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Linda S. Powers

Researcher at University of Arizona

Publications -  185
Citations -  7002

Linda S. Powers is an academic researcher from University of Arizona. The author has contributed to research in topics: Extended X-ray absorption fine structure & Heme. The author has an hindex of 50, co-authored 184 publications receiving 6508 citations. Previous affiliations of Linda S. Powers include Roy J. and Lucille A. Carver College of Medicine & University of Iowa.

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Vitamin D Decreases Respiratory Syncytial Virus Induction of NF-κB–Linked Chemokines and Cytokines in Airway Epithelium While Maintaining the Antiviral State

TL;DR: It is found that vitamin D decreases the inflammatory response to viral infections in airway epithelium without jeopardizing viral clearance, suggesting that adequate vitamin D levels would contribute to reduced inflammation and less severe disease in RSV-infected individuals.
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Respiratory syncytial virus up-regulates TLR4 and sensitizes airway epithelial cells to endotoxin

TL;DR: It is suggested that RSV infection sensitizes airway epithelium to a subsequent environmental exposure (LPS) by altered expression and membrane localization of TLR4 and has the potential to profoundly alter airway inflammation.
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Respiratory Syncytial Virus Induces TLR3 Protein and Protein Kinase R, Leading to Increased Double-Stranded RNA Responsiveness in Airway Epithelial Cells

TL;DR: These studies demonstrate that RSV infection of A549 and human tracheobronchial epithelial cells increases the amounts of TLR3 and PKR in a time-dependent manner, which leads to increased NF-κB activity and production of the inflammatory cytokine IL-8 following a later exposure to dsRNA.
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Identification of an Autophagy Defect in Smokers’ Alveolar Macrophages

TL;DR: The autophagy pathway is identified as a potential target for interventions designed to decrease infection rates in smokers and possibly in individuals with high environmental particulate exposure.
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Variable airway responsiveness to inhaled lipopolysaccharide.

TL;DR: It is demonstrated that an LPS phenotype can be reproducibly elicited in humans, which creates an opportunity to identify genes involved in this response to inhaled LPS.