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William W. Busse

Researcher at University of Wisconsin-Madison

Publications -  740
Citations -  62685

William W. Busse is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Asthma & Eosinophil. The author has an hindex of 115, co-authored 697 publications receiving 56703 citations. Previous affiliations of William W. Busse include National Institutes of Health & University at Buffalo.

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Journal ArticleDOI

Platelet Activation, P-Selectin, and Eosinophil β1-Integrin Activation in Asthma

TL;DR: It is inferred that platelet activation and binding of activated platelets to eosinophils followed by P-selectin-mediated eos inophil β1-integrin activation occur in both nonsevere and severe asthma with rapid movement of platelet-eOSinophil complexes into the lung in more severe disease.
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Biomarkers in asthmatic patients: Has their time come to direct treatment?

TL;DR: The following review will discuss the current use of biomarkers for the diagnosis of asthma, triaging the severity of a patient's disease, and the potential efficacy of treatments.
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Determinants of response to fluticasone propionate and salmeterol/fluticasone propionate combination in the Gaining Optimal Asthma controL study.

TL;DR: In this article, a logistic regression analysis was used to investigate whether covariates influenced the achievement of at least WC asthma in patients with uncontrolled asthma, and predefined criteria were used to assess improvements in 6 clinical outcomes.
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Onset and duration of protection against exercise-induced bronchoconstriction by a single oral dose of montelukast

TL;DR: Montelukast provided significant protection against EIB as soon as 2 hours after a single oral dose, with persistent benefit up to 24 hours, and fewer patients required postexercise beta-agonist rescue at 2Hours after dosing with montelukasts.
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Childhood- versus Adult-Onset Asthma

TL;DR: Data suggest that airway responsiveness, respiratory symptoms, and peripheral blood eosinophilia are independent risk factors for the develop­ ment of chronic obstructive disease and that the mechanism by which these factors predict this development is by reducing max­ imallung function and precipitating early decline in FE~ in young adults.