scholarly journals Exaggerated cation leak from oxygenated sickle red blood cells during deformation: evidence for a unique leak pathway

Blood ◽  
1992 ◽  
Vol 80 (9) ◽  
pp. 2374-2378
Author(s):  
T Sugihara ◽  
RP Hebbel
Keyword(s):  
Shear Stress ◽  
Lipid Hydroperoxide ◽  
Viscous Medium ◽  
Permeability Barrier ◽  
Biochemical Basis ◽  
Rbc Membrane ◽  
Gardos Channel ◽  
Ambient Oxygen ◽  
Applied Shear Stress ◽  
Leak Pathway

An abnormal susceptibility of the sickle red blood cell (RBC) membrane to deformation could compromise its permeability barrier function and contribute to the exuberant cation leakiness occurring during the sickling phenomenon. We examined this hypothesis by subjecting RBCs at ambient oxygen tension to elliptical deformation, applying shear stress in a viscous medium under physiologic conditions. Compared with normal and high-reticulocyte control RBCs, sickle RBCs manifest an exaggerated K leak response to deformation. This leak is fully reversible, is both Cl and Ca independent, and at pHe 7.4 is fully balanced so that Kefflux equals Nainflux. This abnormal susceptibility is also evident in that the K leak in response to deformation occurs at an applied shear stress of only 141 dyne/cm2 for sickle RBCs, as compared to 204 dyne/cm2 for normal RBCs. Fresh sickle RBC membranes contain elevated amounts of lipid hydroperoxide, the presence of which is believed to provide the biochemical basis for enhanced deformation susceptibility. When examined at pHe 6.8, oxygenated sickle RBCs acquire an additional, unbalanced (Kefflux > Nainflux) component to the K leak increment specifically ascribable to deformation. Studies with inhibitors suggest that this additional component is not caused by a known leak pathway (eg, either K:Cl cotransport or the Gardos channel). This abnormal susceptibility of the sickle membrane to development of cation leakiness during deformation probably contributes to the exuberant cation leak taking place during RBC sickling.

scholarly journals Exaggerated cation leak from oxygenated sickle red blood cells during deformation: evidence for a unique leak pathway

Blood ◽  
1992 ◽  
Vol 80 (9) ◽  
pp. 2374-2378 ◽  
Author(s):  
T Sugihara ◽  
RP Hebbel
Keyword(s):  
Shear Stress ◽  
Lipid Hydroperoxide ◽  
Viscous Medium ◽  
Permeability Barrier ◽  
Biochemical Basis ◽  
Rbc Membrane ◽  
Gardos Channel ◽  
Ambient Oxygen ◽  
Applied Shear Stress ◽  
Leak Pathway

Abstract An abnormal susceptibility of the sickle red blood cell (RBC) membrane to deformation could compromise its permeability barrier function and contribute to the exuberant cation leakiness occurring during the sickling phenomenon. We examined this hypothesis by subjecting RBCs at ambient oxygen tension to elliptical deformation, applying shear stress in a viscous medium under physiologic conditions. Compared with normal and high-reticulocyte control RBCs, sickle RBCs manifest an exaggerated K leak response to deformation. This leak is fully reversible, is both Cl and Ca independent, and at pHe 7.4 is fully balanced so that Kefflux equals Nainflux. This abnormal susceptibility is also evident in that the K leak in response to deformation occurs at an applied shear stress of only 141 dyne/cm2 for sickle RBCs, as compared to 204 dyne/cm2 for normal RBCs. Fresh sickle RBC membranes contain elevated amounts of lipid hydroperoxide, the presence of which is believed to provide the biochemical basis for enhanced deformation susceptibility. When examined at pHe 6.8, oxygenated sickle RBCs acquire an additional, unbalanced (Kefflux > Nainflux) component to the K leak increment specifically ascribable to deformation. Studies with inhibitors suggest that this additional component is not caused by a known leak pathway (eg, either K:Cl cotransport or the Gardos channel). This abnormal susceptibility of the sickle membrane to development of cation leakiness during deformation probably contributes to the exuberant cation leak taking place during RBC sickling.

scholarly journals Lipid hydroperoxides permit deformation-dependent leak of monovalent cation from erythrocytes

