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Biomedical subjects

E Mosekilde

Publications and source records attributed to E Mosekilde.

At least 37 records · Page 2Linked to original sources
PubMed2000

Extracting dynamics from threshold-crossing interspike intervals: possibilities and limitations.

In this paper we estimate dynamical characteristics of chaotic attractors from sequences of threshold-crossing interspike intervals, and study how the choice of the threshold level (which sets the equation of a secant plane) influences the results of the numerical computations. Under quite general conditions we show that the largest Lyapunov exponent can be estimated from a series of return times to the secant plane, even in the case when some of the loops of the phase space trajectory fail to cross this plane.

Algorithms↗
PubMed2000

Comment on "Flow-distributed oscillations: stationary chemical waves in a reacting flow"

In a recent paper by Kaern and Menzinger [Phys. Rev. E 60, R3471 (1999)] a successful verification of the stationary space-periodic structures predicted by Andresen et al. [Phys. Rev. E 60, 297 (1999)] was reported. Kaern and Menzinger suggest a mechanism for the formation of such structures that yields a linear relationship between the selected wavelength and the flow rate. We find this mechanism too simple and produce numerical simulations that support the original interpretation of these structures.

Journal Article↗
PubMed1999

Desynchronization of chaos in coupled logistic maps.

When identical chaotic oscillators interact, a state of complete or partial synchronization may be attained in which the motion is restricted to an invariant manifold of lower dimension than the full phase space. Riddling of the basin of attraction arises when particular orbits embedded in the synchronized chaotic state become transversely unstable while the state remains attracting on the average. Considering a system of two coupled logistic maps, we show that the transition to riddling will be soft or hard, depending on whether the first orbit to lose its transverse stability undergoes a supercritical or subcritical bifurcation. A subcritical bifurcation can lead directly to global riddling of the basin of attraction for the synchronized chaotic state. A supercritical bifurcation, on the other hand, is associated with the formation of a so-called mixed absorbing area that stretches along the synchronized chaotic state, and from which trajectories cannot escape. This gives rise to locally riddled basins of attraction. We present three different scenarios for the onset of riddling and for the subsequent transformations of the basins of attraction. Each scenario is described by following the type and location of the relevant asynchronous cycles, and determining their stable and unstable invariant manifolds. One scenario involves a contact bifurcation between the boundary of the basin of attraction and the absorbing area. Another scenario involves a long and interesting series of bifurcations starting with the stabilization of the asynchronous cycle produced in the riddling bifurcation and ending in a boundary crisis where the stability of an asynchronous chaotic state is destroyed. Finally, a phase diagram is presented to illustrate the parameter values at which the various transitions occur.

Journal Article↗
PubMed1999

Stationary space-periodic structures with equal diffusion coefficients.

The paper investigates a chemical reaction-diffusion model in an open flow system. It is shown that such a system may, with particular boundary conditions, exhibit stationary space-periodic structures even in the case of equal diffusion coefficients. This is confirmed through numerical simulations.

Journal Article↗
PubMed1999

Loss of lag synchronization in coupled chaotic systems.

Lag synchronization denotes a particular form of synchronization in which the amplitudes of two interacting, nonidentical chaotic oscillators are correlated but there is a characteristic time delay between them. We study transitions to and between different forms of synchronization for the attractors defined as "in-phase" and "out-of-phase" and investigate the processes by which lag synchronization is lost in two coupled Rössler systems. With a small frequency mismatch between the two systems, these processes are related to the occurrence of a peculiar form of basin structure as more and more periodic orbits embedded into the synchronized chaotic state become unstable in a transverse direction.

Journal Article↗
PubMed1997

Gene therapy of T helper cells in HIV infection: mathematical model of the criteria for clinical effect.

