Publications by authors named "J R Womble"

Background: Airway tissue eosinophilia can be an observed feature of obesity-associated type 2 (T2) asthma, but the processes mediating this inflammation are unknown.

Objective: To investigate a process whereby leptin, an adipokine elevated in obesity, potentiates pulmonary eosinophilia and eotaxin production by airway fibroblasts in T2 asthma.

Methods: We assessed associations between body mass index and airway eosinophilia as well as leptin and eotaxin production in 78 participants with asthma, 36 of whom exhibited obesity.

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Several studies report that ashwagandha, a traditional Ayurvedic supplement, has anti-inflammatory properties. Type 2 (T2) asthma is characterized by eosinophilic airway inflammation. We hypothesized that allergen-induced eosinophilic airway inflammation in mice would be reduced following administration of Withaferin A (WFA), the primary active phytochemical in Ashwagandha.

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Sea otters are apex predators that can exert considerable influence over the nearshore communities they occupy. Since facing near extinction in the early 1900s, sea otters are making a remarkable recovery in Southeast Alaska, particularly in Glacier Bay, the largest protected tidewater glacier fjord in the world. The expansion of sea otters across Glacier Bay offers both a challenge to monitoring and stewardship and an unprecedented opportunity to study the top-down effect of a novel apex predator across a diverse and productive ecosystem.

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Introduction: Asthma is a chronic airway inflammatory disease marked by airway inflammation, remodeling and hyperresponsiveness to allergens. Allergic asthma is normally well controlled through the use of beta-2-adrenergic agonists and inhaled corticosteroids; however, a subset of patients with comorbid obesity experience resistance to currently available therapeutics. Patients with asthma and comorbid obesity are also at a greater risk for severe disease, contributing to increased risk of hospitalization.

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Article Synopsis
  • In a study on asthma and obesity, researchers hypothesized that introducing leptin, a hormone increased in obesity, would worsen airway inflammation and fibrosis in a mouse model of allergic airways disease.
  • The experiment involved exposing mice to an allergen, followed by subcutaneous injections of either leptin or saline, and analyzing lung function and tissue post-treatment.
  • Results showed that leptin increased lung resistance and fibrosis markers, with notable differences in responses between male and female mice, indicating leptin's role in exacerbating asthma conditions.
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