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Shyamala Ganesan

Researcher at University of Michigan

Publications -  27
Citations -  1495

Shyamala Ganesan is an academic researcher from University of Michigan. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 18, co-authored 24 publications receiving 1260 citations.

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Barrier function of airway tract epithelium

TL;DR: In this paper, the authors reviewed the regulation of components of barrier function with respect to chronic airway diseases and showed that impairment of one or more of these essential components may increase susceptibility to infection and promote exaggerated and prolonged innate immune responses to environmental factors including allergens and pathogens resulting in chronic inflammation.
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Increased Cytokine Response of Rhinovirus-infected Airway Epithelial Cells in Chronic Obstructive Pulmonary Disease

TL;DR: Airway epithelial cells from patients with COPD show higher baseline levels of cytokine expression and increased susceptibility to RV infection, despite an increased IFN response.
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Quercetin inhibits rhinovirus replication in vitro and in vivo

TL;DR: Results suggest that quercetin inhibits RV endocytosis and replication in airway epithelial cells at multiple stages of the RV life cycle, which decreases expression of pro-inflammatory cytokines and improves lung function in RV-infected mice.
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Quercetin prevents progression of disease in elastase/LPS-exposed mice by negatively regulating MMP expression

TL;DR: Quercetin prevents progression of emphysema in elastase/LPS-treated mice by reducing oxidative stress, lung inflammation and expression of MMP9 and MMP12 in vivo and in vitro.
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Rhinovirus-Induced Barrier Dysfunction in Polarized Airway Epithelial Cells Is Mediated by NADPH Oxidase 1

TL;DR: It is concluded that Rac1-dependent NOX1 activity is required for RV- or poly(I:C)-induced ROS generation, which in turn disrupts the barrier function of polarized airway epithelia, and suggests that dsRNA generated during RV replication is sufficient to disrupt barrier function.