3,555 research outputs found

    Earth Observing System. Volume 1, Part 2: Science and Mission Requirements. Working Group Report Appendix

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    Areas of global hydrologic cycles, global biogeochemical cycles geophysical processes are addressed including biological oceanography, inland aquatic resources, land biology, tropospheric chemistry, oceanic transport, polar glaciology, sea ice and atmospheric chemistry

    A Lagrangian model of copepod dynamics: Clustering by escape jumps in turbulence

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    Planktonic copepods are small crustaceans that have the ability to swim by quick powerful jumps. Such an aptness is used to escape from high shear regions, which may be caused either by flow per- turbations, produced by a large predator (i.e., fish larvae), or by the inherent highly turbulent dynamics of the ocean. Through a combined experimental and numerical study, we investigate the impact of jumping behaviour on the small-scale patchiness of copepods in a turbulent environment. Recorded velocity tracks of copepods displaying escape response jumps in still water are here used to define and tune a Lagrangian Copepod (LC) model. The model is further employed to simulate the behaviour of thousands of copepods in a fully developed hydrodynamic turbulent flow obtained by direct numerical simulation of the Navier-Stokes equations. First, we show that the LC velocity statistics is in qualitative agreement with available experimental observations of copepods in tur- bulence. Second, we quantify the clustering of LC, via the fractal dimension D2D_2. We show that D2D_2 can be as low as ~ 2.3 and that it critically depends on the shear-rate sensitivity of the proposed LC model, in particular it exhibits a minimum in a narrow range of shear-rate values. We further investigate the effect of jump intensity, jump orientation and geometrical aspect ratio of the copepods on the small-scale spatial distribution. At last, possible ecological implications of the observed clustering on encounter rates and mating success are discussedComment: 13 pages, 9 figure

    SURFO Technical Report No. 17-01

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    The 2017 technical reports written by undergraduate students participating in the SURFO (Summer Undergraduate Research Fellowships in Oceanography) Program while at the University of Rhode Island for ten weeks

    Influence of Tides and Mesoscale Eddies in the Ross Sea

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    The Ross Sea is the most biologically productive region in the Southern Ocean. Primary production is controlled by dissolved iron (dFe), a limiting micronutrient. The main focus of this thesis, motivated by the PRISM-RS project, is to investigate how tides and mesoscale eddies affect the pathways of dFe to the surface ocean. A regional ocean model with four hindcast simulations are used. Tidal forcing is added to simulations and mesoscale eddies are resolved by changing the horizontal grid resolution from 5 to 1.5 km. Simulations cover 1.5 years, ending at the time of the PRISM-RS cruise in early 2012. An extended 20 year simulation provides an estimate of model variability and significance. The model is validated using hydrographic data from the PRISM-RS cruise and climatological values of water mass volumes. Compared to observations, simulations show a salinity offset at depth, that can be attributed to freshening of the Ross Sea in recent years. The model represents water mass volumes well, but has a reduced amount of Ice Shelf Water. Analysis of eddy formation in the model indicates that the weak stratification produces small and short-lived mesoscale eddies in the Ross Sea. The increased resolution approximately doubles the number of eddies seen in one year of simulation and significantly increases the baroclinic eddy kinetic energy. The effect of tidal forcing on sea ice is investigated using a new method to extract a diurnal signal from satellite swath data. In the northwest corner of the Ross Sea continental shelf, strong tidal divergence causes the sea ice to decrease by 20% in winter. Simulation results show a strong heat flux that generates sea ice during spring tide conditions. The supply of dFe in simulations is calculated using four passive tracer dyes representing sources of dFe: sea ice, glacial ice, Circumpolar Deep Water, and benthic supply. The simulation without tides at 5 km resolution estimates the total supply of dFe to the surface at 6.63 μmol m-2 yr-1. Tides increase this by 20%, eddies decrease it by 15%, and the net change from both is not significant. Spatially, the pattern of dFe supply varies significantly between all simulations

    Estimating Bedrock Fracture Density of the Juneau Icefield, AK, to Inform Glacial Erosion Models

