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.
View Article and Find Full Text PDFTargeted 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.
View Article and Find Full Text PDFBackground: 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.
View Article and Find Full Text PDFBackground: 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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