arXiv subjects

Christina Surulescu

Publications and source records attributed to Christina Surulescu.

At least 19 recordsLinked to original sources

arXiv2026

Mathematical modeling of glioma invasion and therapy approaches via kinetic theory of active particles

We propose here a multiscale model for study the effect of combined therapies on glioma spread in the brain under the influence of vascularization. The model accounts for the interplay between the different components of the neoplasm and the healthy tissue and it investigates and compares various therapy approaches. Precisely, these involve radio- and chemotherapy in a concurrent or adjuvant manner together with anti-angiogenic therapy affecting the vascular component of the system. We assess tumor growth and spread on the basis of DTI data, which allows us to reconstruct a realistic brain geometry and tissue structure, and we apply our model to real glioma patient data. In this latter case, a space-dependent radiotherapy description is considered using data about the corresponding isodose curves.

q-bio.CB↗

arXiv2026

Randomness-aware multiscale models of glioma invasion and treatment

In this work, we develop a stochastic multiscale model for glioma growth and invasion in the brain, incorporating the effects of therapeutic interventions. The model accounts for tumor cell migration influenced by brain tissue heterogeneity and anti-crowding mechanisms, while explicitly addressing treatment-related uncertainties through stochastic processes. Starting from a microscopic description of individual cell dynamics, we derive the corresponding system of macroscopic random reaction-diffusion-taxis equations governing cell density and tissue evolution. Finally, we conduct several numerical experiments to assess the efficacy of different treatment protocols, evaluated with respect to both established and newly proposed clinical criteria and measurable outcomes.

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arXiv2025

Global existence of weak solutions to a tissue regeneration model

We study a cross-diffusion model for tissue regeneration which involves the dynamics of human mesenchymal stem cells interacting with chondrocytes in a medium containing a differentiation factor. The latter acts as a chemoattractant for the chondrocytes and influences the (de)differentiation of both cell phenotypes. The stem cells perform haptotaxis towards extracellular matrix expressed by the chondrocytes and degraded by themselves. Cartilage production as part of the extracellular matrix is ensured by condrocytes. The growth factor is provided periodically, to maintain the cell dynamics. We provide a proof for the global existence of weak solutions to this model, which is a simplified version of a more complex setting deduced in \cite{surulescu_AMM}.

math.AP↗

arXiv2025

Mathematical modeling of Buruli ulcer spread

We propose two approaches to a model deduction for Buruli ulcer spread in a tissue, prove global existence of solutions to the obtained macroscopic cross-diffusion PDE-ODE systems, and perform numerical simulations to illustrate the behavior of solutions under various scenarios and compare the outcome of the two approaches.

math.AP↗

arXiv2025

Global existence of weak solutions to a cell migration and (de)differentiation model with double haptotaxis in the context of tissue regeneration

We study a model for the spread and (de)differentiation of mesenchymal stem cells and chondrocytes in a scaffold whose fibers are coated with hyaluron. The chondrocytes produce new extracellular matrix, which, together with hyaluron, serves as haptotactic cue for the stem cell migration. We prove global existence of weak solutions of the corresponding cross-diffusion system with double haptotaxis.

math.AP↗

arXiv2024

Mathematical modeling and analysis of a tumor invasion problem with angiogenesis and taxis cascade

We propose a mathematical model for tumor invasion supported by angiogenesis and interactions with the surrounding tissue. For the model deduction we employ a multiscale approach starting from lower scales and obtaining by an informal parabolic upscaling a system of reaction-diffusion-taxis equations with a so-called 'taxis cascade', where one species is performing taxis towards a signal whose production/decay is controled by the other, for which it also serves as a tactic cue. We prove global existence and uniqueness of solutions to the obtained PDE-ODE system and perform numerical simulations to illustrate the behavior of solutions.

math.AP↗

arXiv2024

On a PDE-ODE-PDE model for two interacting cell populations under the influence of an acidic environment and with nonlocal intra- and interspecific growth limitation

