normal pleura, in adenocarcinoma Prxs I, II, VI and especially IV, and in squamous cell carcinoma Prxs I, II and IV were upregulated.
Tests performed on cultured cells in vitro revealed only a minor increase in the Prx expression after severe oxidant stress in malignant lung cell line originating from alveolar type II pneumocytes (A549) or non-malignant cell line derived from bronchial epithelium. None of the tested growth factors or cytokines affected Prx expression or oxidation state, but severe oxidant stress influenced remarkably the oxidation state of the Prxs.
16
Merikallio, H. (Heta). "Claudins and epitheliomesenchymal transition in lung carcinomas and chronic obstructive pulmonary disease." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526202471.
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Abstract Lung cancers and chronic obstructive pulmonary disease (COPD) are the most common smoking-related lung diseases and both have high mortality rate. Tight junctions (TJ) are apical junctions between epithelial cells that regulate the permeability of epithelium and form the tight junction along with occludin. Dysfunction of the TJ and dysregulation of TJ proteins leads to a loss of cell-cell adhesion and a loss of cohesion as well as epitheliomesenchymal transition. These increase invasion of lung carcinomas and possibly predispose to the exacerbations in COPD. Therefore, the aim of this thesis was to study expression and regulation of claudins in different lung carcinomas and COPD. Carcinomas expressed claudins 1, 2, 3, 4, 5 and 7 in different variations. Claudin 5 expression was weak in all carcinoma types. Strong claudin 1, 4 and 7 expression was associated with better survival in squamous cell carcinoma and adenocarcinoma. Claudin 3 expression was associated with COPD in large airways. Claudins 3 and 4 was found to be stronger in small airways of smokers and COPD patients than in non-smokers. Transcription factor snail had prognostic value in lung carcinomas. Negative snail expression was associated with longer life expectancy in lung carcinoma patients. Negative snail expression was associated with up-regulated claudin 5 and 7 expression, while strong expression was associated with low claudin 1 and 3 expression. Transcription factors slug and twist were inversely associated with claudins 3 and 4 in small and large airways. Slug expression was higher in non-smokers than in COPD patients and smokers. Transcription factor knockdown increased claudin expression in normal bronchial cell line. Except for claudin 2 and 7, which were decreased. Adenocarcinoma-like cell line was not affected by snail knockdown and in squamous cell carcinoma-like cell line claudin 3, 4 and 7 expression was increased. Transcription factor snail knockdown inhibited invasion of cell lines. Twist knockdown increased transepithelial resistance in normal bronchial cell line indicating higher barrier function in cell layerTiivistelmä Keuhkosyöpä ja keuhkoahtaumatauti ovat yleisiä tupakoinnin aiheuttamia keuhkosairauksia, joissa on korkea kuolleisuus. Tupakointi aiheuttaa muutoksia keuhkojen epiteelisoluissa ja solujen välisissä liitoksissa. Tiivisliitokset solujen välillä säätelevät epiteelin rakennetta ja läpäisevyyttä. Klaudiinit ovat proteiineja, jotka muodostavat tiivisliitoksen yhdessä okkludiinin kanssa. Tiivisliitos proteiinien toimintahäiriöt voivat johtaa solujen välisten liitosten katoamiseen ja epiteelin hajoamiseen sekä epiteelisolujen muuntumiseen mesenkymaalisten solujan kaltaisiksi. Nämä seikat lisäävät invaasiota keuhkosyövissä ja saattavat altistaa pahenemisvaiheisiin keuhkoahtaumataudissa. Väitöskirjassa tutkittiin klaudiinien ilmentymistä ja säätelyä keuhkosyövässä ja keuhkoahtaumataudissa. Klaudiinien1, 2, 3, 4, 5 ja 7 esiintyminen keuhkosyövän histologisissa alatyypeissä vaihteli. Klaudiinien 1, 4 ja 7 voimakas ilmentyminen voitiin yhdistää pidempään elinikään potilailla, joilla oli levyepiteeli- tai adenokarsinooma. Klaudiini 3:n ilmentyminen liittyi keuhkoahtaumatautiin suurissa hengitysteissä. Klaudiinien 3 ja 4 voimakas ilmeneminen pienissä ilmateissä oli yleisempää keuhkoahtaumatautipotilailla ja tupakoitsijoilla kuin tupakoimattomilla henkilöillä. Transkriptiotekijä snailin puuttuminen keuhkosyövässä liittyi potilaiden pidempään elinaikaan. Klaudiinien 5 ja 7 ilmeneminen oli voimakkaampaa, kun snailin määrä oli vähäinen. Klaudiinien 1 ja 3 ilmeneminen väheni snail:in ollessa voimakas keuhkosyövässä. Traskriptiotekijöiden (slug ja twist) ilmeneminen liittyi käänteisesti klaudiinien ilmentymiseen pienissä ja suurissa ilmateissä. Slugin ilmeneminen oli voimakkaampaa tupakoimattomilla henkilöillä kuin tupakoivilla tai keuhkoahtaumatautia sairastavilla. Transkriptiotekijöiden snail, slug ja twist toiminnan estäminen lisäsi klaudiinien määrää normaaleissa keuhkon epiteelisoluissa. Poikkeuksen muodostivat klaudiinit 2 ja 7, joiden määrä väheni kun snail:in toiminta oli estetty. Adenokarsinooma-soluissa snailin estolla ei ollut vaikutusta, ja levyepiteelisyövän soluissa klaudiinien 3, 4 ja 7 määrä kasvoi. Snail myös vähensi solujen invaasiota. Transkriptiotekijä twistin toiminnan esto normaaleissa keuhkoepiteelisoluissa nosti solumaton läpi kulkevan sähkön resistenssiä, mikä on osoitus tiiviistä solujen välisistä liitoksista
17
Vyas, Julian Ramesh. "Oxidants and antioxidants in the pathogenesis of chronic lung disease of prematurity." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29464.
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Reactive oxygen species and other radicals (e.g. peroxynitrite) are thought to play a role in the development of chronic lung disease of prematurity (CLD). I hypothesised that serial BAL may washout surfactant and cause persistent radiological changes. I also hypothesised that cellular antioxidants were depleted, and nitric oxide production was increased, in bronchoalveolar lavage fluid (BALF) from infants who developed CLD. Furthermore, my aim was to develop a technique to quantitate nitrite and nitrate in small (<50 microlitres) samples of BALF. 1 studied three groups of infants (those who developed CLD, those who recovered from respiratory distress syndrome (RDS), and control infants ventilated for surgical reasons) and (a) determined the safety of the BAL procedure, (b) developed methods to estimate nitric oxide (NO) products, (c) estimated nitrate and nitrite in BALF and (d) measured glutathione, urate and ascorbate in BALF and plasma. My data showed that serial BAL did not adversely affect radiological appearances. I studied several techniques for reducing nitrite to nitrate, and the Griess reaction and fluorometry to quantitate nitrite. I applied a modified enzymatic method, with fluorometric detection to measure NO products. BALF nitrate concentration was similar in all groups during the first week of life. Thereafter, nitrate concentration was significantly higher (p<0.05) in infants who developed CLD compared to those who did not. Nitrite concentration did not show any trends. There was a delayed increase in BALF ascorbate in the CLD group when compared to the RDS and Control groups. The BALF: plasma ratio of ascorbate was higher in the RDS group at 4 days of age than in the CLD group, suggesting that more mature infants have a better ability to concentrate ascorbate in their lungs. In summary, I noted differences in nitrate and ascorbate concentrations between infants who developed CLD, and those who didn't.
