View clinical trials related to Lung Diseases, Obstructive.
Filter by:Cigarette smoking is the main risk factor for chronic obstructive pulmonary disease (COPD). The cells lining the lung airways (epithelium) and the cells on the surface of the epithelium (alveolar macrophages) of healthy smokers develop characteristic gene expression changes that are different from that of nonsmokers. These gene expression changes include up- and down-regulation of genes in functional categories known to be relevant to the development of COPD. Administration of anti-inflammatory medications (inhaled steroids) in combination with long acting medications that open the airways (bronchodilators), are known to decrease the rate of acute exacerbations and improve the quality of life of individuals with COPD; however, the mechanisms underlying these beneficial effects of are poorly understood. This study will assess the effect of traditional therapy for COPD (inhaled corticosteroids, an anti-inflammatory medication, plus a bronchodilator, a medication that helps open the airways) on smoking-induced gene changes in airway epithelium and alveolar macrophages. Volunteer subjects will be evaluated by bronchoscopy to sample lung cells at 0, 7 and 14 days, with the therapy given at day 1 through day 7. The bronchoscopy aspects of this study will be covered by approved Weill-Cornell IRB protocol # 0005004439 (see below.) To participate in this protocol, the research subject will first be enrolled in Weill-IRB protocol #0005004439 entitled "Evaluation of the Lungs of Normal (Smokers, Ex-smokers, Non-Smokers) Individuals with Segmental Bronchopulmonary Lung Lavage, Bronchial Brushing, and Bronchial Wall Biopsy", fulfilling the inclusion/exclusion criteria of that protocol. They will be invited to participate in this protocol only if they meet the additional inclusion/exclusion criteria of this protocol.
Tadalafil may lower the pulmonary artery pressure in patients with Chronic Obstructive Lung Disease and secondary pulmonary hypertension and thereby improve patients quality of life.
The main purpose of the study is to evaluate the effect of mannitol on the cilia's beat frequency (ciliary beat frequency) in COPD patients.
This study looks at the effect of two drugs (carvedilol and metoprolol) which are used for patients with CHF (chronic heart failure). These agents are beta-blockers and, although effective in heart failure, may cause increases in airways tone and thus limit air getting into the lower parts of the lungs. Carvedilol is more active at blocking the receptor that opens up the airways and therefore theoretically may be more likely to reduce airways tone than metoprolol, although this has never been studied in patients with heart failure, and that is the purpose of the present study. We are looking to enrol 45 patients with heart failure and mild obstruction to the flow of air in their lungs. Patients will be randomised to either carvedilol or metoprolol (standard doses). Following a minimum of 2 weeks of therapy of study medication the patient will undergo a study day involving an assessment of their lung function, an assessment of their heart failure, a "living with heart failure" questionnaire, blood tests and blood pressure and heart rate readings. Patients will then be crossed over to the alternate medication. Following 2 weeks on the target dose the patient will undergo their second study day which will be the same as the first. The results obtained from each study day will be compared.
Comparison of the researchers' standard nebulizer and a breath actuated nebulizer to examine if breathing medication can be delivered more quickly and as effectively or more effectively than the standard nebulizer.
Some patients with chronic obstructive pulmonary disease (COPD) take nebulised treatments to ease the symptom of breathlessness, including the drug ipratropium. Nebulised bronchodilator drugs are taken up to 4 times through the day, and this can take up to 15 minutes each time. Although the treatment isbe effective, patients report that the time taken to set-up and use the nebuliser can be a disincentive to regular use. By contrast, an inhaler device is easy to use following appropriate instruction, and takes only a few seconds to administer. Inhaled tiotropium is a once daily treatment taken by inhaler which has been shown to be effective in COPD. We wish to assess whether inhaled Tiotropium as effective as nebulised ipratropium in patients with stable chronic obstructive pulmonary disease.
Cigarette smoking causes an increase in inflammation in the lungs. In about 20% of smokers this inflammation leads to damage in lungs including making holes in the lung tissue. This damage can not be repaired and these people find it very difficult to breathe. One of the problems with this disease called chronic obstructive pulmonary disease, or COPD for short, is that by the time patients visit their doctor with symptoms, the damage has already been done. At the moment, there is no way to predict which smokers will go on to develop COPD. The aim of this research is to look at smokers who breathe normally and use an imaging technique called a CT scan, to look at their lungs in more detail. Some of these people will have spots on their scan which may be caused by inflammation. We want to look at the cells at these spots to see if they make more proteins and enzymes that cause lung damage when compared to people that do not have these spots. We would then be able to predict which smokers are likely to develop COPD and treat them early before they have damaged their lungs.
The purpose of the study is to compare histone acetyltransferase (HAT) and histone deacetylase (HDAC) expressions and activities in induced sputum macrophages obtained from patients with moderate to severe COPD and age-matched normal non-smokers
A new artificial lung device has been developed that potentially provides added support to mechanical ventilation for severely damaged lungs. The Hattler Respiratory Assist Catheter is designed to provide gas exchange (deliver oxygen and remove carbon dioxide) for a period of up to 7 days, providing more time for the lungs to improve. Extrapolating from large animal data, the hypothesis is that the Hattler Catheter will be capable of providing 30% to 40% of the basal requirements of carbon dioxide exchange in a manner that is dependable and reproducible.
Chronic obstructive pulmonary disease (COPD for short) involves inflammation inside the air passages of the lungs. This inflammation might be partly responsible for the shortness of breath, cough and susceptibility to chest infections that form part of COPD. Inflammation is caused, in part, by white blood cells that are attracted from the blood into the air passages. Once inside the air passages, the white blood cells may change (or 'differentiate') and release substances that produce inflammation and attract more white cells. The hypothesis is that the lifespan of these cells may also be prolonged such that they produce more inflammatory mediators and in turn perpetuate inflammation. The cycle of inflammation may damage the lungs, so we want to see what mediators are released by white blood cells and determine if we can inhibit this effect with existing and new drugs. We would also like to see the effect of these drugs on the life-span and function of white blood cells. We will compare the behaviour and characteristics of white cells with those from healthy smokers and healthy non-smokers to find out if there is anything different about cells from COPD patients.