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Diane S. Krause

Researcher at Yale University

Publications -  170
Citations -  36417

Diane S. Krause is an academic researcher from Yale University. The author has contributed to research in topics: Stem cell & Bone marrow. The author has an hindex of 56, co-authored 162 publications receiving 33122 citations. Previous affiliations of Diane S. Krause include University of Pennsylvania & Johns Hopkins University.

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Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair.

TL;DR: A novel role for SPC in regulating inflammation via JAK/STAT may have clinical applications, and immunofluorescence revealed increased phosphorylated signal transduction and activation of transcription 3 (pSTAT3), suggesting enhanced Janus kinase (JAK)/STAT activation in inflammatory and AT2 cells of SPC-TK/SPC-KO mice.
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C/EBPε directs granulocytic-vs-monocytic lineage determination and confers chemotactic function via Hlx

TL;DR: Two new regulatory functions of C/EBPepsilon in myelopoiesis are shown: in the absence of C/, there is not only incomplete differentiation of granulocytes, but the appearance of an intermediate cell type with monocyte and granulocyte features is disrupted, and the neutrophils have abnormal chemotaxis.
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Acute aspirin overdose: mechanisms of toxicity.

TL;DR: In this case, medical treatment of several critical concurrent metabolic responses was dependent on frequent evaluations of serum electrolytes, blood and urine pH, blood Po2 blood Pco2, and blood HCO3- concentrations.
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Dynamic Migration and Cell‐Cell Interactions of Early Reprogramming Revealed by High‐Resolution Time‐Lapse Imaging

TL;DR: An experimental system with multicolor time‐lapse microscopy that permits direct observation of pluripotency induction at single cell resolution, with temporal intervals as short as 5 minutes, and demonstrates that E‐cadherin is required for proper cellular interactions from an early stage of reprogramming, including the two‐cell intermediate.
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MKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation.

TL;DR: It is shown that MKL1 activation in somatic cells reduces chromatin accessibility and hinders full reprogramming to pluripotency and can be bypassed when the Sun2-containing linker of the nucleoskeleton and cytoskeleton (LINC) complex is inhibited.