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Framing through the concept of precarity, we share our arts-based research on the experiences of creating a collaborative performance-making project focused on connecting students from different education levels, to create a film-dance integrated performance to advocate for social justice issues in education. We, as instructors and researchers, embarked on an arts-based research journey creating sketches, poems, videos, and a dance performance to analyze and represent our research findings. Our performance from the performative inquiry shows our understanding of the collaboration project through the same art form we required our students to utilize: film and dance-integrated arts performance.

What should science, technology, engineering, art, and math (STEAM) education look like? In the context of educational policy, the STEAM conversation has intensified and spread across the United St...

Redefining the educational model of science, technology, engineering, and math curriculum (STEM) to also include art to become STEAM (Fournier, 2013; Guyotte, Sochacka, Constantino, Walther, & Kellam, 2014) is a current method to encourage students to actively participate in 21st-century learning (Saxena, 2014). The skills emphasized for 21st-century learning include critical thinking and problem solving; collaboration and communication; and creativity and innovation (Partnership for 21st Century Skills, 2007). Encouraging students to pursue a STEM career has become an important U.S. educational policy that emphasizes teaching these 21st-century skills along with STEM knowledge in the discourse of future economic growth.

Objective— MicroRNAs are involved in many critical functions, including angiogenesis. Ultrasound-targeted microbubble destruction (UTMD) is a noninvasive technique for targeted vascular transfection of plasmid DNA and may be well suited for proangiogenic microRNA delivery. We aimed to investigate UTMD of miR-126-3p for therapeutic angiogenesis in chronic ischemia. Approach and Results— The angiogenic potential of miR-126-3p was tested in human umbilical vein endothelial cells in vitro. UTMD of miR-126-3p was tested in vivo in Fischer-344 rats before and after chronic left femoral artery ligation, evaluating target knockdown, miR-126-3p and miR-126-5p expression, phosphorylated Tie2 levels, microvascular perfusion, and vessel density. In vitro, miR-126-3p–transfected human umbilical vein endothelial cells showed repression of sprouty-related protein-1 and phosphatidylinositol-3-kinase regulatory subunit 2, negative regulators of vascular endothelial growth factor and angiopoietin-1 signaling, increased phosphorylated Tie2 mediated by knockdown of phosphatidylinositol-3-kinase regulatory subunit 2 and greater angiogenic potential mediated by both vascular endothelial growth factor/vascular endothelial growth factor R2 and angiopoietin-1 /Tie2 effects. UTMD of miR-126-3p resulted in targeted vascular transfection, peaking early after delivery and lasting for >3 days, and resulting in inhibition of sprouty-related protein-1 and phosphatidylinositol-3-kinase regulatory subunit 2, with minimal uptake in remote organs. Finally, UTMD of miR-126-3p to chronic ischemic hindlimb muscle resulted in improved perfusion, vessel density, enhanced arteriolar formation, pericyte coverage, and phosphorylated Tie2 levels, without affecting miR-126-5p or delta-like 1 homolog levels. Conclusions— UTMD of miR-126 results in improved tissue perfusion and vascular density in the setting of chronic ischemia by repressing sprouty-related protein-1 and phosphatidylinositol-3-kinase regulatory subunit 2 and enhancing vascular endothelial growth factor and angiopoietin-1 signaling, with no effect on miR-126-5p. UTMD is a promising platform for microRNA delivery, with applications for therapeutic angiogenesis.

