Noninvasive Morphologic and Hemodynamic Evaluation of Type B Aortic Dissection: State of the Art and Future Perspectives.

Stanford type B aortic dissection (TBAD) is associated with relatively high rates of morbidity and mortality, and appropriate treatment selection is important for optimizing patient outcomes. Depending on individualized risk factors, clinical presentation, and imaging findings, patients are generally stratified to optimal medical therapy anchored by antihypertensives or thoracic endovascular aortic repair (TEVAR). Using standard anatomic imaging with CT or MRI, several high-risk features including aortic diameter, false lumen (FL) features, size of entry tears, involvement of major aortic branch vessels, or evidence of visceral malperfusion have been used to select patients likely to benefit from TEVAR. However, even with these measures, the number needed to treat for TEVAR remains, and improved risk stratification is needed. Increasingly, the relationship between FL hemodynamics and adverse aortic remodeling in TBAD has been studied, and evolving noninvasive techniques can measure numerous FL hemodynamic parameters that may improve risk stratification. In addition to summarizing the current clinical state of the art for morphologic TBAD evaluation, this review provides a detailed overview of noninvasive methods for TBAD hemodynamics characterization, including computational fluid dynamics and four-dimensional flow MRI. Keywords: CT, Image Postprocessing, MRI, Cardiac, Vascular, Aorta, Dissection © RSNA, 2021.

Deletion of caveolin scaffolding domain alters cancer cell migration.

Caveolin-1 (Cav-1) is an integral membrane protein that plays an important role in proliferative and terminally differentiated cells. As a structural component of Caveolae, Cav-1 interacts with signaling molecules via a caveolin scaffolding domain (CSD) regulating cell signaling. Recent reports have shown that Cav-1 is a negative regulator in tumor metastasis. Therefore, we hypothesize that Cav-1 inhibits cell migration through its CSD. HeLa cells were engineered to overexpress Cav-1 (Cav-1 OE), Cav-1 without a functional CSD (∆CSD), or enhanced green fluorescent protein (EGFP) as a control. HeLa cell migration was suppressed in Cav-1 OE cells while ∆CSD showed increased migration, which corresponded to a decrease in the tight junction protein, zonula occludens (ZO-1). The migration phenotype was confirmed in multiple cancer cell lines. Phosphorylated STAT-3 was decreased in Cav-1 OE cells compared to control and ∆CSD cells; reducing STAT-3 expression alone decreased cell migration. ∆CSD blunted HeLa proliferation by increasing the number of cells in the G2/M phase of the cell cycle. Overexpressing the CSD peptide alone suppressed HeLa cell migration and inhibited pSTAT3. These findings suggest that Cav-1 CSD may be critical in controlling the dynamic phenotype of cancer cells by facilitating the interaction of specific signal transduction pathways, regulating STAT3 and participating in a G2/M checkpoint. Modulating the CSD and targeting specific proteins may offer potential new therapies in the treatment of cancer metastasis.