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Michael A Matthay - One of the best experts on this subject based on the ideXlab platform.
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measurement of protein permeability and Fluid Transport of human alveolar epithelial type ii cells under pathological conditions
Methods of Molecular Biology, 2018Co-Authors: Xiaohui Fang, Michael A MatthayAbstract:Alveolar epithelial barrier dysfunction contributes to the influx of protein-rich edema Fluid and the accumulation of inflammatory cells in the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). To study the alveolar epithelial barrier function under pathological conditions, we developed an in vitro model of acute lung injury using cultured human alveolar epithelial type II (ATII) cells. Here we describe the methods that we use to measure protein permeability and Fluid Transport across human ATII cell monolayers under stimulated conditions. Both proinflammatory cytokines and edema Fluid from ALI/ARDS patients can increase protein permeability and decrease Fluid Transport across the human ATII cells monolayer.
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acute lung injury edema Fluid decreases net Fluid Transport across human alveolar epithelial type ii cells
Journal of Biological Chemistry, 2007Co-Authors: Jae W Lee, Xiaohui Fang, Gregory Dolganov, Richard D Fremont, Julie A Bastarache, Lorraine B Ware, Michael A MatthayAbstract:Most patients with acute lung injury (ALI) have reduced alveolar Fluid clearance that has been associated with higher mortality. Several mechanisms may contribute to the decrease in alveolar Fluid clearance. In this study, we tested the hypothesis that pulmonary edema Fluid from patients with ALI might reduce the expression of ion Transport genes responsible for vectorial Fluid Transport in primary cultures of human alveolar epithelial type II cells. Following exposure to ALI pulmonary edema Fluid, the gene copy number for the major sodium and chloride Transport genes decreased. By Western blot analyses, protein levels of alphaENaC, alpha1Na,K-ATPase, and cystic fibrosis transmembrane conductance regulator decreased as well. In contrast, the gene copy number for several inflammatory cytokines increased markedly. Functional studies demonstrated that net vectorial Fluid Transport was reduced for human alveolar type II cells exposed to ALI pulmonary edema Fluid compared with plasma (0.02 +/- 0.05 versus 1.31 +/- 0.56 microl/cm2/h, p < 0.02). An inhibitor of p38 MAPK phosphorylation (SB202190) partially reversed the effects of the edema Fluid on net Fluid Transport as well as gene and protein expression of the main ion Transporters. In summary, alveolar edema Fluid from patients with ALI induced a significant reduction in sodium and chloride Transport genes and proteins in human alveolar epithelial type II cells, effects that were associated with a decrease in net vectorial Fluid Transport across human alveolar type II cell monolayers.
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acute lung injury edema Fluid decreases net Fluid Transport across human alveolar epithelial type ii cells
Journal of Biological Chemistry, 2007Co-Authors: Jae W Lee, Xiaohui Fang, Gregory Dolganov, Richard D Fremont, Julie A Bastarache, Lorraine B Ware, Michael A MatthayAbstract:Most patients with acute lung injury (ALI) have reduced alveolar Fluid clearance that has been associated with higher mortality. Several mechanisms may contribute to the decrease in alveolar Fluid clearance. In this study, we tested the hypothesis that pulmonary edema Fluid from patients with ALI might reduce the expression of ion Transport genes responsible for vectorial Fluid Transport in primary cultures of human alveolar epithelial type II cells. Following exposure to ALI pulmonary edema Fluid, the gene copy number for the major sodium and chloride Transport genes decreased. By Western blot analyses, protein levels of αENaC, α1Na,K-ATPase, and cystic fibrosis transmembrane conductance regulator decreased as well. In contrast, the gene copy number for several inflammatory cytokines increased markedly. Functional studies demonstrated that net vectorial Fluid Transport was reduced for human alveolar type II cells exposed to ALI pulmonary edema Fluid compared with plasma (0.02 ± 0.05 versus 1.31 ± 0.56 μl/cm2/h, p
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alveolar epithelial ion and Fluid Transport recent progress