Left ventricular hypertrophy (LVH) is commonly found in chronic dialysis (CD) recipients, and is associated with impaired microvascular cardiac perfusion and heart failure. In response to LVH and cardiac ischemia, early outgrowth pro-angiogenic cellS(EPCs) mobilize from the bone marrow to facilitate angiogenesis and endothelial repair. In the general population, EPC number and function correlate inversely with cardiovascular risk. In end-stage renal disease (ESRD), EPC number and function are generally reduced.To test whether left ventricular abnormalities retain their potent ability to promote EPC reparative responses in the setting of ESRD.Cross-sectional study.St. Michael's Hospital, Toronto, Ontario, Canada.47 prevalent chronic dialysis recipients.(1) circulating CD34(+) and CD133(+) EPC number, (2) cultured EPC migratory ability, in vitro differentiation potential, and apoptosis rate, and (3) cardiac magnetic resonance-measured LV mass, volume and ejection fraction.Bivariate correlation analysis was performed with Spearman's rho test.Of the 47 patients (mean age: 54 ± 13 years), the mean delivered urea reduction was 74 ± 10 %. Mean LV mass was 123 ± 38 g. Circulating CD34(+) and CD133(+) EPCs represented 0.14 % (IQR: 0.05 - 0.29 %) and 0.05 % (IQR: 0.01 - 0.10 %) of peripheral blood mononuclear cells. There were no significant correlations between any EPC parameter and measures of LV mass or ejection fraction.Lack of a non-ESRD control population, and the inability to measure all parameters of EPC function due to limitations in blood sampling. Our inability to measure cardiac VEGF expression prevented an assessment of changes in cardiac EPC mobilization signals.These data suggest that in ESRD, the reparative EPC response to cardiac hypertrophy may be blunted. Further investigation of the effects of uremia on EPC physiology and its relationship to cardiac injury are required.L’hypertrophie ventriculaire gauche (HVG), qui est associée à la perfusion cardiaque microvasculaire alterée et à l’insuffisance cardiaque, n’est pas rare chez les patients qui reçoivent une dialyse chronique. En réponse à l’HVG et à l’ischémie cardiaque, les cellules proangiogéniques à croissance précoce (CPCP) se mobilisent au sein de la moelle osseuse afin de faciliter l’angiogenèse et la réparation endothéliale. Dans l’ensemble de la population, le nombre et l’activité des CPCP sont inversement proportionnels au risque cardiovasculaire. Dans le cas d’insuffisance rénale chronique terminale (IRT), le nombre et l’activité des CPCP sont généralement réduits.Vérifier si les anomalies du ventricule gauche demeurent aussi efficaces à promouvoir les actions réparatrices des CPCP dans le contexte de l’IRT.St. Michael’s Hospital, à Toronto, en Ontario, au Canada.47 cas prévalents de patients qui reçoivent une dialyse chronique.(1) le nombre de CPCP CD34L’analyse de la corrélation simple a été effectuée au moyen du coefficient de corrélation des rangs de Spearman.On a observé une réduction de 74 ± 10 % en moyenne parmi les 47 participants (moyenne d’âge : 54 ± 13 ans). La masse ventriculaire gauche était de 123 ± 38 g en moyenne. Les CPCP CD34L’absence d’une population témoin non atteinte d’IRT, de même que l’inhabilité de mesurer tous les paramètres de l’activité des CPCP, en raison des limites de l’échantillon sanguin. Notre incapacité à mesurer l’expression du facteur de croissance endothéliale vasculaire nous a empêchés d’effectuer l’analyse des modifications dans les signaux cardiaques de mobilisation des CPCP.Ces données suggèrent que dans le cas d’une IRT, la réponse réparatrice des CPCP à l’hypertrophie cardiaque peut être atténuée. Des observations plus poussées sur les effets de l’urémie sur la physiologie des CPCP et sur le lien avec les lésions cardiaques seraient nécessaires.

Teneurins are a family of highly conserved pair-rule proteins involved in morphogenesis and development of the central nervous system. Their function in adult tissues and in disease is largely unknown. Recent evidence suggests a role for dysregulated expression of Teneurins in human tumors, but systematic investigations are missing. Here, we investigated Teneurin-2 and Teneurin-4 expression in various cancer cell lines and in ovarian tumor tissues. Teneurin-2 and Teneurin-4 were expressed in most of the breast cancer cell lines tested. Teneurin-4 was also detected in ovarian cancer cell lines, and throughout ovarian tumors and normal ovary tissue. Ovarian tumors with low Teneurin-4 expression showed less differentiated phenotypes and these patients had shorter mean overall survival. Similarly, Teneurin-2 expression correlated with overall survival as well, especially in patients with serous tumors. In the various cell lines, 5-Aza-cytidine-induced changes in DNA methylation did not alter expression of Teneurin-2 and Teneurin-4, despite the existence of predicted CpG islands in both genes. Interestingly, however, we found evidence for the control of Teneurin-2 expression by the oncogenic growth factor FGF8. Furthermore, we identified multiple transcript splicing variants for Teneurin-2 and Teneurin-4, indicating complex gene expression patterns in malignant cells. Finally, downregulation of Teneurin-4 expression using siRNA caused a cell-type dependent increase in proliferation and resistance to cisplatin. Altogether, our data suggest that low Teneurin-4 expression provides a growth advantage to cancer cells and marks an undifferentiated state characterized by increased drug resistance and clinical aggressiveness. We conclude that Teneurin-2 and Teneurin-4 expression levels could be of prognostic value in ovarian cancer.