Two elementary cellular automata with a new kind of dynamic

Finite elementary cellular automata (ECAs) are studied, considering periodic and the four types of fixed boundary conditions. It is shown that two of these automata, rules 26 and 154, have particularly interesting dynamics. Both these rules are in Wolfram’s class 2 when subject to periodic boundary conditions but have chaotic dynamics, typical of Wolfram’s class 3, when we consider fixed boundary conditions a ℓ = 1 and a r = 0. The same rules, when fixed null boundary conditions a ℓ = 0 and a r = 0 are used, show complex dynamics with a mixture of order and disorder completely different from the one identified with Wolfram’s class 4: it grows in complexity in order to reach, in just a few time steps, an extremely simple, almost homogeneous configuration, from which the complexification starts again.info:eu-repo/semantics/publishedVersio

Magnetic Cellular Nonlinear Network with Spin Wave Bus for Image Processing

We describe and analyze a cellular nonlinear network based on magnetic nanostructures for image processing. The network consists of magneto-electric cells integrated onto a common ferromagnetic film - spin wave bus. The magneto-electric cell is an artificial two-phase multiferroic structure comprising piezoelectric and ferromagnetic materials. A bit of information is assigned to the cell's magnetic polarization, which can be controlled by the applied voltage. The information exchange among the cells is via the spin waves propagating in the spin wave bus. Each cell changes its state as a combined effect of two: the magneto-electric coupling and the interaction with the spin waves. The distinct feature of the network with spin wave bus is the ability to control the inter-cell communication by an external global parameter - magnetic field. The latter makes possible to realize different image processing functions on the same template without rewiring or reconfiguration. We present the results of numerical simulations illustrating image filtering, erosion, dilation, horizontal and vertical line detection, inversion and edge detection accomplished on one template by the proper choice of the strength and direction of the external magnetic field. We also present numerical assets on the major network parameters such as cell density, power dissipation and functional throughput, and compare them with the parameters projected for other nano-architectures such as CMOL-CrossNet, Quantum Dot Cellular Automata, and Quantum Dot Image Processor. Potentially, the utilization of spin waves phenomena at the nanometer scale may provide a route to low-power consuming and functional logic circuits for special task data processing

Cellular Potts modeling of tumor growth, tumor invasion and tumor evolution

Despite a growing wealth of available molecular data, the growth of tumors, invasion of tumors into healthy tissue, and response of tumors to therapies are still poorly understood. Although genetic mutations are in general the first step in the development of a cancer, for the mutated cell to persist in a tissue, it must compete against the other, healthy or diseased cells, for example by becoming more motile, adhesive, or multiplying faster. Thus, the cellular phenotype determines the success of a cancer cell in competition with its neighbors, irrespective of the genetic mutations or physiological alterations that gave rise to the altered phenotype. What phenotypes can make a cell “successful” in an environment of healthy and cancerous cells, and how? A widely-used tool for getting more insight into that question is cell-based modeling. Cell based models constitute a class of computational, agent-based models that mimic biophysical and molecular interactions between cells. One of the most widely used cell-based modeling formalisms is the cellular Potts model (CPM), a lattice-based, multi particle cell-based modeling approach. The CPM has become a popular and accessible method for modeling mechanisms of multicellular processes including cell sorting, gastrulation, or angiogenesis. The CPM accounts for biophysical cellular properties, including cell proliferation, cell motility, and cell adhesion, which play a key role in cancer. Multiscale models are constructed by extending the agents with intracellular processes including metabolism, growth, and signaling. Here we review the use of the CPM for modeling tumor growth, tumor invasion, and tumor progression. We argue that the accessibility and flexibility of the CPM, and its accurate, yet coarse-grained and computationally efficient representation of cell- and tissue biophysics, make the CPM the method of choice for modeling cellular processes in tumor development

Computational shelf-life dating : complex systems approaches to food quality and safety

