Publications by authors named "D Greif"

Objective: Atherosclerosis underlies the most common etiologies of mortality worldwide, resulting in nearly 10 million deaths annually. In atherosclerosis, inflammation, metabolic factors, and hemodynamics cause the accumulation of extracellular lipids and the formation of plaques in the tunica intima of specific arteries. Atherosclerotic plaques primarily form in the coronary and carotid arteries, the aorta, and the peripheral arteries of the lower extremities.

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Targeted low-throughput studies have previously identified subcellular RNA localization as necessary for cellular functions including polarization, and translocation. Furthermore, these studies link localization to RNA isoform expression, especially 3' Untranslated Region (UTR) regulation. The recent introduction of genome-wide spatial transcriptomics techniques enables the potential to test if subcellular localization is regulated in situ pervasively.

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Background: Early surgical management of full-thickness traumatic rotator cuff tears (RCTs) may optimize functional outcomes, prioritizing timely diagnoses. Ultrasound and magnetic resonance imaging (MRI) are highly sensitive and specific modalities for RCT diagnosis, yet MRI remains the gold standard diagnostic tool despite increased costs and potential delays in care. Ultrasound can provide same-day diagnosis, thus possibly expediting care.

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Background: TGF (transforming growth factor)-β pathway is central to blood-brain barrier development as it regulates cross talk between pericytes and endothelial cells. Murine embryos lacking TGFβ receptor (activin receptor-like kinase 5) in brain pericytes (mutants) display endothelial cell hyperproliferation, abnormal vessel morphology, and gross germinal matrix hemorrhage-intraventricular hemorrhage (GMH-IVH), leading to perinatal lethality. Mechanisms underlying how ALK5 signaling in pericytes noncell autonomously regulates endothelial cell behavior remain elusive.

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Article Synopsis
  • The study explores how chronic hypoxia contributes to the abnormal increase in smooth muscle cells (SMCs) in pulmonary arteries, a condition known as pulmonary hypertension (PH).
  • Researchers found that under low oxygen conditions, lung endothelial cells produce factors that promote SMC survival, while reversing this condition can help reduce the pathological changes, but not always if certain factors are overexpressed.
  • In both mice and human samples, key proteins associated with cell survival and autophagy were upregulated in SMCs, and targeting these pathways showed potential for reversing muscularization and PH.
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