scholarly journals Detecting changes at the leading edge of an interface between oceanic water layers

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Qunshu Tang ◽  
Vincent C. H. Tong ◽  
Richard W. Hobbs ◽  
Miguel Ángel Morales Maqueda

Abstract Many physical phenomena in the ocean involve interactions between water masses of different temperatures and salinities at boundaries. Of particular interest is the characterisation of finescale structure at the marginal interaction zones of these boundaries, where the structure is either destroyed by mixing or formed by stratification. Using high-resolution seismic reflection imaging, we present observations of temporal changes at the leading edge of an interface between sub-thermocline layers in the Panama Basin. By studying time-lapse images of a seismic reflector between two water boundaries with subtle differences, we provide empirical constraints on how stratified layers evolve. The leading edge of this reflector, which is characterised by a gradual lateral decrease in vertical temperature contrast ($$|\Delta T|$$ ∣ Δ T ∣ ), increases in length over ~3 days coupled with an increase in $$|\Delta T|$$ ∣ Δ T ∣ . A critical mixing state, in which turbulent diffusion is gradually replaced by double-diffusion as the dominant mixing process, is thus revealed.

2015 ◽  
Author(s):  
John Salogiannis ◽  
Martin J. Egan ◽  
Samara L. Reck-Peterson

Eukaryotic cells use microtubule-based intracellular transport for the delivery of many subcellular cargos, including organelles. The canonical view of organelle transport is that organelles directly recruit molecular motors via cargo-specific adaptors. In contrast to this view, we show here that peroxisomes move by hitchhiking on early endosomes, an organelle that directly recruits the transport machinery. Using the filamentous fungus Aspergillus nidulans we find that hitchhiking is mediated by a novel endosome-associated linker protein, PxdA. PxdA is required for normal distribution and long-range movement of peroxisomes, but not early endosomes or nuclei. Using simultaneous time-lapse imaging we find that early endosome-associated PxdA localizes to the leading edge of moving peroxisomes. We identify a coiled-coil region within PxdA that is necessary and sufficient for early endosome localization and peroxisome distribution and motility. These results present a new mechanism of microtubule-based organelle transport where peroxisomes hitchhike on early endosomes and identify PxdA as the novel linker protein required for this coupling.


Author(s):  
Joachim Kurzke

Realistic compressor maps are the key to high quality gas turbine performance calculations. When modeling the performance of an existing engine then these maps are usually not known and must be approximated by adapting maps from literature to either measured data or to other available information. There are many publications describing map adaptation processes, simple ones and more sophisticated physically based scaling rules. There are also reports about using statistics, genetic algorithms, neural networks and even morphing techniques for re-engineering compressor maps. This type of methods does not consider the laws of physics and consequently the generated maps are valid at best in the region in which they have been calibrated. This region is frequently very narrow, especially in case of gas generator compressors which run in steady state always on a single operating line. This paper describes which physical phenomena influence the shape of speed and efficiency lines in compressor maps. For machines operating at comparatively low speeds (so that the flow into each stage is subsonic), there is usually considerable range between choke and stall corrected flow. As the speed of the machine is increased the range narrows. For high-speed stages with supersonic relative flow into the rotor the efficiency maximum is where the speed line turns over from vertical to lower than maximum corrected flow. At this operating condition the shock is about to detach from the leading edge of the blades. The flow at a certain speed can also be limited by choking in the compressor exit guide vanes. For high pressure ratio single stage centrifugal compressors this is a normal case, but it can also happen with low pressure ratio multistage boosters of turbofan engines, for example. If the compressor chokes at the exit, then the specific work remains constant along the speed line while the overall pressure ratio varies and that generates a very specific shape of the efficiency contour lines in the map. Also in other parts of the map, the efficiency varies along speed lines in a systematic manner. Peculiar shapes of specific work and corrected torque lines can reveal physically impossibilities that are difficult to see in the standard compressor map pictures. Compressor maps generated without considering the inherent physical phenomena can easily result in misleading performance calculations if used at operating conditions outside of the region where they have been calibrated. Whatever map adaptation method is used: the maps created in such a way should be checked thoroughly for violations of the underlying laws of compressor physics.