Shelf-life is defined as the time that a product is acceptable and meets the consumers expectations regarding food quality. It is the result of the conjunction of all services in production, distribution, and consumption. Shelf-life dating is one of the most difficult tasks in food engineering. Market pressure has lead to the implementation of shelf-life by sensory analyses, which may not reflect the full quality spectra. Moreover, traditional methods for shelf-life dating and small-scale distribution chain tests cannot reproduce in a laboratory the real conditions of storage, distribution, and consumption on food quality. Today, food engineers are facing the challenges to monitor, diagnose, and control the quality and safety of food products. The advent of nanotechnology, multivariate sensors, information systems, and complex systems will revolutionize the way we manage, distribute, and consume foods. The informed consumer demands foods, under the legal standards, at low cost, high standards of nutritional, sensory, and health benefits. To accommodate the new paradigms, we herein present a critical review of shelf-life dating approaches with special emphasis in computational systems and future trends on complex systems methodologies applied to the prediction of food quality and safety.Fundo Europeu de Desenvolvimento Regional (FEDER) - Programa POS-ConhecimentoFundação para a Ciência e a Tecnologia (FCT) - SFRH/BPD/26133/2005, SFRH/ BPD/20735/200

Complex systems dynamics in laser excited ensembles of Rydberg atoms

In this thesis I present experimental and theoretical results showing that an ultracold gas under laser excitation to Rydberg states offers a controllable platform for studying the interesting complex dynamics that can emerge in driven-dissipative systems. The findings can be summarized according to the following three main insights: (i) The discovery of self-organized criticality (SOC) in our Rydberg system under facilitated excitation via three signatures: self-organization of the density to a stationary state; scale invariant behavior; and a critical response in terms of power-law distributed excitation avalanches. Additionally, we explore a mechanism inherent to our system which stabilizes the SOC state. We further investigate this stabilization via a controlled, variable driving of the system. These analyses can help answer the question of why scale invariant behavior is so prevalent in nature. (ii) A striking connection between the power-law growth of the Rydberg excitation number and epidemic spreading is found. Based on this, an epidemic network model is devised which efficiently describes the collective excitation dynamics. The importance of heterogeneity in the emergent Rydberg network and associated Griffiths effects provide a way to explain the observation of non-universal power laws. (iii) A novel quantum cellular automata implementation is proposed using atomic arrays together with multifrequency laser fields. This provides a natural framework to study the relation between microscopic processes and global dynamics, where special rules are found to generate entangled states with applications in quantum metrology and computing

An exploration and validation of computer modeling of evolution, natural selection, and evolutionary biology with cellular automata for secondary students.

The Evolutionary Tool Kit, a new software package, is the prototype of a concept simulator providing an environment for students to create microworlds of populations of artificial organisms. Its function is to model processes, concepts and arguments in natural selection and evolutionary biology, using either Mendelian asexual or sexual reproduction, or counterfactual systems such as \u27paint pot\u27 or blending inheritance. In this environment students can explore a conceptual What if? in evolutionary biology, test misconceptions and deepen understanding of inheritance and changes in populations. Populations can be defined either with typological, or with populational thinking, to inquire into the role and necessity of variation in natural selection. The approach is generative not tutorial. The interface is highly graphic with twenty traits set as icons that are moved onto the \u27phenotypes\u27. Activities include investigations of evolutionary theory of aging, reproductive advantage, sexual selection and mimicry. Design of the activities incorporates Howard Gardner\u27s Theory of Multiple Intelligences. Draft of a teacher and student manual are included