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2757-2763
Author(s):  
T Sugihara ◽  
W Rawicz ◽  
EA Evans ◽  
RP Hebbel
Keyword(s):  
Lipid Hydroperoxide ◽  
Monovalent Cation ◽  
Permeability Barrier ◽  
Lipid Hydroperoxides ◽  
Hydrophobic Membrane ◽  
Cation Homeostasis ◽  
Parallel Control ◽  
Membrane Spanning ◽  
Leak Pathway ◽  
Membrane Defect

Subtle peroxidative perturbation of normal red blood cells (RBC) using t-butylhydroperoxide creates a leak pathway for monovalent cations that is reversibly activated by cell deformation. To determine what factor promotes expression of this unique membrane defect, we have dissected “peroxidation” into components that can be evaluated separately by comparing K leak from suitably modified RBC during elliptical deformation and parallel control incubation. Selective introduction of phospholipid hydroperoxides into normal RBC membranes successfully induces a deformation-dependent leak pathway having the same phenomenology as that previously documented for cells treated with t- butylhydroperoxide itself (fully recoverable; calcium-independent; inhibited at lower pH; K efflux balanced by Na influx). This leak pathway occurs in the absence of detectable secondary peroxidative change and appears to reflect a direct influence of lipid hydroperoxide. Using micropipette examination of vesicular bilayers reconstituted from RBC lipid extracts, we find that lipid from peroxidized RBC exhibits only a slight tendency to be less cohesive than normal lipid, apparently precluding isolated lipid properties as an explanation for altered permeability barrier function. However, addition of a hydrophobic membrane-spanning peptide to these same lipids significantly diminishes bilayer cohesion, an effect that is exacerbated further by the presence of peroxidized lipid. These observations suggest that lipid hydroperoxide is a necessary, but perhaps not sufficient, factor for induction of this unique leak pathway. Our results may be relevant to the abnormal cation homeostasis of sickle RBC in which deformation of an oxidatively perturbed membrane occurs during the sickling phenomenon.

scholarly journals Lipid hydroperoxides permit deformation-dependent leak of monovalent cation from erythrocytes

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2757-2763 ◽  
Author(s):  
T Sugihara ◽  
W Rawicz ◽  
EA Evans ◽  
RP Hebbel
Keyword(s):  
Lipid Hydroperoxide ◽  
Monovalent Cation ◽  
Permeability Barrier ◽  
Lipid Hydroperoxides ◽  
Hydrophobic Membrane ◽  
Cation Homeostasis ◽  
Parallel Control ◽  
Membrane Spanning ◽  
Leak Pathway ◽  
Membrane Defect

Abstract Subtle peroxidative perturbation of normal red blood cells (RBC) using t-butylhydroperoxide creates a leak pathway for monovalent cations that is reversibly activated by cell deformation. To determine what factor promotes expression of this unique membrane defect, we have dissected “peroxidation” into components that can be evaluated separately by comparing K leak from suitably modified RBC during elliptical deformation and parallel control incubation. Selective introduction of phospholipid hydroperoxides into normal RBC membranes successfully induces a deformation-dependent leak pathway having the same phenomenology as that previously documented for cells treated with t- butylhydroperoxide itself (fully recoverable; calcium-independent; inhibited at lower pH; K efflux balanced by Na influx). This leak pathway occurs in the absence of detectable secondary peroxidative change and appears to reflect a direct influence of lipid hydroperoxide. Using micropipette examination of vesicular bilayers reconstituted from RBC lipid extracts, we find that lipid from peroxidized RBC exhibits only a slight tendency to be less cohesive than normal lipid, apparently precluding isolated lipid properties as an explanation for altered permeability barrier function. However, addition of a hydrophobic membrane-spanning peptide to these same lipids significantly diminishes bilayer cohesion, an effect that is exacerbated further by the presence of peroxidized lipid. These observations suggest that lipid hydroperoxide is a necessary, but perhaps not sufficient, factor for induction of this unique leak pathway. Our results may be relevant to the abnormal cation homeostasis of sickle RBC in which deformation of an oxidatively perturbed membrane occurs during the sickling phenomenon.

scholarly journals Synergistic effects of oxidation and deformation on erythrocyte monovalent cation leak

Blood ◽  
1990 ◽  
Vol 75 (5) ◽  
pp. 1192-1198 ◽  
Author(s):  
PA Ney ◽  
MM Christopher ◽  
RP Hebbel
Keyword(s):  
Shear Stress ◽  
Synergistic Effects ◽  
Monovalent Cation ◽  
Microvascular Blood Flow ◽  
Permeability Barrier ◽  
Shear Stresses ◽  
Calcium Dependent ◽  
Rbc Membrane ◽  
Dose Dependent Fashion ◽  
Dose Dependent

