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Biomedical subjects

C DeLisi

Publications and source records attributed to C DeLisi.

At least 91 records · Page 5Linked to original sources
PubMed1981

Effect of nonspecific forces and finite receptor number on rate constants of ligand--cell bound-receptor interactions.

We develop a theory of ligand diffusion in the presence of a central potential toward or away from receptor patches that are uniformly distributed over a spherical cell. The current onto the receptors is reduced to less than that onto the sphere by a factor that is a nonlinear function of the number of free receptors, their size, and their potential energy. Similarly, under conditions defined by the theory, the dissociation rate from a receptor is reduced by the probability of rebinding to some other receptor on the same cell. This complicates the kinetic analysis, leading to the possibility of an occupancy-dependent dissociation rate, but has no effect on the interpretation of thermodynamic data.

Cell Membrane↗
PubMed1979

Quantitative aspects of a unified model of diffusion mediated receptor--cyclase coupling.

A quantitative model is presented of diffusion mediated coupling of adenylate cyclase to multivalent plasma membrane receptors which accounts for a wide range of phenomena including non linear occupation-activation plots with either positive or negative second derivatives, spare receptors, silent receptors, and negative and positive binding cooperativity. A non linear least square fit of the predicted equation for cyclase activation to available data predicts translational diffusion coefficients in the range of (10(-10) - 10(-11))cm2/s.

Adenylyl Cyclases↗
PubMed1979

The influence of cell surface receptor clustering on the thermodynamics of ligand binding and the kinetics of its dissociation.

We show that an equilibrium model for the clustering, by divalent ligand, of homogeneous plasma membrane-bound divalent receptors that do not change conformation predicts Scatchard plots with positive second derivatives (concave up). The result is thermodynamically indistinguishable from predictions based upon receptors that are heterogeneous for ligand, or that change conformation in a negatively cooperative way when ligand binds. A more general formulation of the theory, which allows application to dissociation kinetics, predicts that the dissociation of labeled ligand is accelerated in the presence of excess cold ligand and, moreover, that the accelerated dissociation has at least two components. The theory is briefly illustrated by fitting five different sets of data, at several temperatures for two different systems, with parameter values that are well within physically meaningful ranges. The model presented is the simplest and least ad hoc explanation thus far proposed as the basis for the kinetic phenomena, and raises the possibility that the numerous experiments in which such data are observed are primarily minifestations of cell surface clustering.

Insulin↗
PubMed1978

Secretion rate independent evaluation of IgM antibody avidity at the level of single immunocytes.

The hemolytic plaque inhibition assay has been performed on spleen cells from mice immunized with TNP-HRBC to evaluate avidity of anti-TNP IgM antibodies. At different times after immunization direct plaques were inhibited by soluble TNP-EACA, TNP61-BGG, or anti-mu antiserum. Analysis of the inhibition data provided independent estimates of antibody avidity and secretion rate. Avidity was found to increase with time, to reach a maximum when the antibody response attained the peak value, and then to decline as the response was waning. There was a decrease followed by increase of the secretion rate concomitant with the rise and fall of the antibody response and avidity.

Aminocaproic Acid↗
PubMed1977

Method for quantitating tumor cell removal and tumor cell-invasive capacity in experimental metastases.

An improved method is presented for analyzing the decay of i.v.-injected labeled tumor cells in the lung. A simple compartment analysis yields quantitative values for (a) the rate at which tumor cells are lost or cleared from the lung, and (b) the "invasion" rate at which tumor cells colonize the interstitial space. Statistical methods are outlined for testing the significance of the contribution of each rate to the overall shape of the decay curve and for testing whether or not a given rate is altered significantly during an experiment. The usefulness of the method is demonstrated in analysis of experiments involving perturbations of the host or of the injected tumor cells.

Animals↗