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Kathleen C. Flanders

Researcher at National Institutes of Health

Publications -  150
Citations -  19846

Kathleen C. Flanders is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 68, co-authored 150 publications receiving 19278 citations. Previous affiliations of Kathleen C. Flanders include Gyeongsang National University & New York State Department of Health.

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Effect of overexpression of pparγ on the healing process of corneal alkali burn in mice

TL;DR: It is shown that adenoviral gene introduction of peroxisome proliferator-activated receptor-gamma (PPARgamma) inhibits activation of ocular fibroblasts and macrophages in vitro and also induced anti-inflammatory and anti-fibrogenic responses in an alkali-burned mouse cornea, suggesting that overexpression of PPARGamma may represent an effective new strategy for treatment of oocular surface burns.
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Transforming Growth Factor-βs and Mammary Gland Involution; Functional Roles and Implications for Cancer Progression

TL;DR: The putative role of TGF-β during involution is discussed, as well as its effects on the mammary microenvironment and possible implications for pregnancy-associated tumorigenesis.
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Epithelial-Mesenchymal Transition as a Therapeutic Target for Prevention of Ocular Tissue Fibrosis

TL;DR: EMT in retinal pigment epithelium is involved in the development of another ocular fibrotic disease, proliferative vitreoretinopathy, a fibrosis in the retina, and EMT-related signal transduction cascades, i.
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Antagonizing deactivating cytokines to enhance host defense and chemotherapy in experimental visceral leishmaniasis.

TL;DR: IL-10 appears to be the appropriate target for therapeutic inhibition in visceral L. donovani infection, as it enhances Th1-cell-associated responses, promoting gamma interferon secretion, granuloma assembly, macrophage activation with substantial liver parasite killing, and synergy with pentavalent antimony chemotherapy.
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Smad3 deficiency alters key structural elements of the extracellular matrix and mechanotransduction of wound closure

TL;DR: It is reported that excisional ear wounds in mice lacking Smad3 enlarge compared with wild-type controls resulting from changes in extracellular matrix molecules, which alter the mechanotransduction properties of these wounds.