A spontaneous and controllable removal of condensed microdroplets at high supersaturation via self-propelled jumping is achieved by introducing a designed micropore array on a nanostructured superhydrophobic surface. The fabricated surface was demonstrated to delay the ice formation for 1 hour at -15 °C with a supersaturation of 6.97.

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This paper addresses failure detection in automated parts assembly, using the force signature captured during the contact phase of the assembly process. We use a supervised learning approach, specifically a Support Vector Machine (SVM), to distinguish between successful and failed assemblies. This paper describes our implementation and experimental results obtained with an electronic assembly application. We also analyze the tradeoff between system accuracy and number of training examples. We show that a less expensive sensor (a single-axis load cell instead of a six-axis force/torque sensor) provides enough information to detect failure. Finally, we use Principal Component Analysis (PCA) to compress the force signature and as a result reduce the number of examples required to train the system.

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We used the lattice Boltzmann method to investigate how the hierarchical structure of a rough solid surface, which in this work is modeled as the microstructure (micropillars) covered with nanostructures (nanopillars), affects the contact angle of microdroplets atop of the solid surface and the wetting transition between the Wenzel and Cassie states. Our simulation results show that the Wenzel-to-Cassie state transition can be achieved by decreasing the fluid-solid attraction, increasing the micropillar spacing, or coating the microstructures with nanostructures. For the effect of the hierarchical structure on the contact angle, we find that the micropillars show a negligible effect on the contact angle, but they may affect the sliding angle. In contrast, it is the nanostructure that determines the contact angle. The contact angle increases with the nanopillar length until reaching a maximal value, but its dependence on the nanopillar spacing becomes more complicated. The contact angle may first increase with the nanopillar spacing and then decreases, or decreases monotonously, depending on whether the liquid enters the nanostructure or not. In this work, we also demonstrate in the presence of contact line pinning, that the pinning effect affects the apparent contact angle.

Purpose Neuroblastoma is an embryonic childhood cancer with high mortality. 13-cis retinoic acid (13-cisRA) improves survival for some patients, but many recur, suggesting clinical resistance. The mechanism of resistance, and the normal differentiation pathway, are poorly understood. Three-Amino-acid Loop Extension (TALE) family genes are master regulators of differentiation. Since retinoids promote differentiation in neuroblastoma, we evaluated TALE family gene expression in neuroblastoma. Experimental Design We evaluated expression of TALE family genes in RA-sensitive and -resistant neuroblastoma cell lines, with and without 13cis-RA treatment, identifying genes whose expression correlate with retinoid sensitivity. We evaluated the roles of one gene, PBX1, in neuroblastoma cell lines, including proliferation and differentiation. We evaluated PBX1 expression in primary human neuroblastoma samples by RT-qPCR, and three independent clinical cohort microarray datasets. Results We confirmed induction of PBX1 expression, and no other TALE family genes, was associated with 13-cisRA responsiveness in NB cell lines. Exogenous PBX1 expression in neuroblastoma cell lines, mimicking induced PBX1 expression, significantly impaired proliferation and anchorage-independent growth, and promoted RA-dependent and -independent differentiation. Reduced PBX1 protein levels produced an aggressive growth phenotype and RA resistance. PBX1 expression correlated with histological neuroblastoma subtypes, with highest expression in benign ganglioneuromas and lowest in high-risk neuroblastomas. High PBX1 expression is prognostic of survival, including in multivariate analysis, in the three clinical cohorts. Conclusions PBX1 is an essential regulator of differentiation in neuroblastoma and potentiates retinoid-induced differentiation. Neuroblastoma cells and tumors with low PBX1 expression have an immature phenotype with poorer prognosis, independent of other risk factors.