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Hema Vasavada

Researcher at Yale University

Publications -  11
Citations -  571

Hema Vasavada is an academic researcher from Yale University. The author has contributed to research in topics: Endothelial stem cell & Embryonic stem cell. The author has an hindex of 6, co-authored 9 publications receiving 426 citations.

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A non-canonical Notch complex regulates adherens junctions and vascular barrier function.

TL;DR: The existence of a non-canonical cortical NOTCH1 signalling pathway that regulates vascular barrier function is established, and thus provides a mechanism by which a single receptor might link transcriptional programs with adhesive and cytoskeletal remodelling.
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Development of the fetal bone marrow niche and regulation of HSC quiescence and homing ability by emerging osteolineage cells.

TL;DR: In developing bone marrow, the vasculature can sustain multilineage progenitors, but interactions with osteolineage cells are needed to regulate long-term HSC proliferation and potential, and the timing of murine fetal long bone vascularization and ossification relative to the onset of HSC activity is established.
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Hemogenic endothelial cell specification requires c-Kit, Notch signaling, and p27-mediated cell-cycle control.

TL;DR: This work found that re-expression of c-Kit in RA-deficient (Raldh2(-/-)) primordial endothelium induced Notch signaling and p27 expression, which restored cell-cycle control and rescued hemogenic endothelial cell specification and function.
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Rac2 Modulates Atherosclerotic Calcification by Regulating Macrophage Interleukin-1β Production

TL;DR: In this paper, the authors identify Rac2 as a major inflammatory regulator of signaling that directs plaque osteogenesis, and they found that elevated IL-1β was an independent predictor of cardiovascular death in those subjects with high coronary calcium burden.
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VEGF controls lung Th2 inflammation via the miR-1–Mpl (myeloproliferative leukemia virus oncogene)–P-selectin axis

TL;DR: The expression ofVEGF dampens the expression of microRNA-1, which drives inflammation in part via increasing theexpression of Mpl.VEGF.