The normal red blood cell (RBC) membrane is remarkable for its durability (eg, preservation of permeability barrier function) despite its need to remain deformable for the benefit of microvascular blood flow. Yet, it may be hypothesized that the membrane's tolerance of deformation might be compromised under certain pathologic conditions. We studied this by subjecting normal RBC in viscous suspending medium (20% dextran) to elliptical deformation induced by application of shear stress under physiologic conditions (290 mOsm/L, 37 degrees C, pH 7.40) in the presence of ouabain and furosemide. Measurement of resulting net passive K efflux (“K leak”) demonstrated that shear-induced RBC deformation causes K leak in a dose-dependent fashion at shear stresses far below the hemolytic threshold, an effect shown to be due to deformation per se. To model the specific hypothesis that oxidatively perturbed RBC membranes would be abnormally susceptible to this potentially adverse effect of deformation, we treated normal RBC with the lipid peroxidant t-butylhydroperoxide. Under conditions inducing only minimal K leak due to either oxidation alone or deformation alone, deformation of peroxidant-pretreated RBC showed a markedly enhanced K leak (P less than .001). This highly synergistic oxidation-plus- deformation leak pathway is less active at low pH, is neither chloride- dependent nor calcium-dependent, and allows K efflux to be balanced by Na influx so there is no change in total monovalent cation content or cell density. Moreover, it is fully reversible since deformation- induced K leak terminates on cessation of shear stress (even for oxidant-treated RBC). Control experiments showed that our results are not explained simply by hemolysis, RBC vesiculation, or development of prelytic pores. We conclude that oxidation and deformation individually promote passive leak of monovalent cation through RBC membranes and that a markedly synergistic effect is exerted when the two stresses are combined. We hypothesize that these findings may help explain the abnormal monovalent cation leak stimulated by deoxygenation of sickle RBC.

scholarly journals Synergistic effects of oxidation and deformation on erythrocyte monovalent cation leak

Blood ◽  
1990 ◽  
Vol 75 (5) ◽  
pp. 1192-1198 ◽  
Author(s):  
PA Ney ◽  
MM Christopher ◽  
RP Hebbel
Keyword(s):  
Shear Stress ◽  
Synergistic Effects ◽  
Monovalent Cation ◽  
Microvascular Blood Flow ◽  
Permeability Barrier ◽  
Shear Stresses ◽  
Calcium Dependent ◽  
Rbc Membrane ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Abstract The normal red blood cell (RBC) membrane is remarkable for its durability (eg, preservation of permeability barrier function) despite its need to remain deformable for the benefit of microvascular blood flow. Yet, it may be hypothesized that the membrane's tolerance of deformation might be compromised under certain pathologic conditions. We studied this by subjecting normal RBC in viscous suspending medium (20% dextran) to elliptical deformation induced by application of shear stress under physiologic conditions (290 mOsm/L, 37 degrees C, pH 7.40) in the presence of ouabain and furosemide. Measurement of resulting net passive K efflux (“K leak”) demonstrated that shear-induced RBC deformation causes K leak in a dose-dependent fashion at shear stresses far below the hemolytic threshold, an effect shown to be due to deformation per se. To model the specific hypothesis that oxidatively perturbed RBC membranes would be abnormally susceptible to this potentially adverse effect of deformation, we treated normal RBC with the lipid peroxidant t-butylhydroperoxide. Under conditions inducing only minimal K leak due to either oxidation alone or deformation alone, deformation of peroxidant-pretreated RBC showed a markedly enhanced K leak (P less than .001). This highly synergistic oxidation-plus- deformation leak pathway is less active at low pH, is neither chloride- dependent nor calcium-dependent, and allows K efflux to be balanced by Na influx so there is no change in total monovalent cation content or cell density. Moreover, it is fully reversible since deformation- induced K leak terminates on cessation of shear stress (even for oxidant-treated RBC). Control experiments showed that our results are not explained simply by hemolysis, RBC vesiculation, or development of prelytic pores. We conclude that oxidation and deformation individually promote passive leak of monovalent cation through RBC membranes and that a markedly synergistic effect is exerted when the two stresses are combined. We hypothesize that these findings may help explain the abnormal monovalent cation leak stimulated by deoxygenation of sickle RBC.