American Journal of Respiratory Cell and Molecular Biology, 2006Co-Authors: Hans G Folkesson, Michael A MatthayAbstract:Studies of epithelial ion and Fluid Transport across the distal pulmonary epithelia have provided important new concepts regarding the resolution of pulmonary edema, specifically the removal of edema from the distal airspaces of the lung. Overall, there is convincing evidence that vectorial ion Transport across the alveolar and distal airway epithelia is the primary determinant of alveolar Fluid clearance (AFC). The general paradigm is that active Na and Cl Transport drives net alveolar Fluid clearance, as demonstrated in several different species, including the human lung. The objective of this article is to consider some areas of recent progress in the field of alveolar Fluid Transport under normal and pathologic conditions. More detailed reviews of this field including studies of the immature and the newborn lung are available (1–10). In the lung, as in other epithelia, ion Transporters and other membrane proteins are asymmetrically distributed on opposing cell surfaces, conferring vectorial Transport properties to the polarized epithelial cells (Figure 1). There are epithelial cells in the distal airway epithelia, such as Clara cells, that are capable of vectorial ion Transport. The vast majority of the surface area available for Transport in the distal lung is occupied by the alveolar epithelial type I (ATI) and type II cells (ATII). Tight junctions populate these epithelial cells near their apical surfaces, thereby sustaining apical and basolateral cell polarity (11). The permeability of tight junctions is dynamic and regulated, in part, by cytoskeletal proteins and intracellular Ca concentrations and possibly by ion channels (11). Figure 1. A section of an ARDS lung. Note the Fluid-filled alveolar spaces with significant red blood cell infiltration. Insert demonstrates apical ENaC staining and basolateral Na,K-ATPase staining in lung epithelia. (Reprinted with permission from Ref. 3) Because ATII cells can be isolated from the lung and studied in vitro, they have been studied extensively. ATII cells are responsible for surfactant secretion (12) as well as vectorial Na and Cl Transport. Na uptake occurs on the apical surface, partly through amiloride-sensitive and amiloride-insensitive channels. Subsequently, Na is pumped actively from the basolateral surface into the lung interstitium by the Na,K-ATPase. An epithelial Na channel (ENaC) participating in Na movement across the apical cell membrane has been cloned and well characterized (13, 14). Recent evidence indicates that the CFTR is expressed in ATII cells and plays a role in cAMP-mediated Fluid Transport (15–18). The role of ATI cells for AFC is less known, although several studies have established a possible contribution of ATI cells to vectorial Fluid Transport (19–22). ATI cells express aquaporin 5 (23), Na,K-ATPase (21), and ENaC (21, 22). The presence of Na,K-ATPase is consistent with a role for ATI cells in AFC, but is not conclusive since Na,K-ATPases are needed to maintain cell volume. However, one study using pharmacologic methods to inhibit the α2-subunit of the Na,K-ATPase suggested a role for Na,K-ATPase in driving Fluid clearance across type I cells in vivo (24). Another study reported a role for the α2-Na,K-ATPase under cAMP-stimulated conditions, suggesting that type I cells may be involved, as the α2-subunit seems to be expressed only in type I cells (25). Detailed studies of type I cells have been limited to date because of difficulty maintaining them in cell culture although recent work has demonstrated functional ion channels in freshly isolated ATI cells with electrophysiologic evidence for Na channels (ENaC), K channels, and CFTR Cl channels (26). In addition, there is evidence for ENaC expression (21, 22) and a partial amiloride inhibition of 22Na-uptake in freshly isolated rat ATI cells (22). Evidence for β-adrenoceptor (βAR) expression in ATI cells has also been reported (20, 27). In addition, ATI cells may be involved in macromolecular Transport due to the presence of vesicles and caveolin (28). The distal airway epithelium also actively Transports Na (29–31).
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contribution of cftr to apical basolateral Fluid Transport in cultured human alveolar epithelial type ii cells
American Journal of Physiology-lung Cellular and Molecular Physiology, 2006Co-Authors: Xiaohui Fang, Yuanlin Song, A S Verkman, Gregory Dolganov, Jan Hirsch, Luis J V Galietta, Nicoletta Pedemonte, Rachel L Zemans, Michael A MatthayAbstract:Previous studies in intact lung suggest that CFTR may play a role in cAMP-regulated Fluid Transport from the distal air spaces of the lung. However, the potential contribution of different epitheli...