1997 ◽  
Vol 139 (2) ◽  
pp. 417-434 ◽  
Author(s):  
Clare M. Waterman-Storer ◽  
E.D. Salmon

We have discovered several novel features exhibited by microtubules (MTs) in migrating newt lung epithelial cells by time-lapse imaging of fluorescently labeled, microinjected tubulin. These cells exhibit leading edge ruffling and retrograde flow in the lamella and lamellipodia. The plus ends of lamella MTs persist in growth perpendicular to the leading edge until they reach the base of the lamellipodium, where they oscillate between short phases of growth and shortening. Occasionally “pioneering” MTs grow into the lamellipodium, where microtubule bending and reorientation parallel to the leading edge is associated with retrograde flow. MTs parallel to the leading edge exhibit significantly different dynamics from MTs perpendicular to the cell edge. Both parallel MTs and photoactivated fluorescent marks on perpendicular MTs move rearward at the 0.4 μm/min rate of retrograde flow in the lamella. MT rearward transport persists when MT dynamic instability is inhibited by 100-nM nocodazole but is blocked by inhibition of actomyosin by cytochalasin D or 2,3-butanedione–2-monoxime. Rearward flow appears to cause MT buckling and breaking in the lamella. 80% of free minus ends produced by breakage are stable; the others shorten and pause, leading to MT treadmilling. Free minus ends of unknown origin also depolymerize into the field of view at the lamella. Analysis of MT dynamics at the centrosome shows that these minus ends do not arise by centrosomal ejection and that ∼80% of the MTs in the lamella are not centrosome bound. We propose that actomyosin-based retrograde flow of MTs causes MT breakage, forming quasi-stable noncentrosomal MTs whose turnover is regulated primarily at their minus ends.


2019 ◽  
Vol 116 (43) ◽  
pp. 21445-21449 ◽  
Author(s):  
Barak Hirshberg ◽  
Valerio Rizzi ◽  
Michele Parrinello

Trapped bosons exhibit fundamental physical phenomena and are at the core of emerging quantum technologies. We present a method for simulating bosons using path integral molecular dynamics. The main difficulty in performing such simulations is enumerating all ring-polymer configurations, which arise due to permutations of identical particles. We show that the potential and forces at each time step can be evaluated by using a recurrence relation which avoids enumerating all permutations, while providing the correct thermal expectation values. The resulting algorithm scales cubically with system size. The method is tested and applied to bosons in a 2-dimensional (2D) trap and agrees with analytical results and numerical diagonalization of the many-body Hamiltonian. An analysis of the role of exchange effects at different temperatures, through the relative probability of different ring-polymer configurations, is also presented.


1982 ◽  
Vol 95 (1) ◽  
pp. 127-136 ◽  
Author(s):  
T Soranno ◽  
E Bell

Cytostructural changes during fibroblast spreading and translocation and during the transition between the two states have been studied in living cells and in the same cells after fixation and immunofluorescent staining. In time-lapse sequences we observe that birefringent arcs, sometimes circles, concentric with the cell perimeter, form near the periphery of a spreading cell, or that arcs form near the leading edge of a locomoting cell. The arcs move toward the nucleus, where they disappear. In spreading cells, radial stress fibers extend from the region of the cell nucleus to the periphery. The arcs or circles and the stress fibers are visualized in the same cells after fixation and staining with fluorescein-conjugated antiactin antibodies. Stained images of spreading cells show the arcs and stress fibers in the same plane of focus. At points of intersection with arcs, stress fibers are bent toward the substrate on which the cell is moving. During a transitional stage between spreading and translocation the cytostructure undergoes reproducible changes. Arcs and circle cease to form. The radial stress fibers elongate, spiral around the nucleus, and move to the periphery as a band of filaments. We interpret the moving arcs as condensations of a microfilament network that move toward the nucleus as compression waves. As elements of the net are brought close together by the compression wave, contraction may occur and facilitate the condensations.


1997 ◽  
Vol 139 (2) ◽  
pp. 397-415 ◽  
Author(s):  
Tatyana M. Svitkina ◽  
Alexander B. Verkhovsky ◽  
Kyle M. McQuade ◽  
Gary G. Borisy

While the protrusive event of cell locomotion is thought to be driven by actin polymerization, the mechanism of forward translocation of the cell body is unclear. To elucidate the mechanism of cell body translocation, we analyzed the supramolecular organization of the actin–myosin II system and the dynamics of myosin II in fish epidermal keratocytes. In lamellipodia, long actin filaments formed dense networks with numerous free ends in a brushlike manner near the leading edge. Shorter actin filaments often formed T junctions with longer filaments in the brushlike area, suggesting that new filaments could be nucleated at sides of preexisting filaments or linked to them immediately after nucleation. The polarity of actin filaments was almost uniform, with barbed ends forward throughout most of the lamellipodia but mixed in arc-shaped filament bundles at the lamellipodial/cell body boundary. Myosin II formed discrete clusters of bipolar minifilaments in lamellipodia that increased in size and density towards the cell body boundary and colocalized with actin in boundary bundles. Time-lapse observation demonstrated that myosin clusters appeared in the lamellipodia and remained stationary with respect to the substratum in locomoting cells, but they exhibited retrograde flow in cells tethered in epithelioid colonies. Consequently, both in locomoting and stationary cells, myosin clusters approached the cell body boundary, where they became compressed and aligned, resulting in the formation of boundary bundles. In locomoting cells, the compression was associated with forward displacement of myosin features. These data are not consistent with either sarcomeric or polarized transport mechanisms of cell body translocation. We propose that the forward translocation of the cell body and retrograde flow in the lamellipodia are both driven by contraction of an actin–myosin network in the lamellipodial/cell body transition zone.