18
Joshi, Suchita. "Long term cardiorespiratory outcome in children with chronic lung disease of prematurity." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/55504/.
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The findings of this thesis suggest that children with CLD continue to have airway abnormalities including reversible airway obstruction, air trapping and impaired gas transfer compare to term and preterm controls at 8-12 years of age. Although they had similar exercise capacity to preterm and term control groups, this was at the expense of using greater proportion of their ventilatory reserve. At school age, they do not have evidence of myocardial dysfunction or subclinical pulmonary arterial hypertension.
19
Dai, Jie. "Clinical and genetic associations between lung cancer and chronic obstructive pulmonary disease." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/19263/.
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Lung cancer and chronic obstructive pulmonary disease (COPD) are both leading causes of death in the world, and these two disease are closely linked in the clinical setting and at the genetic level. Previous studies have indicated that COPD confers a higher risk for development of lung cancer, and also affects prognosis once lung cancer has occurred. The present thesis further explored the influences of timing of COPD diagnosis, severity of airflow limitation, radiological emphysema, and genetic variants on lung cancer outcomes. Over 1,000 patients who were diagnosed with non-small cell lung cancer at Mayo Clinic were included. Near two-thirds of patients with COPD were underdiagnosed at the time of lung cancer diagnosis. In comparison to the previously recognized COPD, an incidentally diagnosed COPD was a major factor that increased risks of postoperative complications (incidental COPD versus non-COPD: 28.1% versus 16.5%, p < 0.01) and impaired lung cancer survival (HR, 1.23; 95%CI, 1.05-1.45). Patients with moderate (HR, 1.22; 95%CI, 1.04-1.44) to severe airflow obstruction (HR, 1.75; 1.38-2.23) had a significantly poorer long-term outcome, while similar survival was found between patients with mild COPD and with normal lung function (p=0.97). The severity of regional emphysema was associated with overall survival in early stage lung cancer (p < 0.01), which was independent of tumor location, and it was predictive of quality of life related to dyspnea after lung cancer treatment (p < 0.05). Radiological emphysema was also correlated with postoperative lung function recovery (FEV1% and DLCO%, both p < 0.05) when tumor resection was performed in the emphysematous region. Meta-analysis indicated that the negative impact of COPD was more pronounced in patients with non-small cell lung cancer (pooled HR, 1.23; 95%CI, 1.16-1.30), at an early-stage (pooled HR, 1.35; 95%CI, 1.12-1.63), and who received surgical treatment (pooled HR, 1.31; 95%CI, 1.13-1.51). The effects of single nucleotide polymorphisms on lung cancer survival differed by COPD status; SNP rs74798757 was significantly associated with survival from lung cancer with COPD, whereas SNP rs10218481, CASP7 rs17090907, GPC5 rs1409600 and rs163933, and TAAR8 rs8192627 were independent factors for survival in lung cancer patients who were COPD-free. These results indicate that COPD status may play a significant role in the association between genetic variants and lung cancer outcomes. Further validation from independent cohorts and functional characterization for these associations are necessary, which in future may benefit the COPD-lung cancer population.
20
Jansson, Sven-Arne. "Health economic epidemiology of obstructive airway diseases : the obstructive lung disease in northern Sweden studies - thesis VII /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-805-3/.
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Curley, A. E. "The role of inflammation in the evolution of chronic lung disease in the neonate." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391115.
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Sze, Marc Alexander. "The bacterial lung tissue microbiome in the pathogenesis of chronic obstructive pulmonary disease." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54530.
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Rationale: Several laboratories have shown that the decline in lung function in Chronic Obstructive Pulmonary Disease (COPD) is associated with increased formation of tertiary lymphoid follicles. This provides direct histological evidence in support of the hypothesis that the decline in lung function is associated with activation of an adaptive immune response. The antigens responsible for driving this immune activation remain poorly understood. The recent realization that the human lung contains a bacterial microbiome that changes in association with the presence of COPD suggests the hypothesis that bacteria arising from within this microbiome might be responsible for activating the adaptive immune response in COPD. Approach: The research described in this thesis examines the lung tissue bacterial microbiome from patients with mild to moderate COPD as well as patients with very severe COPD. The bacterial microbiome from these studies utilized either nested or touchdown PCR followed by 454™ pyrotag sequencing of specific variable regions on the 16S rRNA gene. Changes in the microbiome were examined in relation to histological estimates of emphysematous destruction of the lung and inflammatory immune cell infiltration associated with this tissue remodeling process. Finally, Haemophilus influenzae, a bacterium identified from this microbiome, known to cause inflammation was compared to the host tissue repair process.
Results: The different bacterial community was present in control and mild (GOLD 1) compared to moderate (GOLD 2) COPD. The community composition was also different between donor lung tissue and very severe (GOLD 4) COPD. Further, the analysis identified a list of 10 OTUs that discriminated between lung tissue affected by GOLD 4 COPD and controls. In addition, the data presented here indicate that the host immune response to these organisms precedes the structural changes associated with COPD. Conclusion: Collectively, these data confirm that there is a small but diverse microbiome in the normal human lung that becomes less diverse in COPD. Furthermore, the disappearance/appearance of certain OTUs can discriminate between control and COPD affected lung tissue and that some of these OTUs are associated with the inflammatory immune cell infiltration and tissue destruction that occurs in COPD.Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
23
Šileikienė, Virginija. "The effects of bronchial inflammation on lung function in chronic obstructive pulmonary disease." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2013. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2013~D_20130327_100737-84011.
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The aim of the study
To investigate relationship between inflammation of the airways (bronchi) and pulmonary function.
Objectives
1. To examine the levels of peripheral blood cytokines of patients suffering from COPD during exacerbation and remission, in order to detect non-invasive marker/markers of COPD that will enable us to differentiate infectious origin of exacerbation from non-infectious.
2. To investigate relationship between radiology changes of the lungs and respiratory function in patients suffering from chronic obstructive pulmonary disease.
3. To find out whether it is possible to evaluate changes of airway inflammation using classical inflammation and bacterial markers in patients suffering from COPD. To evaluate dependence of these markers on COPD clinical phase.