Jorge Fischbarg - One of the best experts on this subject based on the ideXlab platform.
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net fluorescein flux across corneal endothelium strongly suggests Fluid Transport is due to electro osmosis
The Journal of Membrane Biology, 2016Co-Authors: J M Sanchez, P Iserovich, A A Rubashkin, Veronica Ines Cacace, Carlos Kusnier, R Nelson, Jorge FischbargAbstract:We have presented prior evidence suggesting that Fluid Transport results from electro-osmosis at the intercellular junctions of the corneal endothelium. Such phenomenon ought to drag other extracellular solutes. We have investigated this using fluorescein-Na2 as an extracellular marker. We measured unidirectional fluxes across layers of cultured human corneal endothelial (HCE) cells. SV-40-transformed HCE layers were grown to confluence on permeable membrane inserts. The medium was DMEM with high glucose and no phenol red. Fluorescein-labeled medium was placed either on the basolateral or the apical side of the inserts; the other side carried unlabeled medium. The inserts were held in a CO2 incubator for 1 h (at 37 °C), after which the entire volume of the unlabeled side was collected. After that, label was placed on the opposite side, and the corresponding paired sample was collected after another hour. Fluorescein counts were determined with a (Photon Technology) DeltaScan fluorometer (excitation 380 nm; emission 550 nm; 2 nm bwth). Samples were read for 60 s. The cells utilized are known to Transport Fluid from the basolateral to the apical side, just as they do in vivo in several species. We used 4 inserts for influx and efflux (total: 20 1-h periods). We found a net flux of fluorescein from the basolateral to the apical side. The flux ratio was 1.104 ± 0.056. That difference was statistically significant (p = 0.00006, t test, paired samples). The endothelium has a definite restriction at the junctions. Hence, an asymmetry in unidirectional fluxes cannot arise from osmosis, and can only point instead to paracellular solvent drag. We suggest, once more, that such drag is due to electro-osmotic coupling at the paracellular junctions.
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Fluid Transport across leaky epithelia central role of the tight junction and supporting role of aquaporins
Physical Review, 2010Co-Authors: Jorge FischbargAbstract:The mechanism of epithelial Fluid Transport remains unsolved, which is partly due to inherent experimental difficulties. However, a preparation with which our laboratory works, the corneal endothel...
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the role of the tight junction in paracellular Fluid Transport across corneal endothelium electro osmosis as a driving force
The Journal of Membrane Biology, 2006Co-Authors: Jorge Fischbarg, P Iserovich, Friedrich P J Diecke, A A RubashkinAbstract:The mechanism of epithelial Fluid Transport is controversial and remains unsolved. Experimental difficulties pose obstacles for work on a complex phenomenon in delicate tissues. However, the corneal endothelium is a relatively simple system to which powerful experimental tools can be applied. In recent years our laboratory has developed experimental evidence and theoretical insights that illuminate the mechanism of Fluid Transport across this leaky epithelium. Our evidence points to Fluid being Transported via the paracellular route by a mechanism requiring junctional integrity, which we attribute to electro-osmotic coupling at the junctions. Fluid movements can be produced by electrical currents. The direction of the movement can be reversed by current reversal or by changing junctional electrical charges by polylysine. Aquaporin 1 (AQP1) is the only AQP present in these cells, and its deletion in AQP1 null mice significantly affects cell osmotic permeability but not Fluid Transport, which militates against the presence of sizable water movements across the cell. By contrast, AQP1 null mice cells have reduced regulatory volume decrease (only 60% of control), which suggests a possible involvement of AQP1 in either the function or the expression of volume-sensitive membrane channels/Transporters. A mathematical model of corneal endothelium predicts experimental results only when based on paracellular electro-osmosis, and not when transcellular local osmosis is assumed instead.