We consider a model for the dynamics of active cells interacting with their quiescent counterparts under the influence of acidity characterized by proton concentration. The active cells perform nonlinear diffusion and infer proliferation or decay, according to the strength of spatially nonlocal intra- and interspecific interactions. The two cell phenotypes are interchangeable, the transitions depending on the environmental acidity. We prove global existence of a weak solution to the considered PDE-ODE-PDE system and perform numerical simulations in 1D to informally investigate boundedness and patterning behavior in dependence of the system's parameters and kernels involved in the nonlocal terms.

math.AP↗

arXiv2024

Cell seeding dynamics in a porous scaffold material designed for meniscus tissue regeneration

We study the dynamics of a seeding experiment where a fibrous scaffold material is colonized by two types of cell populations. The specific application that we have in mind is related to the idea of meniscus tissue regeneration. In order to support the development of a promising replacement material, we discuss certain rate equations for the densities of human mesenchymal stem cells and chondrocytes and for the production of collagen-containing extracellular matrix. For qualitative studies, we start with a system of ordinary differential equations and refine then the model to include spatial effects of the underlying nonwoven scaffold structure. Numerical experiments as well as a complete set of parameters for future benchmarking are provided.

math.NA↗

arXiv2024

An in-silico approach to meniscus tissue regeneration: Modeling, numerical simulation, and experimental analysis

We develop a model the dynamics of human mesenchymal stem cells (hMSCs) and chondrocytes evolving in a nonwoven polyethylene terephtalate (PET) scaffold impregnated with hyaluron and supplied with a differentiation medium. The scaffold and the cells are assumed to be contained in a bioreactor with fluid perfusion. The differentiation of hMSCs into chondrocytes favors the production of extracellular matrix (ECM) and is influenced by fluid stress. The model takes deformations of ECM and PET scaffold into account. The scaffold structure is explicitly included by statistical assessment of the fibre distribution from CT images. The effective macroscopic equations are obtained by appropriate upscaling from dynamics on lower (microscopic and mesoscopic) scales and feature in the motility terms an explicit cell diffusion tensor encoding the assessed anisotropic scaffold structure. Numerical simulations show its influence on the overall cell and tissue dynamics.

q-bio.TO↗

arXiv2024

On a mathematical model for tissue regeneration

We propose a PDE-ODE model for tissue regeneration, obtained by parabolic upscaling from kinetic transport equations written for the mesoscopic densities of mesenchymal stem cells and chondrocytes which evolve in an artificial scaffold impregnated with hyaluron. Due to the simple chosen turning kernels, the effective equations obtained on the macroscopic level are of the usual reaction-diffusion-taxis type. We prove global existence of solutions to the coupled macroscopic system and perform a stability and bifurcation analysis, which shows that the observed patterns are driven by taxis. Numerical simulations illustrate the model behavior for various tactic sensitivities and initial conditions.

math.AP↗

arXiv2023

A mathematical model for meniscus cartilage regeneration

We propose a continuous model for meniscus cartilage regeneration triggered by two populations of cells migrating and (de)differentiating within an artificial scaffold with a known structure. The described biological processes are influenced by a fluid flow and therewith induced deformations of the scaffold. Numerical simulations are done for the corresponding dynamics within a bioreactor which was designed for performing the biological experiments.

math.NA↗

arXiv2023

On a mathematical model for cancer invasion with repellent pH-taxis and nonlocal intraspecific interaction

Starting from a mesoscopic description of cell migration and intraspecific interactions we obtain by upscaling an effective reaction-difusion-taxis equation for the cell population density involving spatial nonlocalities in the source term and biasing its motility and growth behavior according to environmental acidity. We prove global existence, uniqueness, and boundedness of a nonnegative solution to a simplified version of the coupled system describing cell and acidity dynamics. A 1D study of pattern formation is performed. Numerical simulations illustrate the qualitative behavior of solutions.

