2,196 research outputs found

    Zombie Vortex Instability. II. Thresholds to Trigger Instability and the Properties of Zombie Turbulence in the Dead Zones of Protoplanetary Disks

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    In Zombie Vortex Instability (ZVI), perturbations excite critical layers in stratified, rotating shear flow (as in protoplanetary disks), causing them to generate vortex layers, which roll-up into anticyclonic zombie vortices and cyclonic vortex sheets. The process is self-sustaining as zombie vortices perturb new critical layers, spawning a next generation of zombie vortices. Here, we focus on two issues: the minimum threshold of perturbations that trigger self-sustaining vortex generation, and the properties of the late-time zombie turbulence on large and small scales. The critical parameter that determines whether ZVI is triggered is the magnitude of the vorticity on the small scales (and not velocity), the minimum Rossby number needed for instability is Rocrit∼0.2Ro_{crit}\sim0.2 for β≡N/Ω=2\beta\equiv N/\Omega = 2, where NN is the Brunt-V\"ais\"al\"a frequency. While the threshold is set by vorticity, it is useful to infer a criterion on the Mach number, for Kolmogorov noise, the critical Mach number scales with Reynolds number: Macrit∼RocritRe−1/2Ma_{crit}\sim Ro_{crit}Re^{-1/2}. In protoplanetary disks, this is Macrit∼10−6Ma_{crit}\sim10^{-6}. On large scales, zombie turbulence is characterized by anticyclones and cyclonic sheets with typical Rossby number ∼\sim0.3. The spacing of the cyclonic sheets and anticyclones appears to have a "memory" of the spacing of the critical layers. On the small scales, zombie turbulence has no memory of the initial conditions and has a Kolmogorov-like energy spectrum. While our earlier work was in the limit of uniform stratification, we have demonstrated that ZVI works for non-uniform Brunt-V\"ais\"al\"a frequency profiles that may be found in protoplanetary disks.Comment: Submitted to Ap

    Identifying influential spreaders and efficiently estimating infection numbers in epidemic models: a walk counting approach

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    We introduce a new method to efficiently approximate the number of infections resulting from a given initially-infected node in a network of susceptible individuals. Our approach is based on counting the number of possible infection walks of various lengths to each other node in the network. We analytically study the properties of our method, in particular demonstrating different forms for SIS and SIR disease spreading (e.g. under the SIR model our method counts self-avoiding walks). In comparison to existing methods to infer the spreading efficiency of different nodes in the network (based on degree, k-shell decomposition analysis and different centrality measures), our method directly considers the spreading process and, as such, is unique in providing estimation of actual numbers of infections. Crucially, in simulating infections on various real-world networks with the SIR model, we show that our walks-based method improves the inference of effectiveness of nodes over a wide range of infection rates compared to existing methods. We also analyse the trade-off between estimate accuracy and computational cost, showing that the better accuracy here can still be obtained at a comparable computational cost to other methods.Comment: 6 page

    Population Structure of the Blue Crab Callinectes sapidus in the Maryland Coastal Bays

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    The population structure of the blue crab Callinectes sapidus was examined in the Maryland Coastal Bays (MCB) from 2014 to 2016. Crabs were sampled from April to December of each year. Size–frequency distributions showed a strong seasonal cycle, with small crabs being abundant in April, increasing in size through September, with adult crabs observed in the highest proportions from August through October of each year. A subsample of crabs was assayed for hemolymph ecdysone concentrations to examine molting patterns in field-collected blue crabs. Molting was observed throughout the sampling season, peaking in April for immature crabs, with lows in all size classes occurring in October. The mean size at maturity (L50) for females collected in this study was 116mmcarapace width (CW), which is comparable to that reported for the lower Chesapeake Bay (CB) and suggests crabs in the MCB are not significantly smaller as previously thought; however, large crabs (\u3e127 mmCW) appear to make up a smaller proportion of the total population in the MCB than in CB. Ovigerous females were observed at two distinct locations depending on the season, with 13/15 (86.7%) in southern Chincoteague Bay in April and May and 24/41 (58.5%) nearest to the Ocean City Inlet in July and August, indicating two potentially distinct spawning grounds and periods. This work suggests that blue crab reproductive success and general population trends are similar across both systems, with fishing pressure or disease in the MCB potentially explaining the low abundance of adult male crabs

    In Vitro Model of Tumor Cell Extravasation

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    Tumor cells that disseminate from the primary tumor and survive the vascular system can eventually extravasate across the endothelium to metastasize at a secondary site. In this study, we developed a microfluidic system to mimic tumor cell extravasation where cancer cells can transmigrate across an endothelial monolayer into a hydrogel that models the extracellular space. The experimental protocol is optimized to ensure the formation of an intact endothelium prior to the introduction of tumor cells and also to observe tumor cell extravasation by having a suitable tumor seeding density. Extravasation is observed for 38.8% of the tumor cells in contact with the endothelium within 1 day after their introduction. Permeability of the EC monolayer as measured by the diffusion of fluorescently-labeled dextran across the monolayer increased 3.8 fold 24 hours after introducing tumor cells, suggesting that the presence of tumor cells increases endothelial permeability. The percent of tumor cells extravasated remained nearly constant from1 to 3 days after tumor seeding, indicating extravasation in our system generally occurs within the first 24 hours of tumor cell contact with the endothelium
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