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epidermal growth factor stimulates Fluid Transport in sv40 transformed rabbit lacrimal gland cells
Advances in Experimental Medicine and Biology, 2002Co-Authors: P Iserovich, Maimaiti Yiming, Z Wang, V N Bildin, Peter S Reinach, Jorge FischbargAbstract:Lacrimal gland Fluid secretion is essential for maintaining the aqueous volume of the precorneal tear film and ocular surface health. A decline in lacrimal gland Fluid output can be a contributing factor to dry eye disease. Lacrimal gland functional activity is dependent on a host of neurohumors and cytokines that control its cells growth, differentiation and protein secretory activity. The release of one of these cytokines, epidermal growth factor (EGF), is regulated through neural control in the lacrimal gland.1–3 Furthermore, rat lacrimal acinar cells possess EGF receptors,4 suggesting that these cells respond to EGF. However, there have been no direct studies on the role of EGF in lacrimal gland Fluid Transport regulation.
A S Verkman - One of the best experts on this subject based on the ideXlab platform.
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Aquaporin water channels in transepithelial Fluid Transport
Faculty of Medicine Tokushima University, 2018Co-Authors: Tradtrantip Lukmanee, Tajima Masato, Li Lihua, A S VerkmanAbstract:Aquaporins (AQPs) are membrane water channels that are involved in a diverse set of functions in mammalian physiology including epithelial Fluid Transport, brain water balance, cell migration, cell proliferation, neuroexcitation, fat metabolism, epidermal hydration, and others. Phenotype analysis of knockout mice has demonstrated an important role for AQPs in transepithelial Fluid Transport in kidney tubules, salivary and airway submucosal glands, choroid plexus and ciliary epithelium. The physiological functions of these epithelia, such as absorption of glomerular filtrate by proximal tubule and secretion of saliva by salivary gland, involve rapid transcellular water Transport across epithelial cell barriers. Studies in knockout mice have also provided evidence that AQPs are not physiologically important in some epithelia where they are expressed, including lacrimal gland, sweat gland, gallbladder, alveoli and airways. Rates of transepithelial Fluid Transport per unit membrane surface area in these epithelia are substantially lower than transepithelial Fluid Transport rates in proximal tubule and salivary gland. Pharmacological inhibition of AQP water permeability in epithelia, with consequent reduced Fluid Transport, offers potential therapy for human diseases involving water imbalance such as congestive heart failure, hypertension and glaucoma
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contribution of cftr to apical basolateral Fluid Transport in cultured human alveolar epithelial type ii cells
American Journal of Physiology-lung Cellular and Molecular Physiology, 2006Co-Authors: Xiaohui Fang, Yuanlin Song, A S Verkman, Gregory Dolganov, Jan Hirsch, Luis J V Galietta, Nicoletta Pedemonte, Rachel L Zemans, Michael A MatthayAbstract:Previous studies in intact lung suggest that CFTR may play a role in cAMP-regulated Fluid Transport from the distal air spaces of the lung. However, the potential contribution of different epitheli...
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lung edema clearance 20 years of progress invited review role of aquaporin water channels in Fluid Transport in lung and airways
Journal of Applied Physiology, 2002Co-Authors: Zea Borok, A S VerkmanAbstract:Water Transport across epithelial and endothelial barriers in bronchopulmonary tissues occurs during airway hydration, alveolar Fluid Transport, and submucosal gland secretion. Many of the tissues ...
