Biomedical subjects

M Scalerandi

Publications and source records attributed to M Scalerandi.

13 recordsLinked to original sources

PubMed2006

Electrical impedance for an electrolytic cell.

We analyze in which experimental conditions the concept of electrical impedance is useful for an electrolytic cell. The analysis is performed by solving numerically the differential equations governing the phenomenon of the redistribution of the ions in the presence of an external electric field and comparing the results with the ones obtained by solving the linear approximation of these equations. The control parameter in our study is the amplitude of the applied voltage, assumed a simple harmonic function of the time. We show that the bulk distribution of ions close to the electrodes differs from the one obtained by means of the linear analysis already for small amplitudes of the applied voltage. Nevertheless, the concept of electrical impedance remains valid. For larger amplitudes, the current in the circuit is no longer harmonic at the same frequency of the applied voltage. Therefore the concept of electrical impedance is no longer meaningful.

Journal Article↗

PubMed2004

Markovian model of growth and histologic progression in prostate cancer.

Models, based on bio-physical and biological considerations, may be very helpful as support tools for traditional diagnostic methodologies and interpretation of statistical data in oncology. This is particularly true when the neoplastic progression and differentiation are rather simple and regular, such as in the case of prostatic adenocarcinomas. Using clinical data as a "statistical ensemble," we propose here a Markovian model to forecast the tumor progression. After validation with clinical data, the model is applied to the determination of the temporal evolution of the risk of metastasis.

Adenocarcinoma↗

PubMed2004

Influence of the ions on the dynamical response of a nematic cell submitted to a dc voltage.

The influence of the ions present in a liquid crystal on the dynamical response of a nematic slab submitted to a dc voltage is studied. The evolution of the system toward the equilibrium state is investigated by solving the continuity equation for the electric charge, taking into account the current of drift and of diffusion. Our analysis shows that the formation of the double layers close to the electrodes strongly modifies the distribution of the electric field across the sample. We evaluate the surface polarization due to the ions movements and the contribution to the anisotropic part of the surface energy having a dielectric origin. We show also that, even if the optical response of the liquid crystal is a slow phenomenon, the distribution of the ionic charge is rather fast. Consequently, the presence of the ions cannot be neglected in the determination of the flexoelectric coefficients when the nematic sample is submitted to a square wave having a period of the order of 1 s.

Journal Article↗

PubMed2002

Inhibition of vascularization in tumor growth.

The transition to a vascular phase is a prerequisite for fast tumor growth. During the avascular phase, the neoplasm feeds only from the (relatively few) existing nearby blood vessels. During angiogenesis, the number of capillaries surrounding and infiltrating the tumor increases dramatically. A model which includes physical and biological mechanisms of the interactions between the tumor and vascular growth describes the avascular-vascular transition. Numerical results agree with clinical observations and predict the influence of therapies aiming to inhibit the transition.

Angiogenesis Inhibitors↗

PubMed2002

Properties of a "phase transition" induced by antiangiogenetic therapeutical protocols.

Inhibiting angiogenesis has been found to be an interesting therapeutical strategy against cancer. In fact, the success of tumor growth is subordinated to the corresponding increase of the vascular system feeding the neoplasm. However, optimization and design of proper antiangiogenetic therapeutical strategies is still an open problem. We apply a recently developed angiogenesis model to study how variations in the relevant parameters, e.g., induced by chemicals, may cause a "phase transition" to a region in the parameter space in which angiogenesis is not succesful. To demonstrate the reliability of our approach and its usefulness, we will study some specific drugs and use our model to investigate the influence of the main variables involved in a clinical treatment: the administration time, the duration of the drug effect, and the drug dose.

Angiogenesis Inhibitors↗

PubMed2002

Competition effects in the dynamics of tumor cords.

A general feature of cancer growth is the cellular competition for available nutrients. This is also the case for tumor cords, neoplasms forming cylindrical structures around blood vessels. Experimental data show that, in their avascular phase, cords grow up to a limit radius of about 100 microm, reaching a quasi-steady-state characterized by a necrotized area separating the tumor from the surrounding healthy tissue. Here we use a set of rules to formulate a model that describes how the dynamics of cord growth is controlled by the competition of tumor cells among themselves and with healthy cells for the acquisition of essential nutrients. The model takes into account the mechanical effects resulting from the interaction between the multiplying cancer cells and the surrounding tissue. We explore the influence of the relevant parameters on the tumor growth and on its final state. The model is also applied to investigate cord deformation in a region containing multiple nutrient sources and to predict the further complex growth of the tumor.

Journal Article↗

PubMed2001

Diffusion with evolving sources and competing sinks: development of angiogenesis.