This paper presents a mathematical analysis of the criteria for gene therapy of T helper cells to have a clinical effect on HIV infection. The analysis indicates that for such a therapy to be successful, it must protect the transduced cells against HIV-induced death. The transduced cells will not survive as a population if the gene therapy only blocks the spread of virus from transduced cells that become infected. The analysis also suggests that the degree of protection against disease-related cell death provided by the gene therapy is more important than the fraction cells that is initially transduced. If only a small fraction of the cells can be transduced, transduction of T helper cells and transduction of haematopoietic progenitor cells will result in the same steady-state level of transduced T helper cells. For gene therapy to be efficient against HIV infection, our analysis suggests that a 100% protection against viral escape must be obtained. The study also suggests that a gene therapy against HIV infection should be designed to give the transduced cells a partial but not necessarily total protection against HIV-induced cell death, and to avoid the production of viral mutants insensitive to the gene therapy.

Cell Death↗
PubMed1996

Quantification of remodeling parameter sensitivity--assessed by a computer simulation model.

During normal aging and menopause, cancellous bone is lost at all skeletal sites due to remodeling-related factors: negative formation balance; temporarily increased remodeling space; and osteoclastic perforations. The relative importance of the various factors in inducing bone mass loss and perforations is still controversial. We have previously used a computer simulation model to describe the effect of several bone remodeling parameters on vertebral cancellous bone loss. The model focused on two different scenarios for the menopause and three different treatment regimens. The aim of the present study was to extend the previous study by quantifying remodeling parameter sensitivity for changes in the bone mass with the use of the computer model we had previously formulated. The menopause scenario, with increased activation frequency and increased resorption depth, was chosen as the base case scenario, and the following parameters were investigated in the sensitivity analysis: activation frequency; formation balance; resorption depth; and critical trabecular thickness. Simulations were performed for a period of 20 years starting at the age of 48 years. The analysis showed that the number of perforations and the perforation-related mass loss both exhibited a large sensitivity toward variations in the final resorption depth. However, the formation balance was the factor that was responsible for the greater part of the bone mass loss. The computer model allowed us to quantify the sensitivity of different output variables with respect to changes in some of the model parameters. This can give information about the biological mechanisms responsible for bone mass loss around the surgically induced or natural menopause and also provide an indication of the type of treatment that would be most useful in preventing the deterioration of the cancellous network.

Adult↗
PubMed1995

Increased adhesion as a mechanism of antibody-dependent and antibody-independent complement-mediated enhancement of human immunodeficiency virus infection.

Enhancement of human immunodeficiency virus (HIV) infection by complement alone or in conjunction with antibodies was studied experimentally and theoretically. Experimental studies showed that while HIV-positive sera neutralize HIV infection, the addition of fresh complement abrogated neutralization and could even cause enhancement. Enhancement was blocked by anti-complement receptor 2 antibodies, and infection under enhancing conditions could be blocked by soluble CD4. Antibody-dependent complement-mediated enhancement (C'ADE) was dependent on the alternative complement activation pathway, as factor B-deficient serum could enhance only after the addition of factor B. The observed enhancement was also antibody dependent, since the addition of antibodies increased the level of enhancement. Under C'ADE conditions, infection reached a plateau within 5 min and was not caused by activation of cells by factors in the human serum. On the contrary, preincubation of cells with complement decreased the level of enhancement. A theoretical model of HIV infection in vitro which exhibited similar enhancement in an antibody- and complement concentration-dependent way was developed. Model studies indicated that the enhanced infection process could be explained by the fact that virions, because of complement deposition on the surface, bind more efficiently to cells. The model also indicated that the saturation of the enhanced infection process seen after a few minutes could be caused by saturation of the complement receptors. The effect of neutralizing antibodies can thus be overcome by the enhancing effect of complement that facilitates the contact between gp120 and CD4. These studies demonstrate that the main features of the complement-dependent enhancement phenomenon can be understood in terms of a simple mathematical model.

CD4 Antigens↗
PubMed1994

Compensation in pancreatic beta-cell function in subjects with glucokinase mutations.

