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Serpil C. Erzurum

Researcher at Cleveland Clinic Lerner Research Institute

Publications -  406
Citations -  34734

Serpil C. Erzurum is an academic researcher from Cleveland Clinic Lerner Research Institute. The author has contributed to research in topics: Asthma & Medicine. The author has an hindex of 87, co-authored 353 publications receiving 29654 citations. Previous affiliations of Serpil C. Erzurum include Pulmonary Vascular Research Institute & National Institutes of Health.

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Association of Ambient Ozone Exposure with Airway Inflammation and Allergy in Adults with Asthma

TL;DR: In adults with asthma but not controls studied during peak ozone season, increasing ozone exposure predicted lower lung function and increased biomarkers of respiratory and systemic inflammation.
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Anti-inflammatory Roles of Glucocorticoids Are Mediated by Foxp3+ Regulatory T Cells via a miR-342-Dependent Mechanism

TL;DR: It is reported that Foxp3+ regulatory T (Treg) cells are irreplaceable GC target cells in vivo, uncovering a previously unknown contribution of Treg cells during glucocorticoid-mediated treatment of inflammation and the underlying mechanisms operated via the Dex-miR-342-Rictor axis.
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Early effect of tidal volume on lung injury biomarkers in surgical patients with healthy lungs.

TL;DR: No tidal volume-related changes were observed in the selected lung injury biomarkers of patients with healthy lungs after 60-min ventilation, which might indicate atelectrauma and lung distention.
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Androgen regulation of pulmonary AR, TMPRSS2 and ACE2 with implications for sex-discordant COVID-19 outcomes.

TL;DR: In this article, the authors investigated the sex-associated TMPRSS2 and ACE2 expression in human and mouse lungs and interrogated the possibility of pharmacologic modification of their expression with anti-androgens.
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Breath Formate Is a Marker of Airway S-Nitrosothiol Depletion in Severe Asthma

TL;DR: EBC formate concentration is significantly higher in the breath of children with asthma than in those without asthma, and this difference is related to asthma pathology and may be a product of increased catabolism of endogenous S-nitrosothiols.