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We hypothesized that non-surgeon, Negative Pressure Wound Therapy (NPWT) naïve participants would better identify device functions and troubleshoot failures after being exposed to a video curriculum (VC) compared to similar participants exposed to clinical practice guidelines (CPGs). VC and critical action step development was followed by randomization of 115 non-surgical, NPWT naïve participants into either the CPG or VC study groups. Participants individually identified components of the NPWT system and then worked as a team to troubleshoot three scenarios on an in vivo porcine model. VC participants better identified all NPWT components and functions (p ​< ​0.001), demonstrated correct cannister attachment (p ​< ​0.001) and performed a seal check (p ​< ​0.001). VC teams performed more critical action steps in the leak (p ​= ​0.011) and obstruction (p ​= ​0.001) scenarios. In post-event surveys, participants were more likely to find the VC easy to use and informative and were likely to recommend the videos to a colleague (p ​= ​0.008, p ​= ​0.019, p ​= ​0.02). VC participants demonstrated improved competency in individual NPWT component identification and team-based troubleshooting of NPWT failures. This VC represents an effective alternative to existing CPGs. •Video curriculum provides more thorough instruction regarding negative pressure wound therapy device functions.•Video curriculum instruction resulted in better troubleshooting of multiple aspects of negative pressure wound therapy care.•Users of the video curriculum would recommend the videos to colleagues.•Video instruction does not replace thorough in-person, hands-on training.

Neural stem cells are reported to lie in a vascular niche, but there is no direct evidence for a functional relationship between the stem cells and blood vessel component cells. We show that endothelial cells but not vascular smooth muscle cells release soluble factors that stimulate the self-renewal of neural stem cells, inhibit their differentiation, and enhance their neuron production. Both embryonic and adult neural stem cells respond, allowing extensive production of both projection neuron and interneuron types in vitro. Endothelial coculture stimulates neuroepithelial cell contact, activating Notch and Hes1 to promote self-renewal. These findings identify endothelial cells as a critical component of the neural stem cell niche.

Mutations in BRAF, a component of extracellular signal-regulated kinases 1 and 2 (ERK) cascade, are frequent in melanoma. It is important to understand how BRAF mutations contribute to malignant traits including anchorage- and growth factor-independence. We have previously shown that efficient activation of ERK in normal human epidermal melanocytes (NHEM) requires both adhesion to the extracellular matrix and growth factors. Mutant V599E BRAF is sufficient to promote ERK activation independent of adhesion and growth factors. Here, we analysed regulation of G1 cell cycle events in NHEM and human melanoma cells. We show that S phase entry in NHEM requires both adhesion and growth factor signaling through the MEK-ERK pathway. This control correlates with induction of cyclin D1 and downregulation of p27 super(Kip1), two key G1 cell cycle events. In melanoma cells expressing V599E BRAF, cyclin D1 was constitutively expressed independent of adhesion but dependent upon MEK activation and nuclear accumulation of ERK. Reduction of cyclin D1 levels by RNA interference inhibited S phase entry in melanoma cells. Importantly, expression of V599E BRAF in NHEM was sufficient to promote cyclin D1 promoter activity in the absence of adhesion. Additionally, p27 super(Kip1) levels were downregulated in V599E BRAF-expressing melanoma cells and active BRAF was sufficient to downregulate p27 super(Kip1) in serum-starved NHEM. Thus, adhesion-growth factor cooperation, leading to efficient activation of ERK, regulates cyclin D1 and p27 super(Kip1) levels in human melanocytes and mutant BRAF overrides adhesion-growth factor control of these two G1 cell cycle proteins in melanomas. These findings provide important insight into how BRAF mutations contribute to aberrant human melanocyte proliferation.