math.AP↗

arXiv2022

Data Driven Modeling of Pseudopalisade Pattern Formation

In this paper we propose a data-driven methodology to gain insight into the formation of different types of pseudopalisade structures. To this end, we start from a state of the art macroscopic model for the dynamics of GBM, that is coupled with the dynamics of extracellular pH, and formulate a terminal value optimal control problem. Thus, given a specific, observed pseudopalisade pattern, we determine the evolution of parameters (bio-mechanisms) that are responsible for its emergence. Random histological images exhibiting pseudopalisade-like structures are chosen to serve as target pattern. Having identified the optimal model parameters that generate the specified target pattern, we then formulate two different types of pattern counteracting ansatzes in order to determine possible ways to impair or obstruct the process of pseudopalisade formation. This provides the basis for designing active or live control of malignant GBM. Furthermore, we also provide a simple, yet insightful, mechanism to synthesize new pseudopalisade patterns by linearly combining the optimal model parameters responsible for generating different known target patterns. This particularly provides a hint that complex pseudopalisade patterns could be synthesized by a linear combination of parameters responsible for generating simple patterns. Going even further, we ask ourselves if complex therapy approaches can be conceived by linearly combining such that are able to reverse or disrupt simple pseudopalisade patterns, which is then positively answered with the help of numerical simulations.

math.AP↗

arXiv2021

A novel derivation of rigorous macroscopic limits from a micro-meso description of signal-triggered cell migration in fibrous environments

In this work we upscale a prototypical kinetic transport equation which models a cell population moving in a fibrous environment with a chemo- or haptotactic signal influencing both the direction and the magnitude of the cell velocity. The presented approach to scaling does not rely on orthogonality and treats parabolic and hyperbolic scalings in a unified manner. It is shown that the steps of the formal limit procedures are mirrored by rigorous operations with finite measures provided that the measure-valued position-direction fiber distribution enjoys some spacial continuity.

math.AP↗

arXiv2021

Multiphase modelling of glioma pseudopalisading under acidosis

We propose a multiphase modeling approach to describe glioma pseudopalisade patterning under the influence of acidosis. The phases considered at the model onset are glioma, normal tissue, necrotic matter, and interstitial fluid in a void-free volume with acidity represented by proton concentration. We start from mass and momentum balance to characterize the respective volume fractions and deduce reaction-cross diffusion equations for the space-time evolution of glioma, normal tissue, and necrosis. These are supplemented with a reaction-diffusion equation for the acidity dynamics and lead to formation of patterns which are typical for high grade gliomas. Unlike previous works, our deduction also works in higher dimensions and involves less restrictions. We also investigate the existence of weak solutions to the obtained system of equations and perform numerical simulations to illustrate the solution behavior and the pattern occurrence.

q-bio.TO↗

arXiv2021

Multiscale modeling of glioma invasion: from receptor binding to flux-limited macroscopic PDEs

We propose a novel approach to modeling cell migration in an anisotropic environment with biochemical heterogeneity and interspecies interactions, using as a paradigm glioma invasion in brain tissue under the influence of hypoxia-triggered angiogenesis. The multiscale procedure links single-cell and mesoscopic dynamics with population level behavior, leading on the macroscopic scale to flux-limited glioma diffusion and multiple taxis. We verify the non-negativity of regular solutions (provided they exist) to the obtained macroscopic PDE-ODE system and perform numerical simulations to illustrate the solution behavior under several scenarios.

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arXiv2020

A flux-limited model for glioma patterning with hypoxia-induced angiogenesis

We propose a model for glioma patterns in a microlocal tumor environment under the influence of acidity, angiogenesis, and tissue anisotropy. The bottom-up model deduction eventually leads to a system of reaction-diffusion-taxis equations for glioma and endothelial cell population densities, of which the former infers flux limitation both in the self-diffusion and taxis terms. The model extends a recently introduced [34] description of glioma pseudopalisade formation, with the aim of studying the effect of hypoxia-induced tumor vascularization on the establishment and maintenance of these histological patterns which are typical for high grade brain cancer. Numerical simulations of the population level dynamics are performed to investigate several model scenarios containing this and further effects.

q-bio.TO↗

arXiv2020

Mathematical modeling of glioma invasion: acid- and vasculature mediated go-or-grow dichotomy and the influence of tissue anisotropy

Starting from kinetic transport equations and subcellular dynamics we deduce a multiscale model for glioma invasion relying on the go-or-grow dichotomy and the influence of vasculature, acidity, and brain tissue anisotropy. Numerical simulations are performed for this model with multiple taxis, in order to assess the solution behavior under several scenarios of taxis and growth for tumor and endothelial cells. An extension of the model to incorporate the macroscopic evolution of normal tissue and necrotic matter allows us to perform tumor grading.

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