4. To evaluate the count of regulatory T lymphocytes (CD4+CD25+), as cells, possibly decreasing inflammation, in blood of the patients suffering from COPD and compare the results with results obtained from the group of patients who are not suffering from COPD.
5. To examine the amount of cells with CD25+ marker in mucosa of bronchi of patients suffering from COPD and compare this result with the result obtained in the control groups of non-smokers and smokers who are not suffering from COPD.
Scientific novelty
In practical work, the problem of timely diagnosis of exacerbation of the disease remains still important, despite significant achievements in research and treatment of COPD. The search of... [to full text]Tyrimo tikslas: ištirti kvėpavimo takų (bronchų) uždegimo sąsajas su plaučių funkcija. Tyrimo uždaviniai 1. Ištirti asmenų, sergančių LOPL, periferinio kraujo citokinų koncentraciją ligos paūmėjimo ir remisijos metu, tikintis rasti neinvazinį LOPL paūmėjimo žymenį (žymenis), leisiantį atskirti infekcinę paūmėjimo kilmę nuo neinfekcinės. 2. Ištirti radiologinių plaučių pokyčių ir kvėpavimo funkcijos rodiklių sąsajas sergant lėtine obstrukcine plaučių liga. 3. Ištirti, ar apie kvėpavimo takų uždegimo pokyčius sergant LOPL galima spręsti iš klasikinių uždegimo ir bakterijų žymenų pokyčių kraujyje. Įvertinti šių kraujo žymenų priklausomybę nuo LOPL klinikinės fazės. 4. Nustatyti T reguliacinių limfocitų (CD4+CD25+), kaip galimai uždegimą slopinančių ląstelių, kiekį LOPL sergančių ligonių kraujyje ir palyginti su LOPL nesergančių asmenų grupe. 5. Ištirti CD25+ žymenį turtinčių ląstelių kiekį LOPL sergančių ligonių bronchų gleivinėje ir palyginti jį su LOPL nesergančių rūkančių ir nerūkančių asmenų kontrolinėmis grupėmis. Mokslinė darbo reikšmė ir naujumas. Nežiūrint didelių pasiekimų tiriant ir gydant LOPL, praktiniame darbe iki šiol išlieka savalaikio ligos paūmėjimo nustatymo problema. Nuolat ieškoma potencialių neinvazinių žymenų, kurie galėtų padėti laiku diagnozuoti LOPL paūmėjimą ir galimai nustatyti jo kilmę (bakterinis ar imuninis). Daug tikimasi iš citokinų, kaip potencialių LOPL paūmėjimo žymenų. Nors pavieniuose darbuose tirta IL-10 ir TNF-α koncentracija LOPL... [toliau žr. visą tekstą]
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Powell, Wendy Elizabeth. "The role of IL-6 trans-signalling in chronic lung disease of prematurity." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/55501/.
Full textAbstract:
IL-6 trans-signalling was investigated in transformed airway epithelial cells (A549 and BEAS2B cells) and primary small airway epithelial cells (SAEC) in vitro. The cells expressed gp130 but not IL-6R. MCP-1 in response to IL-6 trans-signalling was variable and generally weak. Furthermore, IL-8 release was not downregulated by IL-6 trans-signalling. Instead, an increase in MCP-1 and IL-8 release was observed in response to a combined stimulation of IL-6 trans-signalling and IL-1[Special characters omitted]. This suggests that the pro-resolution paradigm of IL-6 trans-signalling may not be the case in airway epithelial cells.
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Ahmed, Bushra. "Longitudinal investigation of the airway microbiota in children with chronic suppurative lung disease." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/62315.
Full textAbstract:
Recurrent airway infection and its complications are the leading cause of death in Cystic Fibrosis (CF) but remain poorly understood. Molecular microbiology demonstrates that the CF airways are more polymicrobial than previously thought. The role of the microbiota in disease prognosis is unclear. There have been few longitudinal studies of the airway microbiota in children, partly because sampling the lower airways is difficult as many children cannot expectorate. Part one of this thesis determined whether upper airway samples could act as surrogates for the lower airway microbiota in children. Cough swabs [CS], throat swabs [TS] and lower airway samples (bronchoalveolar lavage and bronchial brushings) were collected for 16S rRNA gene sequencing. There was good correlation between TS and the lower airways at a community but not an individual level; TS distinguished disease differences, suggesting that they could be used in longitudinal studies of the airway microbiota in children. CS sequenced poorly, thus precluding their use for molecular microbiology. The longitudinal study had two arms; infants with CF diagnosed on newborn screening (NBS), in whom molecular microbiology revealed a small increase in diversity of the airway microbiota until 2 years of age; Streptococcus spp. and Haemophilus spp. were the most common organisms and showed an inverse relationship in their relative abundances over time. The second compared older children with CF with Primary Ciliary Dyskinesia (PCD), which shares a similar pathology to CF but rarely the same rate of disease progression. This revealed similar trends to those seen in NBS in the relative abundance of Streptococcus spp. and Haemophilus spp. in PCD but not in CF. This suggests that early changes in CF mirror those seen in later childhood in PCD and a switch occurs in CF during childhood from a milder to a more pathological community composition.
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Liu, Shiu Cheong Patrick. "Effects of xanthine oxidase inhibitors in pulmonary hypertension associated with chronic lung disease." Thesis, University of Dundee, 2019. https://discovery.dundee.ac.uk/en/studentTheses/ee8678d8-e7c7-498c-b501-ff5522f32ae5.
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Chronic lung diseases are often complicated with pulmonary hypertension (PH). This can lead to disability and poor prognosis. Oxidative stress has been implicated in the development of PH and right ventricular hypertrophy (RVH).A possible new way to treat lung disease related pulmonary hypertension is allopurinol (a xanthine oxidase inhibitor) which decreases both uric acid and oxidative stress. We hypothesised that allopurinol could regress RVH in patients with pulmonary hypertension associated with chronic lung disease (PH-CLD).In a double-blind, randomised controlled clinical trial, 72 patients with PH-CLD (93% diagnosed with chronic obstructive pulmonary disease and 17% with interstitial lung disease) were randomised to receive either allopurinol 300 mg twice daily or placebo for twelve months. The primary outcome was the mean change in right ventricular mass (RVM) as assessed by cardiac magnetic resonance imaging (CMRI) at twelve months. The secondary outcomes were the change in other cardiac parameters measured by CMRI, St George's Respiratory Questionnaire, Short Form 36, spirometry and six-minute walk test (6MWT).The mean age was 71 years, the mean FEV1 was 60% with mean resting SaO2 of 96%. After 12 months, there was no significant change in RVM. There were also no significant changes in other cardiac parameters measured on CMRI, quality of life questionnaires, spirometry and 6MWT. Post-hoc subgroup analysis showed that allopurinol reduced RVM (allopurinol -6.16 g vs placebo 0.75 g, p = 0.02) in COPD patients with more severe airflow limitation. Patients with higher NT-proBNP (> 489 pg/ml) had a greater improvement in left ventricular ejection fraction with allopurinol 5.12 vs placebo -1.62, p = 0.02.In summary, allopurinol had no overall impact but reduced RV mass in COPD patients with more severe airflow limitation. Further studies are warranted to assess the longer term impact of allopurinol in more severe COPD.
