View clinical trials related to Emphysema.
Filter by:The purpose of this study is to show that one form of mechanical airway clearance techniques, High Frequency Chest Wall Oscillation (HFCWO)using a pneumatic vest, will diminish exacerbations of COPD which will improve respiratory health status.
Systemic inflammation is present in chronic obstructive pulmonary disease (COPD), which has been linked to cardiovascular morbidity and mortality. We determined the effects of oral and inhaled corticosteroids on serum markers of inflammation in patients with stable COPD.
The aim of this study is to investigate the mechanisms whereby lung function is decreased in COPD. The hypothesis is that in diseases such as COPD, inflammatory cells including neutrophils, macrophages and lymphocytes migrate to the lung and release either more or different types of inflammatory mediators and/or destructive enzymes compared to subjects without COPD. We aim to investigate these separate cell types in the blood of subjects with COPD and identify which genes are more highly expressed when compared to cells obtained from patients without COPD. We will also investigate the lung macrophages from these subjects to identify whether the same or different genes are expressed in these cells. We will isolate different leukocyte populations from the blood and extract ribonucleic acid (RNA) from these samples. The type and quantity of RNA in these samples is a reflection of the specific genes expressed in these cells. This RNA will be sent to Gene Logic and this company will test these samples to identify which genes have been expressed. Similar experiments will be performed using macrophages obtained following bronchoalveolar lavage of these subjects. We would aim to examine the responses of leukocytes from three groups of subjects, namely (i) non-smoking controls (ii) smokers without clinical or histological signs of COPD and (iii) smokers with COPD. The isolated leukocytes will either be immediately solubilized in solutions to purify RNA or we will then use these isolated cells in vitro and following stimulation investigate whether different genes are expressed or at a differential rate in the disease state. The objective is to identify which genes are specifically expressed in patients with COPD with a view to identify novel targets for drug therapy. We will examine both leukocytes derived from peripheral blood and macrophages obtained from bronchoalveolar lavage with the aim to determine whether differences attributable to disease can be identified in both circulating cells and those at the site of disease. This is a preliminary study to determine the profile of inflammatory mediator expression from leukocytes and as such power calculations to determine the number of subjects is not appropriate.
The aim of this study is to investigate the mechanisms whereby leukocytes are recruited to the lung in chronic obstructive pulmonary disease (COPD) and cause tissue destruction. The hypothesis is that in COPD more leukocytes enter the lung and it is these cells that are responsible for the degradation of lung tissue. We, the researchers at Imperial College London, will isolate leukocytes from the blood of patients with COPD, healthy smokers and normal subjects and measure the movement of the leukocytes to chemoattractants. We will examine further, which cell surface receptors are responsible for this trafficking of cells. Furthermore, the differentiation of these cells in vitro will be compared with cells from healthy smokers and normal subjects. Specifically, the expression of enzymes that are responsible for tissue destruction and the cell surface receptors on these cells will be investigated. The objective is to identify the mechanisms whereby leukocytes from COPD patients behave differently to cells from healthy smokers and normal subjects with a view to identify novel targets for drug therapy.
The aim of this study is to examine the inflammatory mechanisms involved in the pathogenesis of inflammatory lung disease, in particular to compare the inflammatory profile seen in asthma and COPD. Evidence for inflammation in asthma and COPD is based on the finding of increased numbers of macrophages and neutrophils in the lungs and respiratory secretions of these patients. The inflammatory cells produce proteases, as well as, reactive oxidant species resulting in a protease/anti-protease imbalance which favours lung destruction. The aim is to examine the inflammatory mediators released by inflammatory cells (such as, macrophages and lymphocytes) in order to determine whether there are differences between non-smoking subjects, smoking subjects and patients with asthma or COPD. Monocytes are precursors of alveolar macrophages, and both monocytes and neutrophils are recruited to the lung from the blood via the action of specific chemoattractants. We have evidence that in inflammation there are higher levels of these chemoattractants. Therefore these cells might also demonstrate the same changes seen in alveolar macrophages from these patients. We also aim to assess the role of the macrophage precursor (monocyte) and neutrophils in the blood. We will also assess lymphocyte/monocyte interaction. We will do this as the lymphocyte may be involved in the initial recruitment of inflammatory cells. We will also assess the role of cytokines involved with monocyte/macrophage/neutrophil migration in induced sputum as well as the role of induced sputum in the migration of monocytes and neutrophils into the lung. Our aim is to link the initial changes in blood to the changes causing disease in the lungs. We aim to examine cellular responses in four groups of subjects, namely (i) non-smoking controls, (ii) smokers without clinical evidence of COPD or asthma, (iii) smokers with COPD (iv) asthmatic patients.
The aim of this study is to investigate the mechanisms whereby specific white cells called macrophages found in the lung release inflammatory mediators or chemicals together with enzymes that destroy the surrounding lung tissue. The hypothesis is that in diseases such as chronic obstructive pulmonary disease (COPD), lung macrophages release either more or different types of inflammatory mediators and/or destructive enzymes compared to subjects without COPD. We will isolate macrophages from small pieces of lung parenchyma. These samples are derived from lobes resected for carcinoma of the lung. We would aim to examine the responses of tissue derived macrophages in three groups of subjects, namely (i) non-smoking controls (lung carcinoma as secondary metastasis), (ii) smokers without clinical or histological signs of COPD and (iii) smokers with COPD. The resected lung tissue will be cut into small pieces and washed in order to release the macrophages from the tissue. The macrophages will then be isolated from other cell types in the washings. We will then use these isolated cells in vitro to examine the cell surface receptors in order to compare these macrophage cells with macrophages reported from bronchoalveolar lavage and monocyte derived macrophage models. We will then examine inflammatory mediator synthesis and release following stimulation of these cells. We will also examine the regulation and release of enzymes known to damage lung tissue. Using these two models we will then examine the signal transduction pathways that lead to this activation of the macrophages and investigate the effects of novel therapeutic agents to inhibit inflammatory mediator and/or enzyme synthesis and release. The objective is to identify the mechanisms whereby macrophages respond to pro-inflammatory conditions seen in COPD with a view to identify novel targets for drug therapy.
The Spiration Intra-Bronchial Valve is intended for use as a minimally invasive treatment for severe emphysema, using standard bronchoscopy. The valve is designed to limit airflow to a selected portion of the lung, producing a reduction in lung volume, which may improve pulmonary function in patients with emphysema.
The purpose of this study is to assess the safety and efficacy of the Emphasys Endobronchial Valve (EBV) and procedure (with pulmonary rehabilitation) compared to optimal medical management (with pulmonary rehabilitation) in patients with heterogeneous emphysema.
The purpose of this study was to compare the effect of exercise treatment combined with breathing retraining (a computerized feedback program), with exercise treatment combined with heliox (a helium and oxygen combination), with exercise only in patients with moderate to severe chronic obstructive pulmonary disease. This was an 8-week intervention study.
The purpose of this study is to evaluate a multifaceted intervention to improve the quality of end-of-life communication between patients with COPD and their primary care providers using information about patients preferences for end of life care and how to communicate and use this information to activate patients, family members, and healthcare providers.