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John C. Olsen

Researcher at University of North Carolina at Chapel Hill

Publications -  81
Citations -  8085

John C. Olsen is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Genetic enhancement & Cystic fibrosis transmembrane conductance regulator. The author has an hindex of 42, co-authored 81 publications receiving 7761 citations. Previous affiliations of John C. Olsen include Cardiff University.

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Journal ArticleDOI

CFTR as a cAMP-dependent regulator of sodium channels.

TL;DR: In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport.
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A controlled study of adenoviral-vector-mediated gene transfer in the nasal epithelium of patients with cystic fibrosis

TL;DR: In patients with cystic fibrosis, adenoviral-vector-mediated transfer of the CFTR gene did not correct functional defects in nasal epithelium, and local inflammatory responses limited the dose of adenvirus that could be administered to overcome the inefficiency of gene transfer.
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Role of mutant CFTR in hypersusceptibility of cystic fibrosis patients to lung infections

TL;DR: Pseudomonas aeruginosa lipopolysaccharide (LPS)-core oligosaccharide was identified as the bacterial ligand for epithelial cell ingestion; exogenous oligosACcharide inhibited bacterial ingestion in a neonatal mouse model, resulting in increased amounts of bacteria in the lungs.
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Efficiency of gene transfer for restoration of normal airway epithelial function in cystic fibrosis

TL;DR: Mixed populations of a CF airway cell line expressing either the normal cystic fibrosis transmembrane conductance regulator (CFTR) cDNA (corrected cells) or a reporter gene in defined percentages suggest that in vivo correction of allCF airway cells may not be mandatory.
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Cloning and expression of a human P2U nucleotide receptor, a target for cystic fibrosis pharmacotherapy.

TL;DR: expression of the human P2U receptor (HP2U) in 1321N1 cells revealed evidence for autocrine ATP release and stimulation of transduced receptors, which will be useful for studying autocrine regulatory mechanisms and in screening of potential therapeutic drugs.