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aquaporin water channels and endothelial cell function
Journal of Anatomy, 2002Co-Authors: A S VerkmanAbstract:The aquaporins (AQP) are a family of homologous water channels expressed in many epithelial and endothelial cell types involved in Fluid Transport. AQP1 protein is strongly expressed in most microvascular endothelia outside of the brain, as well as in endothelial cells in cornea, intestinal lacteals, and other tissues. AQP4 is expressed in astroglial foot processes adjacent to endothelial cells in the central nervous system. Transgenic mice lacking aquaporins have been useful in defining their role in mammalian physiology. Mice lacking AQP1 manifest defective urinary concentrating ability, in part because of decreased water permeability in renal vasa recta microvessels. These mice also show a defect in dietary fat processing that may involve chylomicron absorption by intestinal lacteals, as well as defective active Fluid Transport across the corneal endothelium. AQP1 might also play a role in tumour angiogenesis and in renal microvessel structural adaptation. However, AQP1 in most endothelial tissues does not appear to have a physiological function despite its role in osmotically driven water Transport. For example, mice lacking AQP1 have low alveolar-capillary water permeability but unimpaired lung Fluid absorption, as well as unimpaired saliva and tear secretion, aqueous Fluid outflow, and pleural and peritoneal Fluid Transport. In the central nervous system mice lacking AQP4 are partially protected from brain oedema in water intoxication and ischaemic models of brain injury. Therefore, although the role of aquaporins in epithelial Fluid Transport is in most cases well-understood, there remain many questions about the role of aquaporins in endothelial cell function. It is unclear why many leaky microvessels strongly express AQP1 without apparent functional significance. Improved understanding of aquaporin-endothelial biology may lead to novel therapies for human disease, such as pharmacological modulation of corneal Fluid Transport, renal Fluid clearance and intestinal absorption.
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lung Fluid Transport in aquaporin 5 knockout mice
Journal of Clinical Investigation, 2000Co-Authors: Norimasa Fukuda, Michael A Matthay, Yuanlin Song, A S Verkman, A S VerkmanAbstract:The mammalian lung expresses water channel aquaporin-1 (AQP1) in microvascular endothelia, AQP4 in airway epithelia, and AQP5 at the apical plasma membrane in type I cells of alveolar epithelia. We previously studied the role of AQP1 and AQP4 in lung Fluid Transport using knockout mice. Here, we examined the role of AQP5 using AQP5 knockout mice, which were recently shown to manifest defective saliva secretion. AQP5 deletion did not affect lung morphology at the light microscopic level, nor did it affect the distribution or expression of aquaporins 1, 3, or 4. Airspace-capillary osmotic water permeability (Pf) was measured in isolated perfused lungs by pleural surface fluorescence and gravimetric methods. Pf was reduced 10-fold by AQP5 deletion and was further reduced by 2- to 3-fold in AQP1/AQP5 double-knockout mice. Hydrostatic lung edema in response to acute increases in pulmonary artery pressure was not affected by AQP5 deletion. Active alveolar Fluid absorption was measured in an in situ lung model from the increase in concentration of a volume marker in an isosmolar alveolar instillate. Interestingly, Fluid absorption did not differ in litter-matched AQP5 knockout mice, nor was there an effect of AQP5 deletion when Fluid absorption was maximally stimulated by pretreatment of mice with keratinocyte growth factor. These results indicate that AQP5 is responsible for the majority of water Transport across the apical membrane of type I alveolar epithelial cells. The unimpaired alveolar Fluid clearance in AQP5-null mice indicates that high alveolar water permeability is not required for active, near-isosmolar Fluid Transport.
Jeremie Roux - One of the best experts on this subject based on the ideXlab platform.
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transforming growth factor β1 inhibits cystic fibrosis transmembrane conductance regulator dependent camp stimulated alveolar epithelial Fluid Transport via a phosphatidylinositol 3 kinase dependent mechanism
Journal of Biological Chemistry, 2010Co-Authors: Jeremie Roux, Michel Carles, Hidefumi Koh, Arnaud Goolaerts, Michael T Ganter, Brian B Chesebro, Marybeth Howard, Benjamin T Houseman, Walter E Finkbeiner, Kevan M ShokatAbstract:Exogenous or endogenous β2-adrenergic receptor agonists enhance alveolar epithelial Fluid Transport via a cAMP-dependent mechanism that protects the lungs from alveolar flooding in acute lung injury. However, impaired alveolar Fluid clearance is present in most of the patients with acute lung injury and is associated with increased mortality, although the mechanisms responsible for this inhibition of the alveolar epithelial Fluid Transport are not completely understood. Here, we found that transforming growth factor β1 (TGF-β1), a critical mediator of acute lung injury, inhibits β2-adrenergic receptor agonist-stimulated vectorial Fluid and Cl− Transport across primary rat and human alveolar epithelial type II cell monolayers. This inhibition is due to a reduction in the cystic fibrosis transmembrane conductance regulator activity and biosynthesis mediated by a phosphatidylinositol 3-kinase (PI3K)-dependent heterologous desensitization and down-regulation of the β2-adrenergic receptors. Consistent with these in vitro results, inhibition of the PI3K pathway or pretreatment with soluble chimeric TGF-β type II receptor restored β2-adrenergic receptor agonist-stimulated alveolar epithelial Fluid Transport in an in vivo model of acute lung injury induced by hemorrhagic shock in rats. The results demonstrate a novel role for TGF-β1 in impairing the β- adrenergic agonist-stimulated alveolar Fluid clearance in acute lung injury, an effect that could be corrected by using PI3K inhibitors that are safe to use in humans.