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Choate, Radmila. "ESTIMATING DISEASE SEVERITY, SYMPTOM BURDEN AND HEALTH-RELATED BEHAVIORS IN PATIENTS WITH CHRONIC PULMONARY DISEASES." UKnowledge, 2019. https://uknowledge.uky.edu/epb_etds/22.
Full textAbstract:
Chronic pulmonary diseases include a wide range of illnesses that differ in etiology, prevalence, symptomatology and available therapy. A common link among these illnesses is their impact on patients’ vital function of breathing, high symptom burden and significantly impaired quality of life.
This dissertation research evaluates disease severity, symptom burden and health behaviors of patients with three different chronic pulmonary conditions. First, alpha-1 antitrypsin deficiency (AATD) is an inherited condition that typically is associated with an increased risk of early onset pulmonary emphysema. This study examines differences in demographic, health, and behavioral characteristics and compares clinical outcomes and health related behaviors and attitudes between two severe genotypes of AATD - ZZ and SZ. The findings of the study suggest that patients with SZ genotype and less severe form of deficiency report higher number of exacerbations, comorbidities, as well as unhealthy behaviors such as lack of exercise and current smoking. In addition, individuals with the more severely deficient ZZ genotype are more adherent to disease management and prevention program recommendations and maintain a healthier lifestyle than individuals with SZ genotype.
Second chronic lung disease examined in this research was chronic obstructive pulmonary disease (COPD), the fourth leading cause of death and second leading cause of disability in the United States. Prevalence and burden of cough and phlegm, two of the most common symptoms of the COPD, were assessed among participants of the COPD Foundation’s Patient-Powered Research Network (COPD PPRN). In addition, association between patient-reported levels of phlegm and cough, clinical outcomes and patients’ quality of life were evaluated. Participants’ quality of life was assessed using Patient Reported Outcome Measurement Information System instrument PROMIS-29. Association between changes in symptom severity over time and patient-reported quality of life were examined. Findings of this study indicated that severity of cough and phlegm were associated with higher number of exacerbations, greater dyspnea, and worsened patient-reported quality of life including physical and social functioning. Improvement in cough and phlegm severity over time was associated with better patient-reported quality of life.
Third pulmonary illness described in this dissertation is non-cystic fibrosis bronchiectasis (NCFB), a rare and etiologically diverse condition characterized by dilated bronchi, poor mucus clearance and susceptibility to bacterial infection. Association between presence of Pseudomonas aeruginosa (PA), one of the most frequently isolated pathogens in patients with NCFFB, and disease severity was assessed utilizing enrollment data from the Bronchiectasis and NTM Research Registry (BRR). NCFB disease severity was evaluated using modified versions of validated in large international cohorts instruments, the Bronchiectasis Severity Index (BSI) and FACED. The findings of this study indicate that PA infection is common in NCFB patients, and presence of PA in patients’ sputum is associated with having moderate and high severity of bronchiectasis. In addition, the results of this study suggest that the two severity assessment instruments classify patients with NCFB differently which may be attributed to a greater number of severity markers utilized in the calculation of the BSI compared to FACED.
In conclusion, the proposed dissertation aims to enhance understanding of differences in health outcomes between genotypes of AATD within AlphaNet registry, and to guide future health-promoting behaviors. It highlights the burden of common symptoms such as cough and phlegm in patients with COPD within COPD PPRN and their association with patients’ quality of life. In addition, it introduces modified indices of NCFB severity and emphasizes high burden of the disease in patients with presence of PA within the US BRR.
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McColm, Janet R. "Inflammatory mediators in the lungs of preterm infants and their role in the development of chronic lung disease." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21402.
Full textAbstract:
The clinical pilot study enrolled 26 infants and measured IL-8, TNF-α and inflammatory cells in bronchoalveolar lavage samples. The results demonstrated that it may be possible to predict a group of babies at extremely high risk for developing chronic lung disease by early measurement of IL-8 in tracheal secretions. To further investigate the role of the genital mycoplasmas, Ureaplasma urealyticum and Mycoplasma hominis, a randomised study using an effective antibiotic, erythromycin, was carried out. A low grade untreated infection could persistently stimulate an in vivo inflammatory response, but we also wished to investigate the reported anti-inflammatory properties of erythromycin. The infection rate in the study was lower than expected (12% compared to 30% in a pilot study) and did not correlate with outcome. There was also no correlation between outcome and treatment and the inflammatory response, as measured by IL-8, did not correlate with outcome as it had in our pilot study. As part of a randomised trial of a natural and synthetic surfactant taking place on our unit, bronchoalveolar lavage samples both pre and post surfactant were analysed for cytokines and cells. Our results showed that Curosurf produced a significantly lower inflammatory response compared to Exosurf 24 hours after administration but there was no correlation between surfactant type and development of chronic lung disease. The cell population present in the lung effluent has been an area of controversy. Standard cytospin smears of bronchoalveolar lavage samples were compared using a differential stain and an immunocytochemical stain which relies on monoclonal antibodies to identify specific cell surface markers. Our results confirm that the differential stain identifies neutrophils but it significantly under-estimates cells of the monocyte/macrophage lineage. Laboratory investigations were carried out to further elucidate and quantify the response of A549 human lung epithelial cells to Ureaplasma urealyticum, and other genital isolates, a Gram-positive (Staphylococcus albus) and a Gram-negative (Eschericia coli). The cells were stimulated in the presence of TNF-α and high oxygen concentrations, and with used in the clinical management of these infants, including surfactants, antibodies and steroids.
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Li, Yinghua. "Ureaplasma urealyticum induced pulmonary inflammation in the development of chronic lung disease of prematurity /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-073-3/.
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Lindberg, Anne. "Chronic obstructive pulmonary disease (COPD) : prevalence, incidence, decline in lung function and risk factors." Doctoral thesis, Umeå : Public Health and Clinical Medicine, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-347.
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Jónsson, Baldvin. "Chronic lung disease of prematurity : a study of selected causative factors and preventive measures /." Stockholm, 1998. http://diss.kib.ki.se/1998/19981204jons/.
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Huang, Jing-Qi. "The immunoreactive expression of neuroendocrine cells or neuroendocrine bodies in human chronic lung disease /." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61879.
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Bragman, Felix J. S. "Quantitative lung CT analysis for the study and diagnosis of Chronic Obstructive Pulmonary Disease." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10045444/.
