Publications by authors named "Nazanin ZounematKermani"

Volatile organic compounds (VOCs) in asthmatic breath may be associated with sputum eosinophilia. We developed a volatile biomarker signature to predict sputum eosinophilia in asthma. VOCs emitted into the space above sputum samples (headspace) from patients with severe asthma ( = 36) were collected onto sorbent tubes and analyzed using thermal desorption gas chromatography-mass spectrometry (GC-MS).

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Article Synopsis
  • Multi-omics data integration in biomedical research faces challenges, especially with traditional consensus clustering methods that often assume similar sample coverages, which doesn't align with real-world biological data.
  • A new strategy called "ccml," implemented in R, addresses this by allowing for unequal missing labels during the consensus clustering process, accommodating varying data coverage from multiple predictive labels.
  • The ccml method has shown promise in effectively grouping molecular data in studies on chronic obstructive pulmonary disease and adult asthma, providing a valuable toolkit for researchers dealing with incomplete multi-omics datasets.
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Background: Patients with asthma often suffer from frequent respiratory viral infections and reduced virus clearance. Lung resident memory T cells provide rapid protection against viral reinfections.

Objective: Because the development of resident memory T cells relies on the lung microenvironment, we investigated the impact of allergen sensitization on the development of virus-specific lung resident memory T cells and viral clearance.

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Background: Interleukin-1-dependent increases in glycolysis promote allergic airways disease in mice and disruption of pyruvate kinase M2 (PKM2) activity is critical herein. Glutathione-S-transferase P (GSTP) has been implicated in asthma pathogenesis and regulates the oxidation state of proteins via S-glutathionylation. We addressed whether GSTP-dependent S-glutathionylation promotes allergic airways disease by promoting glycolytic reprogramming and whether it involves the disruption of PKM2.

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