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Asthma phenotyping and endotyping has emerged as a novel approach to asthma classification inspired by precision medicine which separates the clinical presentations of asthma, or asthma phenotypes, from their underlying causes, or asthma endotypes. The best-supported endotypic distinction is the type 2-high/type 2-low distinction.
Bronchial hyperresponsiveness is a hallmark of asthma but also occurs frequently in people with chronic obstructive pulmonary disease (COPD). [2] In the Lung Health Study, bronchial hyperresponsiveness was present in approximately two-thirds of patients with non-severe COPD, and this predicted lung function decline independently of other ...
Research by sports scientist John Dickinson found that 70 percent of UK-based members of the British swimming team had some form of asthma, as did a third of Team Sky cyclists, compared to a national asthma rate of eight to ten percent, [24] whilst a study by the United States Olympic Committee in 2000 found that half of cross-country skiers ...
During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways. [3]
The effects of bronchial thermoplasty on smooth muscle mass are seen up to at least 12 months post-treatment; however, the procedure does not seem to impact other features of airway remodelling. [4] Thus far, no pharmacological treatment modality for asthma has been developed nor shown to prevent or attenuate the progression of airway remodelling.
Like other β adrenergic agonists, they cause smooth muscle relaxation. β 2 adrenergic agonists' effects on smooth muscle cause dilation of bronchial passages, vasodilation in muscle and liver, relaxation of uterine muscle, and release of insulin. They are primarily used to treat asthma and other pulmonary disorders.
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