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Emanuela M. Bruscia

Researcher at Yale University

Publications -  52
Citations -  3472

Emanuela M. Bruscia is an academic researcher from Yale University. The author has contributed to research in topics: Cystic fibrosis & Inflammation. The author has an hindex of 26, co-authored 43 publications receiving 3038 citations. Previous affiliations of Emanuela M. Bruscia include California Pacific Medical Center & European Institute.

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Lack of a Fusion Requirement for Development of Bone Marrow-Derived Epithelia

TL;DR: This work uses the Cre/lox system together with β-galactosidase and enhanced green fluorescent protein expression in transgenic mice to identify epithelial cells in the lung, liver, and skin that develop from BMDCs without cell fusion.
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Targeting the Intracellular Environment in Cystic Fibrosis: Restoring Autophagy as a Novel Strategy to Circumvent the CFTR Defect.

TL;DR: Recent pre-clinical evidence indicating that targeting the intracellular environment surrounding the misfolded mutant CFTR instead of protein itself could constitute an attractive therapeutic option to sensitize patients carrying the F508del-CFTR mutation to the beneficial action of CFTR potentiators on lung inflammation is reviewed.
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Plasticity of bone marrow-derived stem cells.

TL;DR: The literature that lends credibility to the theory that highly plastic BMCs have a role in maintenance and repair of nonhematopoietic tissue is reviewed and the possible mechanisms by which this may occur are discussed.
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Innate immunity in cystic fibrosis lung disease

TL;DR: Dissecting the complex network of innate immune regulation and associated pro-inflammatory cascades in CF lung disease may pave the way for novel immune-targeted therapies in CF and other chronic infective lung diseases.
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Macrophages Directly Contribute to the Exaggerated Inflammatory Response in Cystic Fibrosis Transmembrane Conductance Regulator−/− Mice

TL;DR: The hypothesis that macrophages play a role in the exuberant cytokine production and secretion that characterizes CF is supported, suggesting that the macrophage response may be an important therapeutic target for decreasing the morbidity of CF lung disease.