Full textAbstract:
The importance of medical imaging in the research of Chronic Obstructive Pulmonary Dis- ease (COPD) has risen over the last decades. COPD affects the pulmonary system through two competing mechanisms; emphysema and small airways disease. The relative contribu- tion of each component varies widely across patients whilst they can also evolve regionally in the lung. Patients can also be susceptible to exacerbations, which can dramatically ac- celerate lung function decline. Diagnosis of COPD is based on lung function tests, which measure airflow limitation. There is a growing consensus that this is inadequate in view of the complexities of COPD. Computed Tomography (CT) facilitates direct quantification of the pathological changes that lead to airflow limitation and can add to our understanding of the disease progression of COPD. There is a need to better capture lung pathophysiology whilst understanding regional aspects of disease progression. This has motivated the work presented in this thesis. Two novel methods are proposed to quantify the severity of COPD from CT by analysing the global distribution of features sampled locally in the lung. They can be exploited in the classification of lung CT images or to uncover potential trajectories of disease progression. A novel lobe segmentation algorithm is presented that is based on a probabilistic segmen- tation of the fissures whilst also constructing a groupwise fissure prior. In combination with the local sampling methods, a pipeline of analysis was developed that permits a re- gional analysis of lung disease. This was applied to study exacerbation susceptible COPD. Lastly, the applicability of performing disease progression modelling to study COPD has been shown. Two main subgroups of COPD were found, which are consistent with current clinical knowledge of COPD subtypes. This research may facilitate precise phenotypic characterisation of COPD from CT, which will increase our understanding of its natural history and associated heterogeneities. This will be instrumental in the precision medicine of COPD.
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Harman, Katharine. "Exploring the relationship between loss of CFTR protein function and markers of disease severity in chronic suppurative lung disease." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/57500.
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Cystic fibrosis (CF) and Primary Ciliary Dyskinesia (PCD) are chronic suppurative lung diseases (CSLD). CF is characterised by inherited mutations affecting the cystic fibrosis transmembrane regulator (CFTR) protein, which is thought to be normal in PCD, however the role of CFTR in disease is incompletely understood. This thesis investigates the relationship between CFTR, inflammation and airway health, firstly in the context of the CF gene therapy Multidose trial followed by contrasting CF, PCD and control patients. The first study explored the relationship between lower airway potential difference (LAPD) measurements performed in the Multidose trial as a measure of CFTR function, and physiological, radiographic and inflammatory markers of disease severity. At baseline, FEV1 correlated with basal LAPD measurements, however not between restored chloride secretion and change in airway disease following treatment; implicating the role of sodium transport, not chloride in disease pathogenesis. As no direct correlation was seen, I went on to explore an alternative theory that a bi-directional relationship exists between CFTR and inflammation; CFTR dysfunction triggers a hyper-inflammatory state and inflammation causes secondary CFTR dysfunction. Cell cultures were cultivated from the nasal epithelium of patients with CF, PCD and controls. Both at baseline and following stimulation with common respiratory pathogens, the levels of inflammatory mediators in the supernatant from each group of cells were comparable. The numbers involved with this study were small, however did not indicate that CF cells cultured in these conditions (in vitro) were hyper-inflammatory. The final study explored in vivo whether inflammation causes secondary CFTR dysfunction. Nasal potential difference (NPD) measurements were compared with localised levels of inflammation in subjects with CF, PCD and controls. PCD traces showed reduced chloride secretion, however it was not possible to differentiate secondary CFTR dysfunction from damage to epithelial cell integrity. Elevated levels of inflammatory mediators were detected in PCD nasal fluid, however the results were variable and these levels did not correlate with NPD measurements of ion channel function. These studies did not support the hypothesis that there is a direct relationship between CFTR function and airway disease, that in vitro CF cells are hyperinflammatory, or in vivo that inflammation leads to secondary CFTR dysfunction. The experiments performed in this thesis provide a basis for future work exploring this relationship, and may help guide future trials for novel therapies in CF.
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Sharma, Pramod. "The Effect of Experimental Changes in Physiological and Psychological Factors on Perception of Exertional Dyspnea in Healthy Individuals." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/365245.
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Dyspnea is a clinical term for the sensation of shortness of breath. It is a subjective experience perceived and reported by an affected person when referring to a feeling of the unpleasantness and discomfort related to breathing (Epstein, Manning, and Schwartzstein, 1995; Mukerji, 1990). Both healthy subjects and patients with heart and lung disease can experience this sensation, but a key difference is the level of activity at which this sensation becomes particularly troublesome (West et al., 2010). Typically, healthy subjects experience substantial dyspnea during heavy to severe exertion when demands on the cardiorespiratory system are high, e.g. during running, stair climbing or at high altitude (Mukerji, 1990). By contrast, patients with heart and lung disease are likely to experience this sensation during their day to day activities (Hajiro et al., 1999; Simon et al., 1990; Vivodtzev et al., 2006) which may, as a consequence, become more limited as their condition progresses. So, dyspnea becomes an issue of clinical concern, likely indicative of disease, when it occurs at a level of activity in an individual that would not usually cause any difficulty (Mukerji, 1990).
Although dyspnea is associated with a wide range of clinical conditions, it is a particularly significant symptom in Chronic Obstructive Pulmonary Disease (COPD) where it has a major impact on exercise capacity and quality of lifeThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Allied Health
Griffith Health
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Stevens, Daniel. "Exercise testing and the physiological responses to exercise in young patients with chronic chest diseases." Thesis, University of Exeter, 2009. http://hdl.handle.net/10036/86037.