1980 ◽  
Vol 86 (2) ◽  
pp. 402-416 ◽  
Author(s):  
D H Tippit ◽  
J D Pickett-Heaps ◽  
R Leslie

Prometaphase in two large species of diatoms is examined, using the following techniques: (a) time-lapse cinematography of chromosome movements in vivo; (b) electron microscopy of corresponding stages: (c) reconstruction of the microtubules (MTs) in the kinetochore fiber of chromosomes attached to the spindle. In vivo, the chromosomes independently commence oscillations back and forth to one pole. The kinetochore is usually at the leading edge of such chromosome movements; a variable time later both kinetochores undergo such oscillations but toward opposite poles and soon stretch poleward to establish stable bipolar attachment. Electron microscopy of early prometaphase shows that the kinetochores usually laterally associate with MTs that have one end attached to the spindle pole. At late prometaphase, most chromosomes are fully attached to the spindle, but the kinetochores on unattached chromosomes are bare of MTs. Reconstruction of the kinetochore fiber demonstrates that most of its MTs (96%) extend past the kinetochore and are thus apparently not nucleated there. At least one MT terminates at each kinetochore analyzed. Our interpretation is that the conventional view of kinetochore function cannot apply to diatoms. The kinetochore fiber in diatoms appears to be primarily composed of MTs from the poles, in contrast to the conventional view that many MTs of the kinetochore fiber are nucleated by the kinetochore. Similarly, chromosomes appear to initially orient their kinetochores to opposite poles by moving along MTs attached to the poles, instead of orientation effected by kinetochore MTs laterally associating with other MTs in the spindle. The function of the kinetochore in diatoms and other cell types is discussed.


1998 ◽  
Vol 111 (15) ◽  
pp. 2085-2095 ◽  
Author(s):  
J. Kolega

Different isoforms of non-muscle myosin II have different distributions in vivo, even within individual cells. In order to understand how these different distributions arise, the distribution and dynamics of non-muscle myosins IIA and myosin IIB were examined in cultured cells using immunofluorescence staining and time-lapse imaging of fluorescent analogs. Cultured bovine aortic endothelia contained both myosins IIA and IIB. Both isoforms distributed along stress fibers, in linear or punctate aggregates within lamellipodia, and diffusely around the nucleus. However, the A isoform was preferentially located toward the leading edge of migrating cells when compared with myosin IIB by double immunofluorescence staining. Conversely, the B isoform was enriched in structures at the cells' trailing edges. When fluorescent analogs of the two isoforms were co-injected into living cells, the injected myosins distributed with the same disparate localizations as endogenous myosins IIA and IIB. This indicated that the ability of the myosins to ‘sort’ within the cytoplasm is intrinsic to the proteins themselves, and not a result of localized synthesis or degradation. Furthermore, time-lapse imaging of injected analogs in living cells revealed differences in the rates at which the two isoforms rearranged during cell movement. The A isoform appeared in newly formed structures more rapidly than the B isoform, and was also lost more rapidly when structures disassembled. These observations suggest that the different localizations of myosins IIA and IIB reflect different rates at which the isoforms transit through assembly, movement and disassembly within the cell. The relative proportions of different myosin II isoforms within a particular cell type may determine the lifetimes of various myosin II-based structures in that cell.


1998 ◽  
Vol 111 (12) ◽  
pp. 1649-1658 ◽  
Author(s):  
C. Ballestrem ◽  
B. Wehrle-Haller ◽  
B.A. Imhof

The actin cytoskeleton maintains the cellular architecture and mediates cell movements. To explore actin cytoskeletal dynamics, the enhanced green fluorescent protein (EGFP) was fused to human β-actin. The fusion protein was incorporated into actin fibers which became depolymerized upon cytochalasin B treatment. This functional EGFP-actin construct enabled observation of the actin cytoskeleton in living cells by time lapse fluorescence microscopy. Stable expression of the construct was obtained in mammalian cell lines of different tissue origins. In stationary cells, actin rich, ring-like structured ‘actin clouds’ were observed in addition to stress fibers. These ruffle-like structures were found to be involved in the reorganization of the actin cytoskeleton. In migratory cells, EGFP-actin was found in the advancing lamellipodium. Immobile actin spots developed in the lamellipodium and thin actin fibers formed parallel to the leading edge. Thus EGFP-actin expressed in living cells unveiled structures involved in the dynamics of the actin cytoskeleton.


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