Interaction Between Lattice Dislocations and Grain Boundaries In Ordered Compounds

1990 ◽  
Vol 213 ◽  
Author(s):  
B.J. Pestman ◽  
J. Th. M. De Hosson ◽  
V. Vitek ◽  
F.W. Schapink
Keyword(s):  
Shear Stress ◽  
Grain Boundary ◽  
Grain Boundaries ◽  
Partial Dislocation ◽  
Atomistic Simulations ◽  
Many Body ◽  
Shockley Partial Dislocation ◽  
Screw Dislocations ◽  
Applied Shear Stress ◽  
Tilt Boundaries

ABSTRACTThe interaction of 1/2<1 1 0> screw dislocations with symmetric [1 1 0] tilt boundaries was investigated by atomistic simulations using many-body potentials representing ordered compounds. The calculations were performed with and without an applied shear stress. The observations were: absorption into the grain boundary, attraction of a lattice Shockley partial dislocation towards the grain boundary and transmission through the grain boundary under the influence of a shear stress. It was found that the interaction in ordered compounds shows similarities to the interaction in fcc.

MAGNETOPHORETIC CIRCUIT BIOCOMPATIBILITY

2020 ◽  
Vol 20 (07) ◽  
pp. 2050050
Author(s):  
ROOZBEH ABEDINI-NASSAB
Keyword(s):  
Shear Stress ◽  
Single Cell ◽  
Single Cell Analysis ◽  
Cell Behavior ◽  
Cell Analysis ◽  
Applied Shear Stress ◽  
Cell Handling ◽  
Magnetic Labeling ◽  
Long Term Studies

Recently, we introduced magnetophoretic circuits, composed of overlaid magnetic and metallic layers, as a novel single-cell analysis (SCA) tool. We showed the ability of these circuits in organizing large single-particle and particle-pair arrays. Assembling the cells in microarrays is performed with the ultimate goal of running temporal phenotypic analyses. However, for long-term studies, a suitable microenvironment for the cells to normally grow and differentiate is needed. Towards this goal, in this study, we run required biocompatibility tests, based on which we make the magnetophoretic-based microchip a suitable home for the cells to grow. The results confirm the ability of these chips in cell handling and show no unwanted cell behavior alteration due to the applied shear stress on them, the magnetic labeling, or the microenvironment. After this achievement, this tool would be ready for running important single-cell studies in oncology, virology, and medicine.

First-Principles Study of Structural and Defect Properties in FeCo Intermetallics

2004 ◽  
Vol 842 ◽  
Author(s):  
M. Krcmar ◽  
C. L. Fu ◽  
J. R. Morris
Keyword(s):  
Shear Stress ◽  
Ab Initio ◽  
Structural Stability ◽  
First Principles ◽  
Statistical Thermodynamic ◽  
Internal Stresses ◽  
Applied Shear Stress ◽  
Defect Energies ◽  
Antisite Defects ◽  
B2 Structure

ABSTRACTEmploying ab-initio calculations and statistical thermodynamic modeling, we investigated the structural stability, defect energies, and ordering of B2 FeCo intermetallics. We find that FeCo in the B2 structure is a marginally stable and weakly ordered system, with a high density of antisite defects on both sublattices and low APB energies for the <111> slip on both {110} and {112} planes. The structural stability of B2 FeCo is very sensitive to the change in local atomic environment, as the system transforms to a lower-symmetry L10 phase under the effects of reduced dimensionality or applied shear stress. We suggest that internal stresses near dislocation cores might be closely connected with the intrinsic brittleness of ordered FeCo, as it is likely to induce a local structural transformation from the B2 structure to the L10 structure.

Dislocation—like Defects in an Amorphous Lennard—jones Solid

1986 ◽  
Vol 82 ◽  
Author(s):  
L. T. Shi ◽  
P. Chaudhari
Keyword(s):  
Computer Simulation ◽  
Shear Stress ◽  
Screw Dislocations ◽  
Lennard Jones ◽  
Simulation Techniques ◽  
Applied Shear Stress ◽  
Computer Simulation Techniques

ABSTRACTIt has been found, using computer simulation techniques, that both edge and screw dislocations can be stably introduced into an amorphous Lennard-Jones solid, and can be moved through the model under an applied shear stress.

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