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The use of exercise is a valuable tool in the healthcare management of young patients with chronic chest diseases (CCD). Indeed, exercise testing yields important prognostic data which are a strong predictor of survival. Such information can indicate to the clinician to increase drug therapy treatment, and functional capacity of the patient can be monitored over time with repeated testing. Exercise training has been shown to improve both aerobic and anaerobic fitness and quality of life in patients with lung disease. The use of exercise testing and training in the healthcare of patients with lung disease in the UK, however, has not been investigated. In order for recommendations for exercise testing and training based on scientific evidence to be implemented, they should relate to current standards and resources. Therefore, the first study of the present thesis sought to characterise the use of both exercise testing and training in UK Cystic fibrosis (CF) clinics through a nationwide audit. Data from the audit showed that exercise testing and training are underused despite recognition of the importance of each in the healthcare of the patient by clinicians and other healthcare providers. Indeed, resources for exercise testing in UK CF clinics are limited. A patient over the age of 8 y will only have a 41.1 % chance of receiving an exercise test of any type over a 12 month period, and the exercise test will be quite crude. Exercise training is frequently discussed with the patient; however, there is a strong likelihood (72.9 %) that the advice given will only be general encouragement. The prognostic value of exercise testing is becoming increasingly recognised. Indeed, peak oxygen uptake (VO2peak) derived through maximal cardiopulmonary exercise testing (CPET) has been reported to be equal or superior to that of resting spirometric lung function tests in the prognostic evaluation of patients with CCD. Furthermore, a high correlation between VO2peak and long term survival in both adults and children with CF has been reported. Other physiological data from CPET, such as oxygen uptake (VO2) recovery following CPET, has not been investigated in young patients with CCD and may provide an additional physiological marker of patient health. The aim of study two, therefore, was to investigate recovery following CPET in young patients with CCD, and determine if any significant relationships exist between VO2 recovery and measures of disease severity in these patients. Data from study two showed that young patients with CCD compared to healthy controls had significantly reduced aerobic fitness (t52 = - 2.64, P = 0.011), and the fast component of the VO2 recovery following CPET, analysed by a mono-exponential model, is significantly prolonged (t52 = 2.63, P = 0.011). Furthermore, the fast component of the VO2 recovery is significantly related to disease severity, as assessed by the Shwachman score (SS), in the CF subgroup (r = - 0.75, P < 0.001), and as assessed by forced expiratory volume in 1 s (FEV1), in the young patients with CCD (r = - 0.49, P = 0.009). Thus, indicating that greater disease severity is associated with a longer VO2 recovery following CPET. A significant relationship between VO2peak and VO2 recovery was shown in the young patients with CCD (r = - 0.45, P = 0.018). Although the relationship is significant, however, it is still quite weak, and, therefore, indicates that the VO2 recovery is not closely related to the VO2peak in these patients. Quality of life and likelihood of survival are greater in patients with CCD with higher levels of aerobic fitness, and regular exercise has been shown to improve both lung function and exercise capacity in these patients. Indeed, exercise training programmes tailored to the individual patient are recommended in the standards of patient healthcare in the UK. Whilst the chronic effects of regular exercise have been investigated, the acute physiological responses to exercise training have not been studied in young patients with CCD. In study three young patients with CCD and healthy controls performed intermittent exercise (IE) designed to replicate the typical activity and exercise patterns of young people. Following IE, in the healthy controls the VO2 required to sustain moderate steady-state exercise fell significantly from 3 min to 1 h and 1 h to 24 h, however, in the young patients with CCD VO2 during moderate steady-state exercise increased significantly from 3 min to 1 h and then decreased significantly from 1 h to 24 h (main effect for time: F1.5,79.2 = 22.82, P < 0.001). A significant time × group interaction between young patients with CCD and controls in VO2 during moderate steady-state exercise 3 min, 1 h and 24 h following IE (interaction: F1.5,79.4 = 30.01, P < 0.001) may suggest that metabolic stress is still evident over this time period, which may be indicative of fatigue. Data from the present thesis shows that exercise is underused in UK CF clinics, with the availability of equipment and personnel both being limiting factors. Furthermore, a lack of standardisation in the provision of exercise between clinics is evident. In studies two and three, data shows different physiological responses following CPET and IE, respectively, between children with CCD and controls. The present thesis has advanced our understanding of the provision of exercise in the healthcare of CF in the UK, and furthered knowledge in how young patients with CCD respond physiologically to exercise.
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Subhedar, Nim. "The importance of pulmonary hypertension in the development of chronic lung disease in preterm infants." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264301.
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Leong-Smith, Phe. "Oxidative stress and metal homeostasis at the air-lung interface in Chronic Obstructive Pulmonary Disease." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/oxidative-stress-and-metal-homeostasis-at-the-airlung-interface-in-chronic-obstructive-pulmonary-disease(9c8de9c8-c5a1-4b40-9100-4a654a1e6274).html.
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Background: Chronic obstructive pulmonary disease (COPD) represents a spectrum of disorders encompassing chronic bronchitis and emphysema, associated with cough, excess mucus and exercise-related dyspnoea and characterized by a progressive reduction in airflow. Development of these symptoms is associated with chronic exposure to noxious particles or gas, most commonly from tobacco smoking, which triggers abnormal inflammation in the lung. Consistent with this increased inflammatory burden, oxidative stress has been demonstrated in COPD patients, largely through determination of antioxidant and oxidative damage marker concentrations in exhaled breath condensate and induced sputum. Whilst these samples are easier to obtain than bronchoscopy-based lavage, there remains contention concerning how well they reflect the distal airway lining fluids and hence the actual disease state. In the present study, I therefore investigated the oxidative status of bronchoalveolar lavage fluids (BAL) from well defined groups of COPD patients; current and ex-smoker, as well as aged and smoking matched controls. In addition, as COPD has been argued to be a disease of accelerated ageing a group of young controls was included to examine the extent to which age influences the endpoints under consideration. Chapter 2: In the first experimental chapter I investigated the evidence for oxidative stress in the airways of subjects with COPD (smokers and ex-smoking) relative to age and smoking matched controls. In addition, young healthy non-smokers and mild asthmatics were included to investigate the impact of age on the examined parameters, as well as to compare antioxidant defences in the context of acute and chronic inflammation. In this chapter, I examined respiratory tract lining fluid antioxidants sampled in bronchoalveolar lavage fluid, focusing on low molecular weight antioxidants (glutathione, urate and ascorbate) and their oxidation products (glutathione disulphide and dehydroaspresence) of COPD, but observed smoking-related increases in glutathione and ferritin, and age-related increases in dehydroascorbate and 4-hydroxy-2-nonenal. Chapter 3: In the second experimental chapter I attempted to understand the age-related increase in oxidation markers observed in the lavage samples from chapter 2. Pro-oxidant metal (Fe and Cu) concentrations were determined in the lavage samples from each of the groups used in chapter 2, by inductively coupled plasma mass spectrometry and a novel assay was developed based on metal catalysed oxidation of ascorbate, to provide a functional measure of the catalytically active metal pools at the surface of the lung. Through the use of selective chelators, the relative contribution of labile Fe and Cu pools was assessed. In this chapter I was able to demonstrate that respiratory tract lining fluid Cu concentrations increased with age, in parallel to an increased pro-oxidant status in the RTLF and evidence of a non-transferrin bound Fe pool. These indices appeared related to the concentration of oxidation markers reported in chapter 2. Chapter 4: Given the failure to detect increases in gross measures of oxidative damage in COPD patients, it was decided that the focus should shift toward a more refined focus on specific oxidations to proteins functionally related to the pathogenesis of the disease. I decided based on the pre-existing literature, that there was merit in focusing on 4-hydroxy-2-nonenal adduction of proteins. To achieve this, I attempted to develop a mass spectrometry-based method for the identification of adducted proteins and protein sequences. This was an ambitious undertaking and unfortunately I was only able to take these experiments so far, but at least was able to demonstrate the feasibility of the method. The methodology developed was sufficiently promising to warrant further investigation after the completion of my PhD. Short conclusion: In this study I was unable to demonstrate any evidence of oxidative stress in the airways of patients with COPD, either ex- or current smokers. I did however, observe evidence of increased oxidative damage, catalytic metal (Cu) concentrations and pro-oxidant metal activities (Cu and non-transferrin bound Fe) with age. At the end of this thesis, despite the attempt to investigate markers of oxidative stress in a relevant compartment (the distal lung) and in carefully controlled groups (aged and smoking matched), the role of oxidative processes in COPD remains oblique.
