Drop splashing after impact onto immiscible pools of different viscosities

Droplet impact onto liquid pools is a canonical scenario relevant to numerous natural phenomena and industrial processes. However, despite their ubiquity, multi-fluid systems with the drop and pool consisting of different liquids are far less well understood. Our hypothesis is that the post-impact dynamics greatly depends on the pool-to-droplet viscosity ratio , which we explore over a range of six orders of magnitude using a combination of experiments and theoretical approaches (mathematical modelling and direct numerical simulation). Our findings indicate that in this scenario the splashing threshold and the composition of the ejecta sheet are controlled by the viscosity ratio. We uncover that increasing the pool viscosity decreases the splashing threshold for high viscosity pools () when the splash comes from the droplet. By contrast, for low viscosity pools, the splash sheet comes from the pool and increasing the pool viscosity increases the splashing threshold. Surprisingly, there are conditions for which no splashing is observed under the conditions attainable in our laboratory. Furthermore, considering the interface velocity together with asymptotic arguments underlying the generation of the ejecta has allowed us to understand meaningful variations in the pressure during impact and rationalise the observed changes in the splashing threshold

Transcriptional activation of the Axl and PDGFR-α by c-Met through a ras- and Src-independent mechanism in human bladder cancer

<p>Abstract</p> <p>Background</p> <p>A cross-talk between different receptor tyrosine kinases (RTKs) plays an important role in the pathogenesis of human cancers.</p> <p>Methods</p> <p>Both NIH-Met5 and T24-Met3 cell lines harboring an inducible human c-Met gene were established. C-Met-related RTKs were screened by RTK microarray analysis. The cross-talk of RTKs was demonstrated by Western blotting and confirmed by small interfering RNA (siRNA) silencing, followed by elucidation of the underlying mechanism. The impact of this cross-talk on biological function was demonstrated by Trans-well migration assay. Finally, the potential clinical importance was examined in a cohort of 65 cases of locally advanced and metastatic bladder cancer patients.</p> <p>Results</p> <p>A positive association of Axl or platelet-derived growth factor receptor-alpha (PDGFR-α) with c-Met expression was demonstrated at translational level, and confirmed by specific siRNA knock-down. The transactivation of c-Met on Axl or PDGFR-α <it>in vitro </it>was through a <it>ras</it>- and Src-independent activation of mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway. In human bladder cancer, co-expression of these RTKs was associated with poor patient survival (<it>p </it>< 0.05), and overexpression of c-Met/Axl/PDGFR-α or c-Met alone showed the most significant correlation with poor survival (<it>p </it>< 0.01).</p> <p>Conclusions</p> <p>In addition to c-Met, the cross-talk with Axl and/or PDGFR-α also contributes to the progression of human bladder cancer. Evaluation of Axl and PDGFR-α expression status may identify a subset of c-Met-positive bladder cancer patients who may require co-targeting therapy.</p

Droplet impact dynamics on shallow pools

When a fast droplet impacts a pool of the same fluid, a thin ejecta sheet that dominates the early-time dynamics emerges within the first few microseconds. Fluid and impact properties are known to affect its evolution; we experimentally reveal that the pool depth is a critical factor too. Whilst ejecta sheets can remain separate and subsequently fold inwards on deeper pools, they instead develop into outward-propagating lamellae on sufficiently shallow pools, undergoing a transition that we delineate by comprehensively varying impact inertia and pool depth. Aided by matching direct numerical simulation results, we find that this transition stems from a confinement effect of the pool base on the impact-induced pressure, which stretches the ejecta sheet to restrict flow into it from the droplet on sufficiently shallow pools. This insight is also applied to elucidate the well-known transition due to Reynolds number

Rapid production of new oligodendrocytes is required in the earliest stages of motor-skill learning

We identified mRNA encoding the ecto-enzyme Enpp6 as a marker of newly forming oligodendrocytes, and used Enpp6 in situ hybridization to track oligodendrocyte differentiation in adult mice as they learned a motor skill (running on a wheel with unevenly spaced rungs). Within just 2.5 h of exposure to the complex wheel, production of Enpp6-expressing immature oligodendrocytes was accelerated in subcortical white matter; within 4 h, it was accelerated in motor cortex. Conditional deletion of myelin regulatory factor (Myrf) in oligodendrocyte precursors blocked formation of new Enpp6+ oligodendrocytes and impaired learning within the same ~2−3 h time frame. This very early requirement for oligodendrocytes suggests a direct and active role in learning, closely linked to synaptic strengthening. Running performance of normal mice continued to improve over the following week accompanied by secondary waves of oligodendrocyte precursor proliferation and differentiation. We concluded that new oligodendrocytes contribute to both early and late stages of motor skill learning