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A. Wesley Burks

Researcher at University of North Carolina at Chapel Hill

Publications -  305
Citations -  31163

A. Wesley Burks is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Peanut allergy & Food allergy. The author has an hindex of 82, co-authored 288 publications receiving 27987 citations. Previous affiliations of A. Wesley Burks include Boston Children's Hospital & University of Arkansas at Little Rock.

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Long-term sublingual immunotherapy for peanut allergy in children: Clinical and immunologic evidence of desensitization.

TL;DR: Extended-therapy peanut SLIT provided clinically meaningful desensitization in the majority of children with peanut allergy that was balanced with ease of administration and a favorable safety profile.
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Phenotypic Characterization of Eosinophilic Esophagitis in a Large Multicenter Patient Population from the Consortium for Food Allergy Research.

TL;DR: Gastrointestinal eosinophilia is present in approximately 10% of patients with EoE; the symptom-diagnosis time gap is influenced by age, race, food allergy, and atopic dermatitis; symptoms vary with race; concurrent infectious/immunologic disorders and mental health disorders are common; and the level of esophageal eOSinophils is comparable in patients with and without fibrostenotic features.
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Clinical Characteristics of Peanut-Allergic Children: Recent Changes

TL;DR: In the past decade, the ages of first peanut exposure and reaction have declined among peanut-allergic children seen in a referral clinic, and sesame seeds should perhaps be considered one of the major food allergens.
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Anaphylaxis: a history with emphasis on food allergy.

TL;DR: Treatment with intramuscular epinephrine continues to be the recommended first‐line therapy, although studies indicate that education of both the patients and the medical community is needed.
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Mast cell desensitization inhibits calcium flux and aberrantly remodels actin

TL;DR: It is found that displacement of the actin cytoskeleton and its continued association with FcεRI impede the capacity of desensitized MCs to evoke the calcium response that is essential for MC degranulation.