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Jonathan Ma

Researcher at Virginia Commonwealth University

Publications -  11
Citations -  318

Jonathan Ma is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Neutrophil elastase & Cystic fibrosis. The author has an hindex of 4, co-authored 8 publications receiving 171 citations. Previous affiliations of Jonathan Ma include Boston Children's Hospital.

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Mucins, Mucus, and Goblet Cells

TL;DR: Insight into the innate immune properties of mucins and goblet cells support a shift from the current paradigm of repressing increased mucin expression to targeting regulation of specific mucins or mucin hyperconcentration in the abnormal airway milieu.
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Cystic Fibrosis Sputum Rheology Correlates With Both Acute and Longitudinal Changes in Lung Function.

TL;DR: There are dramatic increases in dynamic viscosity and elasticity during a pulmonary exacerbation with return to baseline at recovery, which suggests that sputum viscoelastic properties are tightly associated with lung function and disease status.
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Neutrophil Extracellular Traps Increase Airway Mucus Viscoelasticity and Slow Mucus Particle Transit.

TL;DR: It is hypothesized that the extracellular DNA and/or oxidative stress e.g. by the release of reactive oxygen species (ROS) and myeloperoxidase (MPO) during NETs formation in the airways would increase mucus viscoelasticity.
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Dry powder aerosol containing muco-inert particles for excipient enhanced growth pulmonary drug delivery.

TL;DR: The MIP released from the EEG aerosol had human airway mucus and CF sputum diffusion properties comparable to the suspension formulation, which makes this formulation a promising pulmonary drug delivery system for CF lung infections.
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Neutrophil Elastase Triggers the Release of Macrophage Extracellular Traps: Relevance to CF.

TL;DR: In this paper, neutrophil extracellular traps increase cystic fibrosis (CF) airway inflammation by clipping of chromatin binding proteins and the release of METs, a mechanism to augment NE-induced airway inflammatory in CF.