Active clinical trials for "Asthma"

The purpose of this study is to evaluate the immunomodulatory effect of treatment of allergic rhinitis symptoms with specific immunotherapy by measurement of pulmonary inflammatory markers, and among others, exhaled nitric oxide.

The purpose of this study is to evaluate the multiple mechanisms through which stress, physical environment, and genetic predisposition contribute to asthma in urban children.

The objective of this pilot study is to assess the feasibility and the potential differential impact of a novel intervention of induced positive affect and self-affirmation to increase physical activity in asthma patients.

To investigate genetic factors that affect asthma severity.

We are testing the following two hypotheses: 1) Peaks in hourly exposures to airborne particulate matter (PM) of outdoor origin will be more closely associated with acute asthmatic responses to particles than 24-hour average exposures in susceptible individuals; 2) Personal exposure to PM, and estimated particle dose to the lungs, will be more closely associated with daily asthma severity than standard outdoor particle concentrations measured as 24-hour averages at governmental monitoring sites.

To study work-related asthma in a low-income, urban population.

In this project, we hypothesize that polymorphisms of genes expressed by the airway epithelia in asthmatics following specific airway challenges predispose individuals to the development of asthma. To test this hypothesis, we identify the genes that are differentially expressed by airway epithelial cells following challenge with stimuli that induce acquired (house dust mite) or innate (LPS) immune responses, and then determine whether polymorphisms in these genes are associated with the development of asthma in a separate, well characterized, familial cohort of asthmatics. This is a powerful approach that is designed to identify novel genes that are associated with both asthma pathogenesis (differentially expressed in the exposure-response study) and asthma susceptibility (genetically associated with asthma in a linkage/association study).

To examine whether or not primary school-aged children with asthma from low-income households have lower household environmental tobacco smoke (ETS) exposure than matched control children.

Asthma is a chronic inflammatory disease. We propose to study inflammatory changes in the lungs of subjects with atopic asthma of different severity in vivo using positron emission tomography (PET) with 2-deoxy-2-[18F]fluoro-D-glucose (FDG). It has been shown that the uptake of FDG as detected by PET scanning correlates with inflammation in animal models as well as in human disease processes such as sarcoidosis, tuberculosis and abscess formation. In addition, it has been shown that the inflammation associated with allergen challenge in patients with atopic asthma can be visualized using PET scanning with FDG. We hypothesize that the degree of FDG-uptake as a measure of inflammation correlates with the severity of asthma as determined by pulmonary function tests and clinical signs and symptoms. In addition, information about the spatial distribution of the inflammatory changes will be obtained. To compare the characteristics of the inflammation in asthma with non-asthmatic inflammation of the lung, the images obtained in asthmatic subjects will be compared with images from subjects who have inflammatory changes of the lung caused by Wegener's granulomatosis. Subjects with atopic asthma and non-atopic control subjects will be selected from the community and, if eligible for the study, undergo skin testing against common allergens and pulmonary function testing. Subjects with Wegener's granulomatosis will be selected from a large group of subjects followed with this disease at NIAID. PET scanning with FDG will be used to measure inflammation in the PET scanning facility at the Clinical Center of the NIH and the results of the scanning will be correlated with the severity of the disease. We expect that for the first time this methodology will permit an objective measure of the basic pathogenic process, the allergic inflammation, in patients with atopic asthma. Using this methodology it will be possible to study the efficacy of currently available therapies for allergic inflammation. In addition, this methodology will provide an extremely useful tool for the development of new therapeutic approaches to the treatment of asthma.

To identify susceptibility genes associated with asthma and asthma related phenotypes.