Thursday, March 28, 2019
Asthma :: essays research papers
Asthma is a degenerative illness that affects many people. Asthma affects approximately 155 one thousand thousand people around the world. The pharmaceutical industry approximates $5.5 billion in sales for asthma attack medication per year for a condition that is incurable.Asthma is an incendiary disease of the airways. The narrowing of airways occurs receivable to inflammation and excessive mucous secretion. The minginess of the airway gives rise to common asthmatic symptoms of wheezing, coughing, tightness in the chest, and brusqueness of breath. The usual form of control for asthma is bronchiodilators and corticosteriods.Although, bronchiodilators be used in asthma therapy they have no effect on the inflammatory process. Bronchiodilators are a class of drug that relaxes airway smooth muscle by increasing cAMP and opening potassium channels. Corticosteriods on the other fall out are now considered the first line of treatment for patients with severe and chronic asthma. Cor ticosteriods bind to a receptor in the cytosol, which translocates to the nucleus and binds DNA to stir up genes. The main action of corticosteriods is to suppress multiple inflammatory genes, such as cytokines, inflammatory enzymes and adhesion molecules. The effectiveness of the corticosteriod is in most part due to the inhibition of transcription factors, such as AP-1 (activation protein 1), Nuclear factor-&61547b (NF-&61547b), and nuclear factor of activated T-cells (NF-AT), which are required for inflammatory response.The Fc&61541RI is the receptor for the immunoglobulin E antibody. The Fc&61541RI is composed of a &61537 chain that binds the Fc portion of the immunoglobulin E, the &61538 chain and the &61543 chain unitedly form a tetrameric structure. Due to the fact that release of mediators from mast cells in asthma is IgE-E dependent one approach would be to block the activation of IgE using blocking antibodies that do not result in mast cells. A humanized murine monoclona l antibody directed to the Fc&61541RI-binding domain of human IgE (rhuMAb-E25) reduces allergen special IgE after intravenous administration. RhuMAb reduces early and late responses to inhaled allergen and eosinophils counts from induced sputum.
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