The relationship between the in vivo insulin secretory responsiveness of the pancreatic beta-cell to glucose and the flux of glucose through the enzyme glucokinase was investigated in six subjects with heterozygous glucokinase mutations and in six matched control subjects. This was done by combining data published previously on the in vivo dose-response relationships between glucose and insulin secretion and on the in vitro enzymatic properties of wild-type and mutant forms of glucokinase. The flux of glucose through glucokinase (GK flux) in these subjects was estimated using a model based on the approximate Michaelis-Menten kinetics of wild-type and mutant forms of the enzyme. In two subjects with glucokinase mutations, which resulted in only a small reduction in enzymatic activity, the decrease in insulin secretion was directly proportional to the decrease in GK flux predicted using a Michaelis-Menten model for both mutant and wild-type glucokinase. However, in four subjects with glucokinase mutations, which resulted in severe reductions in enzymatic activity, insulin secretion was reduced compared with control subjects but less than predicted. This latter result implies the existence of a compensatory change in the beta-cells of such subjects, which results in a relative increase in insulin secretory response. We propose modifications to the simple model relating glucose concentration and GK flux, including glucose-induced overexpression of the normal allele and a role of glucokinase regulatory protein. The modifications take into account the possibility that the degree of compensation may be directly related to the severity of the mutation.

Adolescent↗
PubMed1993

[Is the new chaos- and fractal research of importance to medical science?].

Living systems are characterized by a complexity of structure and function which goes well beyond the descriptive capacity of classical physical and mathematical methods. During the latest decade, the development of non-linear dynamics has introduced a series of new concepts and tools to describe even extremely complex systems. This has led to a better understanding of the processes through which complex structures can arise from very simple interactions. The present and a following paper will give a brief introduction to some concepts and methods of this new science.

Biological Evolution↗
PubMed1992

Minimal model for Ca(2+)-dependent oscillations in excitable cells.

A minimal model for calcium controlled oscillations is presented. The model considers only an exchange of potassium and calcium ions over the plasma membrane. Calcium ions leak into the cell through a potential dependent channel and is extruded by a pump. Potassium leaks out through a calcium dependent, but voltage independent, channel. The cytosolic calcium concentration is buffered, so a fixed fraction is free. Inactivation, membrane capacity, and time delays for the conductance changes are not included, so the time dependence is solely introduced through the temporal changes of the intracellular Ca(2+)-concentration. With continuous parameter changes the model can switch between five states: (1) a non-excitable, stable state; (2) single-spike excitability; (3) slow, spontaneous oscillations; (4) reverse-spike excitability; and (5) another non-excitable, stable state. One of the key parameters for this switching behavior is the rate constant for the calcium pump.

Action Potentials↗
PubMed1991

The significance of an erroneous recording of the centre of mandibular rotation in orthognathic surgery.

The effect of post-operative jaw position of an error in locating the true centre of mandibular rotation was evaluated using a computer-simulation model and a mock surgery model. The centre of the condyle serves as a reference point in surgical procedures involving the maxilla. The purpose of this study was to describe the amount of malpositioning of the jaws at surgery due to a discrepancy between a simulated true centre of rotation and the centre of the condyle. The results showed, that a 20 mm error in location of the true centre of rotation could result in a 3 mm horizontal malpositioning of the maxilla.

Analysis of Variance↗
PubMed1991

Computer model for mechanisms underlying ultradian oscillations of insulin and glucose.

Oscillations in human insulin secretion have been observed in two distinct period ranges, 10-15 min (i.e. rapid) and 100-150 min (i.e., ultradian). The cause of the ultradian oscillations remains to be elucidated. To determine whether the oscillations could result from the feedback loops between insulin and glucose, a parsimonious mathematical model including the major mechanisms involved in glucose regulation was developed. This model comprises two major negative feedback loops describing the effects of insulin on glucose utilization and glucose production, respectively, and both loops include the stimulatory effect of glucose on insulin secretion. Model formulations and parameters are representative of results from published clinical investigations. The occurrence of sustained insulin and glucose oscillations was found to be dependent on two essential features: 1) a time delay of 30-45 min for the effect of insulin on glucose production and 2) a sluggish effect of insulin on glucose utilization, because insulin acts from a compartment remote from plasma. When these characteristics were incorporated in the model, numerical simulations mimicked all experimental findings so far observed for these ultradian oscillations, including 1) self-sustained oscillations during constant glucose infusion at various rates; 2) damped oscillations after meal or oral glucose ingestion; 3) increased amplitude of oscillation after increased stimulation of insulin secretion, without change in frequency; and 4) slight advance of the glucose oscillation compared with the insulin oscillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity Cycles↗