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ho 1 induction restores c amp dependent lung epithelial Fluid Transport following severe hemorrhage in rats
The FASEB Journal, 2005Co-Authors: Hyon Lee, Michael A Matthay, Jeremie Roux, Melissa H Pespeni, Phyllis A Dennery, Jeanfrancois PittetAbstract:Inhibition of cAMP-dependent stimulation of the vectorial Fluid Transport across the lung epithelium following hemorrhagic shock is mediated by NO released within the airspaces of the lung. We tested here the hypothesis that prior induction of HO-1 would attenuate the release of NO in the airspaces, thus preventing the inhibition of the c-AMP stimulation of alveolar Fluid clearance (ALC) in rats. Indeed, HO-1 induction restored the cAMP-mediated up-regulation of ALC after hemorrhage by decreasing NO released within the airspaces of the lung. In vitro studies demonstrated that HO-1 induction significantly reduced the iNOS-mediated release of NO by alveolar macrophages stimulated with endotoxin for 24 h. This effect is explained in part by a HO-1-dependent attenuation of the LPS-mediated nuclear translocation of NF-kappaB. In addition, HO-1 induction also significantly reduced the iNOS-mediated release of NO by MH-S cells that were stimulated with interferon-gamma by decreasing the phosphorylation of STAT 1, another transcription factor important for the activation of the iNOS promoter. In contrast, HO-1 induction did not affect the production of NO by rat alveolar epithelial type II cells that were stimulated with cytomix (a mixture of TNF-alpha, IL-1beta, and IFN-gamma) for 24 h. In summary, these results provide the first in vivo evidence that the induction of HO-1 in the lung restores a normal Fluid Transport capacity of the alveolar epithelium following hemorrhagic shock by inhibiting the iNOS-mediated release of NO by alveolar macrophages.
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transforming growth factor β1 decreases expression of the epithelial sodium channel αenac and alveolar epithelial vectorial sodium and Fluid Transport via an erk1 2 dependent mechanism
Journal of Biological Chemistry, 2003Co-Authors: James A Frank, Xiaohui Fang, Jeremie Roux, Marybeth Howard, Hisaaki Kawakatsu, George Su, Andre Dagenais, Yves Berthiaume, Cecilia M Canessa, Dean SheppardAbstract:Abstract Acute lung injury (ALI) is characterized by the flooding of the alveolar airspaces with protein-rich edema Fluid and diffuse alveolar damage. We have previously reported that transforming growth factor-β1 (TGF-β1) is a critical mediator of ALI after intratracheal administration of bleomycin or Escherichia coli endotoxin, at least in part due to effects on lung endothelial and alveolar epithelial permeability. In the present study, we hypothesized that TGF-β1 would also decrease vectorial ion and water Transport across the distal lung epithelium. Therefore, we studied the effect of active TGF-β1 on 22Na+ uptake across monolayers of primary rat and human alveolar type II (ATII) cells. TGF-β1 significantly reduced the amiloride-sensitive fraction of 22Na+ uptake and Fluid Transport across monolayers of both rat and human ATII cells. TGF-β1 also significantly decreased αENaC mRNA and protein expression and inhibited expression of a luciferase reporter downstream of the αENaC promoter in lung epithelial cells. The inhibitory effect of TGF-β1 on sodium uptake and αENaC expression in ATII cells was mediated by activation of the MAPK, ERK1/2. Consistent with the in vitro results, TGF-β1 inhibited the amiloride-sensitive fraction of the distal airway epithelial Fluid Transport in an in vivo rat model at a dose that was not associated with any change in epithelial protein permeability. These data indicate that increased TGF-β1 activity in the distal airspaces during ALI promotes alveolar edema by reducing distal airway epithelial sodium and Fluid clearance. This reduction in sodium and Fluid Transport is attributable in large part to a reduction in apical membrane αENaC expression mediated through an ERK1/2-dependent inhibition of the αENaC promoter activity.