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Coxson, Harvey Owen. "Quantification of the tissue changes in the human lung with chronic lung disease using a combination of computed tomography and stereology." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0035/NQ27124.pdf.
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Hallin, Runa. "Nutritional Depletion in Chronic Obstructive Pulmonary Disease (COPD) : Effect on Morbidity, Mortality and Physical Capacity." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9512.
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The overall aim of this work was to examine the effects of depleted nutritional status on some aspects of Chronic Obstructive Pulmonary Disease (COPD). Morbidity. In paper І, we found that energy intake was lower than the calculated energy demand for all patients. A low body mass index (BMI) at inclusion and weight loss, during the one year follow-up period were independent risk factors for having a new exacerbation (p = 0.003 and 0.006, respectively). Mortality. Nineteen percent of the patients in paper ІІ, where underweight (BMI<20). A significant positive correlation was found between BMI and FEV1, and this correlation remained significant after adjustment for age, sex and pack years (p<0.0001). Being underweight was related to increased overall mortality and respiratory mortality but not to mortality of other causes, 19% of the patients had died within 2 years. The lowest mortality was found among the overweight patients (BMI 25-30 kg/m). Physical capacity and effect of training. In paper ІІІ we investigated baseline characteristics of patients that were starting physical training. We found that peak working capacity was positively related to BMI (r=0.35, p=0.02) and fat free mass index (FFMI) (r=0.49, p=0.004) and negatively related to S-Fibrinogen and serum C reactive protein (S-CRP). BMI and FFMI were significantly related to the 12 minutes walking distance when adjusted for body weight. Fifty to 76% of the variation in physical capacity was accounted for when age, gender, FEV1, FFMI and CRP were combined in a multiple regression model. In Paper ІV the median change in fat free mass (FFM), after 4 months of physical training was 0.5 kg. Old age, low FEV1 and high level of dyspnoea were independent negative predictors of FFM increase after the training period. In conclusion nutritional status is an important determinant of morbidity, mortality and physical capacity in COPD. Low FEV1 and high level of dyspnea are negative predictors for increased FFM after physical training.
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Arne, Mats. "Chronic Obstructive Pulmonary Disease : Patients´ Perspectives, Impact of the Disease and Utilization of Spirometry." Doctoral thesis, Uppsala universitet, Lungmedicin och allergologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-113813.
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The overall aim of this thesis was to describe subjects with chronic obstructive pulmonary disease (COPD) from different perspectives. Focus was on patients at the time of diagnosis, impact of the disease in comparison to other chronic diseases, factors associated with good health and quality of life (QoL), and diagnostic spirometry in clinical practice. Methods: Qualitative method, grounded theory, was used to analyse patients´ perspectives at the time of diagnosis in a primary care setting (n=10). Public health surveys in the general population were used to compare chronic diseases (n=10,755) and analyse factors associated with health outcomes in COPD (n=1,475). Medical records and spirometry reports, from primary and secondary care, were analysed to assess diagnosis of COPD in clinical practice (n=533). Results: In clinical practice, 70% of patients at the time of diagnosis of COPD lacked spirometry results confirming the diagnosis. Factors related to consequences of smoking, shame and restrictions in physical activity (PA) in particular, were described by patients at the time of diagnosis of COPD. In general subjects with COPD (84%), rheumatoid arthritis (74%) and diabetes mellitus (72%) had an activity level considered too low to maintain good health. In COPD, the most important factor associated with good health and quality of life was a high level of PA. Odds ratios (OR (95%CI)) varied from 1.90 (1.47-2.44) to 7.57 (4.57-12.55) depending on the degree of PA, where subjects with the highest PA level had the best health and QoL. Conclusions: Subjects with COPD need to be diagnosed at an early stage, and health professionals should be aware that feelings of shame could delay patients from seeking care and thus obtaining a diagnosis. The use of spirometry and the diagnostic quality should be emphasised. In patients with COPD greater attention should be directed on increasing the physical activity level, as patients with a low level of physical activity display worse health and quality of life.
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Kammerl, Ilona [Verfasser], and Silke [Akademischer Betreuer] Meiners. "Proteasome and immunoproteasome function in cigarette smoke-mediated chronic lung disease / Ilona Kammerl. Betreuer: Silke Meiners." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/108831807X/34.
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Sridhar, Mangalam K. "An investigation into aspects of energy balance and nutritional status of patients with chronic lung disease." Thesis, University of Glasgow, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295327.
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Jackson, Victoria Emily. "Investigation into the role of rare genetic variation in lung function and chronic obstructive pulmonary disease." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/38645.
Full textAbstract:
Lung Function is a physiological measurement used for monitoring respiratory health and in the diagnosis of chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Lung function and COPD are influenced by a combination of environmental and genetic factors. This thesis aims to investigate the genetic basis of these traits, with a particular focus on the effect of low frequency and rare genetic variants, so far largely overlooked in genome-wide association studies (GWAS). An analysis of exome array data and COPD identifies novel associations between COPD risk and low frequency single nucleotide polymorphisms (SNPs) in MOCS3 and IFIT3 and between a rare SNP in SERPINA12 and percent predicted forced expiratory volume in one second (FEV1) in COPD cases. Recently developed methods for the meta-analysis of gene-based tests are empirically evaluated and shown to be approximately equivalent to a mega-analysis using individual level data for a quantitative trait. These methods are then applied in a meta-analysis of exome array data and quantitative lung function measures. This meta-analysis identifies no gene-based associations; however genome-wide significant (P < 5x10⁻⁸) single variant associations are identified in two novel regions: a SNP near LY86 associated with the ratio of FEV1 to forced vital capacity (FVC) and a SNP near FGF10 associated with FVC in ever smokers. Finally the largest GWAS to date of two lung function flow measures (peak expiratory flow [PEF] and forced expiratory flow between 25% and 75% of FVC [FEF25-75]) is described. The overlap in variants associated with PEF and FEF25-75 and volumetric measures of lung function (FEV1, FVC and FEV1/FVC) is examined, and 10 SNPs are identified as showing association with PEF (P < 5x10⁻⁸), but no other lung function trait with P < 5x10⁻⁵. These findings have the potential to provide insight into the biological mechanisms underlying lung health and disease.
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Young, Jeanne. "Providing ethical care: cardiopulmonary resuscitation (CPR) for chronic obstructive pulmonary disease (COPD) exacerbations in patients with end stage lung disease (ESLD)." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=92266.