Tumors ensure their long-time growth by emitting molecular messengers that induce cellular modifications in neighboring capillaries. These modifications are conducive to the enlargement of the vascular system feeding the tumor. This phenomenon, termed angiogenesis, is controlled by the diffusion and competitive trapping of nutrients and molecular messengers by several cell species. The number, location, and properties of these traps change continuously. The angiogenic process also implies that nutrient sources are time dependent. Starting from assumptions at the cellular level, we formulate a mathematical model that predicts the evolution of angiogenesis and the increase in the blood flow to the tumor. The model also predicts the emergence of directed growth and the possibility of therapeutical synergy. Simulations permit a careful analysis of the influence of the main parameters.

Absorption↗

PubMed2001

Emergence of taxis and synergy in angiogenesis.

Angiogenesis, the expansion of the vascular system feeding a tumor, is crucial to both primary tumors long-time growth and for the successful implantation of metastases. We formulate a model that relates the energetic requirements of the cancer cells to the production and diffusion of an angiogenic factor and to the ensuing evolution of neighboring endothelial cells. The model yields predictions for the development of neovascularization and for the increase in the blood flow to the tumor. We show that the directed growth of the vascular net is an emergent property and that therapies targeting different stages of the angiogenic process might have a synergistic effect.

Angiogenesis Inducing Agents↗

PubMed2001

Effects of anatomical constraints on tumor growth.

Competition for available nutrients and the presence of anatomical barriers are major determinants of tumor growth in vivo. We extend a model recently proposed to simulate the growth of neoplasms in real tissues to include geometrical constraints mimicking pressure effects on the tumor surface induced by the presence of rigid or semirigid structures. Different tissues have different diffusivities for nutrients and cells. Despite the simplicity of the approach, based on a few inherently local mechanisms, the numerical results agree qualitatively with clinical data (computed tomography scans of neoplasms) for the larynx and the oral cavity.

Cell Division↗

PubMed2000

Local interaction simulation approach for the response of the vascular system to metabolic changes of cell behavior.

The self-regulatory interactions between cells and the vascular system are mediated by signals propagating at a finite speed. In order to build up a physical model of these processes, several features, such as storing of internal energy, nonclassical nonlinear behavior, and delay and threshold effects, have to be taken into account. Considering cells as particles in different metabolic states according to their internal energy, we have developed a model based on the local interaction simulation approach. Several numerical results, in qualitative agreement with biological observations, illustrate the applicability of the model and the method to implement it.

Animals↗

PubMed2000

A physical-based model for the simulation of neoplastic growth and metastasis.

BACKGROUND AND OBJECTIVES: It is possible to formulate models capable of reproducing the main details of the physical processes involved in the evolution of biological systems. The complexity of the problem requires to begin with a simple and universal model for the description of the cellular growth, to be adapted successively to the local conditions found in clinically observed neoplastic growths. METHODS: A model based on the Local Interaction Simulation Approach (LISA) has been formulated for the simulation of growth, diffusion, and metastasis of neoplasms. The vascularization is described by a blood vessel located on one edge of the specimen in which a constant and homogeneous flow is assumed. A nutrient density is defined to mimic the blood flow within the tissue. RESULTS: Photograms taken at proper times may identify the main characteristics of the tumor evolution and describe its volume variations in a transversal section. Furthermore, it is possible to monitor constantly the volume of the neoplasm and of the necrotic tissue as a function of time, as well as the portion of cells that have migrated in the blood vessel. CONCLUSIONS: In spite of strong simplifying assumptions, the model presents good qualitative agreement with clinical data, which may be further improved by more detailed information about cancer cells properties or local vascular system patterns.

Animals↗

PubMed2000

Analysis of a "phase transition" from tumor growth to latency.

A mathematical model, based on the local interaction simulation approach, is developed in order to allow simulations of the spatiotemporal evolution of neoplasies. The model consists of a set of rules, which govern the interaction of cancerous cells among themselves and in competition with other cell populations for the acquisition of essential nutrients. As a result of small variations in the basic parameters, it leads to four different outcomes: indefinite growth, metastasis, latency, and complete regression. In the present contribution a detailed analysis of the dormant phase is carried on and the critical parameters for the transition to other phases are computed. Interesting chaotic behaviors can also be observed, with different attractors in the parameters space. Interest in the latency phase has been aroused by therapeutical strategies aiming to reduce a growing tumor to dormancy. The effect of such strategies may be simulated with our approach.

Cell Division↗

PubMed1999

Non-linear model of cancer growth and metastasis: a limiting nutrient as a major determinant of tumor shape and diffusion.

A new approach for modelling the spatio-temporal evolution of tumors is presented. To test its validity, a very basic model is considered, which, in spite of its simplicity, is capable of generating a multiplicity of morphologies and growth and migration rates. From an in-vivo scenario of basic life processes, cancer cell proliferation is described as a competition for basic nutrients. The chosen mathematical treatment and simulation techniques permit a direct implementation of the local nonlinear couplings existing between the various cell populations and the free and bound nutrient concentration. A discussion of the results and proposed improvements and applications of the model is also presented.

Cell Division↗