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Wenli Zhang

Researcher at University of North Carolina at Chapel Hill

Publications -  9
Citations -  701

Wenli Zhang is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Chemokine & Virus. The author has an hindex of 9, co-authored 9 publications receiving 652 citations.

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Journal ArticleDOI

Diesel exhaust enhances influenza virus infections in respiratory epithelial cells

TL;DR: Results presented here suggest that in human respiratory epithelial cells oxidative stress generated by DE(as) increases the susceptibility to influenza infection and that exposure to DE increases the ability of the virus to attach to and enter respiratory epithel cells.
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Zinc-induced PTEN Protein Degradation through the Proteasome Pathway in Human Airway Epithelial Cells

TL;DR: Exposure to Zn2+ ions causes PTEN degradation and loss of function, which is mediated by an ubiquitin-associated proteolytic process in the airway epithelium.
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Hydrogen Peroxide Has Opposing Effects on IKK Activity and I κ B α Breakdown in Airway Epithelial Cells

TL;DR: The results demonstrate that treatment with H2O2 increased IKK activity, phosphorylation, and ubiquitination of I κ B α in NHBE cells, but there was no significant proteolytic degradation of Iδ B α, nuclear translocation of p65, or NF- δ B DNA binding activity in cells treated with H 2O2.
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Selenium deficiency alters epithelial cell morphology and responses to influenza

TL;DR: It is demonstrated that selenium deficiency has a significant impact on the morphology and influenza-induced host defense responses in human airway epithelial cells.
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Reduced expression of IRF7 in nasal epithelial cells from smokers after infection with influenza.

TL;DR: It is demonstrated that infection with influenza results in the reduced expression of transcription factor IRF7 in NECs from smokers, and that these effects may be mediated by an epigenetic modification of theIRF7 gene, thus providing a potential mechanism rendering smokers more susceptible to respiratory virus infections.