Full textAbstract:
Cardiopulmonary resuscitation should generally not be offered to patients who suffer from a chronic obstructive pulmonary disease (COPD) exacerbation in the setting of end-stage lung disease (ESLD). Requests for CPR in this context may sometimes be uninformed, misguided, and the result of an unresolved grieving process by familial surrogates. While understandable, these requests rarely represent a truly autonomous patient perspective that is grounded in a competent, informed, and enlightened deliberation.Alternatively, life-support technology and resuscitation is used appropriately when it is offered to patients with reversible disease, a disease for which functional recovery is possible, or to maintain a patient in an acceptable quality of life. It was never intended as, nor should it become, a treatment to delay the inevitable trajectory of a conscious or permanently unconscious and imminently dying patient.
When juxtaposed against perspectives of professional integrity, non-maleficence, distributive justice and basic human dignity, requests for CPR in this context rarely seem to be ethically persuasive or in the patient's best interests.
Pour les gens souffrant d'exacerbation en stade final des maladies respiratoires (SFMR) causée par une maladie pulmonaire obstructive chronique (MPOC), la réanimation cardio-pulmonaire est généralement à proscrire. Dans un tel contexte, la demande de réanimation peut être le résultant de mauvais renseignements, d'un choix malavisé ou même etre l'expression du refus des members de la famille face au deuil qu'ils auront à faire. Quoiqu'il est compréhensible de faire une telle demande, il est rare qu'elle soit bien fondée et représentative d'un choix éclairé et autonome de la part du patient ou de la patiente.
D'autre part, les technologies maintenant la vie ainsi que la réanimation sont utilisées de facon appropriée et juste lorsqu'elles sont offertes aux patient(e)s chez qui la maladie est réversible, où le rétablissent fonctionnel est possible ou afin de maintenir une qualité de vie acceptable. En aucun temps devrait-on considérer la reanimation afin de prolonger l'inévitable parcours du patient inconscient ou conscient et du patient pour qui la mort est imminente. fr
Lorsque juxtaposée aux notions d'intégrité professionnelle, la bienfaisance, une justice distributive et de celle de la dignité humaine, la demande de réanimation cardio-pulmonaire dans ce contexte semble rarement être éthiquement persuasive ou être dans les meilleurs intérêts du patient. fr
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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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Binder, William, Scott Clark, Edina Hall, Ferena Salek, and Jon Glover. "Effect of Adherence to the GOLD Guidelines on Chronic Obstructive Pulmonary Disease Related Readmissions in a Community Hospital." The University of Arizona, 2016. http://hdl.handle.net/10150/613978.
Full textAbstract:
Class of 2016 AbstractObjectives: To assess the relationship between adherence to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines for the management of chronic obstructive pulmonary disease (COPD) exacerbations and the corresponding 30-day, all-cause readmissions rate in a community hospital. Methods: A retrospective chart review was conducted on patients admitted with the primary diagnosis of a COPD exacerbation. Medications administration records relevant to the GOLD guidelines were examined as separate independent variables in relation to a readmission within 30 days of discharge. Additional factors examined included: demographic data, resident of a long-term care facility, pre-index hospitalization, pulmonary consult, vaccines, length of stay (LOS), discharge medications, and follow-up appointments. Results: Electronic health records of 120 patients were reviewed and divided into non-readmitted patients (n = 65, mean age 73.4 ± 10.1 years), all-cause readmissions (n = 55, mean age 70.15 ± 9.69 years), and COPD-related readmissions (n = 21, mean age 70.7 ± 11.1 years). Patients with heart failure (p = 0.024), a LOS >5 days (p = 0.045), a pre-index hospitalization (p = 0.001), or who were long-term care residents (p = 0.024) experienced more all-cause readmissions. Females experienced less all-cause readmissions (p = 0.035). Significantly more patients with a pre-index hospitalization had a COPD-related readmission (p = 0.027). Lastly, adherence to the GOLD treatment parameters was not significantly different across all groups. Conclusions: COPD is a complex disease and adherence to the GOLD guidelines during an exacerbation is unlikely to significantly impact 30-day readmission rates.
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Finney-Hayward, Tricia Kate. "Monocyte-derived macrophages as a lung macrophage model in chronic obstructive pulmonary disease : characterisation and functional output." Thesis, Imperial College London, 2005. http://hdl.handle.net/10044/1/8330.
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Ling, Sean Hilton. "The relationship of particulate matter retention in the lung to the severity of chronic obstructive pulmonary disease." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/23319.
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Particulate matter (PM) deposited into the lung is removed predominantly by ciliary action of epithelial cells in the airways and by macrophages that phagocytose these particles in the peripheral air space. We hypothesize that the particle load or burden in the lungs’ of patients with Chronic Obstructive Pulmonary Disease (COPD) are
responsible for perpetuating the chronic inflammatory response in the lung of subjects
with COPD (even after smoking cessation).
Samples were selected to cover the whole range of severity of COPD. Quantitative histological methods were used to quantify and characterize the particle burden in the lung tissue. The volume fraction (Vv) of PM in the lung tissue, including
the parenchyma, airways, alveolar macrophages, blood vessels, and lymphoid follicles
was determined using the aforementioned methods. To determine the chemical composition of the PM, Raman spectroscopy was used to analyze samples in situ. PM could be found in virtually all compartments of the lung: the parenchyma,
blood vessels, airways, lymphoid follicles, and alveolar macrophages. The total burden of
PM in all tissues of the lung was higher in subjects with COPD compared to controls
(p
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Green, Clara Emily. "Understanding shared pathogenesis between chronic obstructive pulmonary disease (COPD) and lung cancer by means of cell specific genomics." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8230/.
Full textAbstract:
Introduction: COPD (Chronic Obstructive Pulmonary Disease) and lung cancer are related conditions associated with inflammation. Relatively little focus has been given to the endothelium, through which inflammatory cells transmigrate to reach the lung. We sought to determine if coding and non-coding alterations in pulmonary endothelium exist in COPD and lung cancer. Methods: Patients with and without COPD undergoing thoracic surgery were recruited. Pulmonary Endothelial Cells were isolated from lung and tumour and extracted RNA (ribonucleic acid) used for miRNA (micro-RNA) and mRNA (messenger RNA) microarrays. Ingenuity pathway analysis (IPA) was also carried out. Results: 2071 genes and 43 miRNAs were significantly upregulated in COPD. 4 targets were validated by quantitative polymerase chain reaction, of which miR-181b-3p was chosen for functional validation. Another target, miR-429, was also increased in lung tumour. Several cancer-related pathways such as transforming growth factor- β were altered in the IPA. There was significantly reduced tube formation and endothelial sprouting in Human umbilical vein endothelial cells transfected with miR-181b-3p, consistent with an effect on angiogenesis. Conclusions: Upregulation of miR-181b-3p reduces tube formation and sprouting by endothelial cells. This might be significant in the development of emphysema as lung vasculature is important in the structural maintenance of alveoli.