John O Dabiri - One of the best experts on this subject based on the ideXlab platform.
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effect of swarm configuration on Fluid Transport during vertical collective motion
Bioinspiration & Biomimetics, 2019Co-Authors: M M Wilhelmus, Janna Nawroth, Bhargav Rallabandi, John O DabiriAbstract:: Understanding the hydrodynamics of self-propelled organisms is critical to evaluate the role of migrating zooplankton aggregations in sustaining marine ecosystems via the Transport of nutrients and mixing of Fluid properties. Analysis of Transport and mixing during swimming is thus essential to assess whether biomixing is a relevant source of kinetic energy in the upper ocean. In this study, dilute swarms of the ephyral Aurelia aurita were simulated under different configurations to analyze the effects of inter-organism spacing and structure of a migrating aggregation on Fluid Transport. By using velocimetry data instead of numerically simulated velocity fields, our study integrates the effects of the near- and far-field flows. Lagrangian analysis of simulated Fluid particles, both in homogeneous and stratified Fluid, shows that the near-field flow ultimately dictates Fluid dispersion. The discrepancy between our results and predictions made using low-order models (both in idealized Fluid and within the Stokes limit) highlights the need to correctly represent the near-field flow resulting from swimming kinematics and organism morphology. Derived vertical stirring coefficients for all cases suggest that even in the limit of dilute aggregations, self-propelled organisms can play an important role in Transporting Fluid against density gradients.
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lagrangian analysis of Fluid Transport in empirical vortex ring flows
Physics of Fluids, 2006Co-Authors: Shawn C Shadden, John O Dabiri, Jerrold E MarsdenAbstract:In this paper we apply dynamical systems analyses and computational tools to Fluid Transport in empirically measured vortex ring flows. Measurements of quasisteadily propagating vortex rings generated by a mechanical piston-cylinder apparatus reveal lobe dynamics during entrainment and detrainment that are consistent with previous theoretical and numerical studies. In addition, the vortex ring wake of a free-swimming Aurelia aurita jellyfish is measured and analyzed in the framework of dynamical systems to elucidate similar lobe dynamics in a naturally occurring biological flow. For the mechanically generated rings, a comparison of the net entrainment rate based on the present methods with a previous Eulerian analysis shows good correspondence. However, the current Lagrangian framework is more effective than previous analyses in capturing the Transport geometry, especially when the flow becomes more unsteady, as in the case of the free-swimming jellyfish. Extensions of these results to more complex flow geometries is suggested.
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the role of optimal vortex formation in biological Fluid Transport
Proceedings of The Royal Society B: Biological Sciences, 2005Co-Authors: John O Dabiri, Morteza GharibAbstract:Animal phyla that require macro-scale Fluid Transport for functioning have repeatedly and often independently converged on the use of jet flows. During flow initiation these jets form Fluid vortex rings, which facilitate mass transfer by stationary pumps (e.g. cardiac chambers) and momentum transfer by mobile systems (e.g. jet-propelled swimmers). Previous research has shown that vortex rings generated in the laboratory can be optimized for efficiency or thrust, based on the jet length-to-diameter ratio (L/D), with peak performance occurring at 3.5
vortex ring formation. This new approach identifies simple rules for effective Fluid Transport, facilitates comparative biological studies of jet flows across animal phyla irrespective of their specific functions and can be extended to unify theories of optimal jet-based and flapping-based vortex ring formation.