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    Understanding glacial erosion rates is important because debris eroded by a glacier can impact glacier flow speeds, protect tidewater glaciers from rapid retreat, and impact the productivity of marine ecosystems. Traditionally, glacial erosion models rely on a rock’s inherent “erodibility”, typically presented as a constant, to predict how much debris will be eroded by the glacier. However, the erodibility of bedrock varies spatially as a function of its fracture density, fracture orientation, and lithology, so the notion of applying a constant erodibility term to a whole field site does not fully capture the actual bedrock dynamics of the system. In this work, I present a novel approach to quantify bedrock fracture density and orientation through the generation of a 3D Structure from Motion (SfM) model and the application of a series of machine learning algorithms. To test this approach, I quantified the fracture density of a glacial bedrock nunatak in the Juneau Icefield of Southeast (SE) Alaska. The spatial variation in fracture density across this nunatak was found to be highly variable. Bedrock in the SE region of this field site showed a relatively high fracture density (\u3e20% fractured), whereas the central region of this field site showed a relatively low fracture density (0-10% fractured). Fracture orientations were shown to have a bimodal distribution, with the most common fracture orientations being approximately 0 and ± 90 degrees. This fracture density methodology and associated results can applied across the Juneau Icefield and other glacier systems to improve glacial bedrock erosion models

    Modelling the Pelagic Ecosystem Dynamics: The NW Mediterranean

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    26 páginas. 11 figuras,1 tabla.Peer reviewe

    Hydrogen peroxide induces apoptotic-like cell death in Microcystis aeruginosa (Chroococcales, Cyanobacteria) in a dose-dependent manner

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    We investigated the capability of Microcystis aeruginosa to cause apoptosis by pursuing morphological, molecular and physiological characteristics after exposure to H2O2. Microcystis proliferation was only weakly affected after exposure to 150 mu M H2O2 but cell numbers decreased dramatically after exposures of 250 and 325 mu M H2O2. Cells exposed to 250 and 325 mu M H2O2 were examined using transmission electron microscopy, and they exhibited membrane deformation and partial disintegration of thylakoids. Correspondingly, fluorescence imaging of DNA by Hoechst 33342 staining revealed the condensation of nucleoid chromatin. Moreover, cellular injury was concomitant with dramatic decreases in photosynthetic efficiency (ratio of variable fluorescence to maximum fluorescence [Fv/Fm], maximum electron transport rate [ETRmax]) and elevated caspase-3-like activity after exposure of 250 and 325 mu M H2O2. Terminal deoxynucleotidyl transferase Deoxyuridine 5-triphosphate nick end labelling (TUNEL) positive staining appeared in cells exposed to 250 mu M and 325 mu M H2O2, and the percentage staining increased with increasing H2O2 concentration. These data suggested that M. aeruginosa exposed to H2O2 underwent an apoptotic event. Additionally, cells exposed to H2O2 had increased cytoplasmic vacuolation and nontypical DNA laddering. Increased caspase-3-like activity was not inhibited in the presence of the synthetic caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone. Therefore, H2O2 induced apoptotic-like cell death in a dose-dependent manner. Taken together, our results provided a novel mechanism for explaining cyanobacterial bloom dynamics in response to environmental stress. The results also contributed to the understanding of the origin and evolution of programmed cell death.We investigated the capability of Microcystis aeruginosa to cause apoptosis by pursuing morphological, molecular and physiological characteristics after exposure to H2O2. Microcystis proliferation was only weakly affected after exposure to 150 mu M H2O2 but cell numbers decreased dramatically after exposures of 250 and 325 mu M H2O2. Cells exposed to 250 and 325 mu M H2O2 were examined using transmission electron microscopy, and they exhibited membrane deformation and partial disintegration of thylakoids. Correspondingly, fluorescence imaging of DNA by Hoechst 33342 staining revealed the condensation of nucleoid chromatin. Moreover, cellular injury was concomitant with dramatic decreases in photosynthetic efficiency (ratio of variable fluorescence to maximum fluorescence [Fv/Fm], maximum electron transport rate [ETRmax]) and elevated caspase-3-like activity after exposure of 250 and 325 mu M H2O2. Terminal deoxynucleotidyl transferase Deoxyuridine 5-triphosphate nick end labelling (TUNEL) positive staining appeared in cells exposed to 250 mu M and 325 mu M H2O2, and the percentage staining increased with increasing H2O2 concentration. These data suggested that M. aeruginosa exposed to H2O2 underwent an apoptotic event. Additionally, cells exposed to H2O2 had increased cytoplasmic vacuolation and nontypical DNA laddering. Increased caspase-3-like activity was not inhibited in the presence of the synthetic caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone. Therefore, H2O2 induced apoptotic-like cell death in a dose-dependent manner. Taken together, our results provided a novel mechanism for explaining cyanobacterial bloom dynamics in response to environmental stress. The results also contributed to the understanding of the origin and evolution of programmed cell death
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