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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 346 (1990), S. 277-279 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] A quantitative infectivity assay requires the number of infectious events to be linear (unsaturated) in the target cell concentration21,22. Figure 1 shows results for six concentrations of CEM-SS cells23,24. Results were linear at lower cell concentrations and showed only minor assay saturation at ...
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Bulletin of mathematical biology 51 (1989), S. 715-730 
    ISSN: 1522-9602
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Mathematics
    Notes: Abstract In a separate paper, we developed a mathematical model describing HIV infection and used it to suggest experiments for quantifying characteristic viral parameters. In this paper we generalize the model to any well-mixed assay system. We also present complete and rigorous derivations of fundamental results needed for the design and analysis of HIV infectivity assays. The model is applicable to infectious agents with multiple receptors for their target cell (e.g. HIV, Epstein-Barr virus and Plasmodium), and to blockers (both reversible and irreversible), as long as blocker and target cells are the same diffusion compartment.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1572-9613
    Keywords: Lattice Boltzmann BGK equations ; nonslip boundary conditions ; analytic solutions of simple flows
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract In this paper we analytically solve the velocity of the lattice Boltzmann BGK equation (LBGK) for several simple flows. The analysis provides a framework to theoretically analyze various boundary conditions. In particular, the analysis is used to derive the slip velocities generated by various schemes for the nonslip boundary condition. We find that the slip velocity is zero as long as Σαfαeα=0 at boundaries, no matter what combination of distributions is chosen. The schemes proposed by Nobleet al. and by Inamuroet al. yield the correct zeroslip velocity, while some other schemes, such as the bounce-back scheme and the equilibrium distribution scheme, would inevitably generate a nonzero slip velocity. The bounce-back scheme with the wall located halfway between a flow node and a bounce-back node is also studied for the simple flows considered and is shown to produce results of second-order accuracy. The momentum exchange at boundaries seems to be highly related to the slip velocity at boundaries. To be specific, the slip velocity is zero only when the momentum dissipated by boundaries is equal to the stress provided by fluids.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 31 (1995), S. 225-240 
    ISSN: 0886-1544
    Keywords: cell-substratum adhesion ; lamellar contractility ; locomotion ; silicone rubber ; traction forces ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A means of determining quantitative maps of the tractions exerted by locomoting cells on a substratum has been developed. This method is similar to the Harris silicone substratum assay [Harris et al., 1980: Science 208:177-179], but uses an improved non-wrinkling film that deforms more predictably in response to traction forces. The method also utilizes a mathematical analysis of rubber deformation to produce the final map of the distribution of tractions. The resulting maps consistently showed that fish keratocytes exert a steady-state “pinching” on the substratum, perpendicular to the cell's direction of locomotion. No significant rearward tractions were detected at or near the front edge of the cell. Likewise, no significant forward tractions associated with peeling of adhesions were found at the back of the cell. A second assay uses deflection of a lightly attached glass microneedle to measure the total force exerted by locomoting cells. Forces of approximately 4.5 × 10-3 dyn were required to “stall” locomoting keratocytes. The implications of these findings for cell movement are discussed.
    Additional Material: 11 Ill.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 1 (1981), S. 205-235 
    ISSN: 0886-1544
    Keywords: capping of receptors ; cell locomotion ; cell-surface interactions ; frictional force ; membrane flow ; polymorphonuclear leukocytes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: As a cell moves over a surface, the distribution of membrane proteins that adhere to the surface will be changed relative to the distribution of these molecules on a static cell. Observations of this redistribution offer, in principle, evidence as to the mechanisms of membrane dynamics during cell locomotion. Toward extracting such information we present and analyze a mathematical model of receptor transport in the membrane by diffusion and convection, as affected by the making and breaking of the bonds between the receptors and the surface as the cell moves.We show that the disruption of receptor-surface bonds at the tail of the cell provides a mechanism by which the frictional force opposing a cell's motion is exerted, and calculate the magnitude of this force as a function of cell velocity. Assuming this to be the major contribution to the frictional force, we show that when the shear force on a cell is above a critical value it is no longer possible for the cell to slide across the surface. For such large forces, it is still possible for the cell to roll; alternatively the cell can be torn free of the surface.Our analysis of existing data on movement of polymorphonuclear leukocytes indicates that cell motion is not accompanied by a bulk flow of membrane from the front to the back of the cell. The data also indicate that cells do not tend to roll as they move over a surface under normal conditions. The data are most consistent with a model where the membrane as a whole is stationary but where receptors that bind to the surface become coupled to sub-membrane contractile proteins.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Annals of biomedical engineering 23 (1995), S. 322-331 
    ISSN: 1573-9686
    Keywords: Cell Adhesion ; Ligand-Coated Substrate ; Peel Test ; Membrane Mechanics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Technology
    Notes: Abstract Cell adhesion to substratum is often mediated by binding between cell surface receptors and substrate ligands. Substrates can be derivatized with different types and densities of ligands, but how substrate chemistry determines cellular function, such as adhesion strength, has not been demonstrated quantitatively. We employ a numerical methodology developed by Dembo and colleagues (9), who investigated membrane peeling under conditions of excess ligand density, to investigate the kinetics and strength of cell peeling from ligand coated surfaces for arbitrary ligand density. We show there are two asymptotic limits to peeling strength, as quantified by the critical tension: a high ligand density limit, where the critical tension is independent of ligand density and depends logarithmically on the receptor density; and a low ligand density limit, in which the critical tension depends logarithmically on the ligand density but is independent of receptor density. In between these limits, we numerically determine the critical tension. The critical tension is always a weak function of the dissociation constant between ligand and receptor. Furthermore, we show how the rate of peeling, for tensions above the critical tension, depends on ligand density and the mechanical properties of the receptor-ligand bonds. Interestingly, we illustrate when small increases in ligand density should alter cellular behavior, inducing a change to spreading onto a substrate from peeling up from a substrate. In total the predictions of this paper provide criteria for the design of ligand-coated substrate that provide for the proper adhesion strength and dynamics of detachment of cells from surfaces.
    Type of Medium: Electronic Resource
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