Lattice-gas cellular automata for the analysis of cancer invasion

Cancer cells display characteristic traits acquired in a step-wise manner during carcinogenesis. Some of these traits are autonomous growth, induction of angiogenesis, invasion and metastasis. In this thesis, the focus is on one of the latest stages of tumor progression, tumor invasion. Tumor invasion emerges from the combined effect of tumor cell-cell and cell-microenvironment interactions, which can be studied with the help of mathematical analysis. Cellular automata (CA) can be viewed as simple models of self-organizing complex systems in which collective behavior can emerge out of an ensemble of many interacting "simple" components. In particular, we focus on an important class of CA, the so-called lattice-gas cellular automata (LGCA). In contrast to traditional CA, LGCA provide a straightforward and intuitive implementation of particle transport and interactions. Additionally, the structure of LGCA facilitates the mathematical analysis of their behavior. Here, the principal tools of mathematical analysis of LGCA are the mean-field approximation and the corresponding Lattice Boltzmann equation. The main objective of this thesis is to investigate important aspects of tumor invasion, under the microscope of mathematical modeling and analysis: Impact of the tumor environment: We introduce a LGCA as a microscopic model of tumor cell migration together with a mathematical description of different tumor environments. We study the impact of the various tumor environments (such as extracellular matrix) on tumor cell migration by estimating the tumor cell dispersion speed for a given environment. Effect of tumor cell proliferation and migration: We study the effect of tumor cell proliferation and migration on the tumor’s invasive behavior by developing a simplified LGCA model of tumor growth. In particular, we derive the corresponding macroscopic dynamics and we calculate the tumor’s invasion speed in terms of tumor cell proliferation and migration rates. Moreover, we calculate the width of the invasive zone, where the majority of mitotic activity is concentrated, and it is found to be proportional to the invasion speed. Mechanisms of tumor invasion emergence: We investigate the mechanisms for the emergence of tumor invasion in the course of cancer progression. We conclude that the response of a microscopic intracellular mechanism (migration/proliferation dichotomy) to oxygen shortage, i.e. hypoxia, maybe responsible for the transition from a benign (proliferative) to a malignant (invasive) tumor. Computing in vivo tumor invasion: Finally, we propose an evolutionary algorithm that estimates the parameters of a tumor growth LGCA model based on time-series of patient medical data (in particular Magnetic Resonance and Diffusion Tensor Imaging data). These parameters may allow to reproduce clinically relevant tumor growth scenarios for a specific patient, providing a prediction of the tumor growth at a later time stage.Krebszellen zeigen charakteristische Merkmale, die sie in einem schrittweisen Vorgang während der Karzinogenese erworben haben. Einige dieser Merkmale sind autonomes Wachstum, die Induktion von Angiogenese, Invasion und Metastasis. Der Schwerpunkt dieser Arbeit liegt auf der Tumorinvasion, einer der letzten Phasen der Tumorprogression. Die Tumorinvasion ensteht aus der kombinierten Wirkung von den Wechselwirkungen Tumorzelle-Zelle und Zelle-Mikroumgebung, die mit die Hilfe von mathematischer Analyse untersucht werden können. Zelluläre Automaten (CA) können als einfache Modelle von selbst-organisierenden komplexen Systemen betrachtet werden, in denen kollektives Verhalten aus einer Kombination von vielen interagierenden "einfachen" Komponenten entstehen kann. Insbesondere konzentrieren wir uns auf eine wichtige CA-Klasse, die sogenannten Zelluläre Gitter-Gas Automaten (LGCA). Im Gegensatz zu traditionellen CA bieten LGCA eine einfache und intuitive Umsetzung der Teilchen und Wechselwirkungen. Zusätzlich erleichtert die Struktur der LGCA die mathematische Analyse ihres Verhaltens. Die wichtigsten Werkzeuge der mathematischen Analyse der LGCA sind hier die Mean-field Approximation und die entsprechende Lattice - Boltzmann - Gleichung. Das wichtigste Ziel dieser Arbeit ist es, wichtige Aspekte der Tumorinvasion unter dem Mikroskop der mathematischen Modellierung und Analyse zu erforschen: Auswirkungen der Tumorumgebung: Wir stellen einen LGCA als mikroskopisches Modell der Tumorzellen-Migration in Verbindung mit einer mathematischen Beschreibung der verschiedenen Tumorumgebungen vor. Wir untersuchen die Auswirkungen der verschiedenen Tumorumgebungen (z. B. extrazellulären Matrix) auf die Migration von Tumorzellen dürch Schätzung der Tumorzellen-Dispersionsgeschwindigkeit in einem gegebenen Umfeld. Wirkung von Tumor-Zellenproliferation und Migration: Wir untersuchen die Wirkung von Tumorzellenproliferation und Migration auf das invasive Verhalten der Tumorzellen durch die Entwicklung eines vereinfachten LGCA Tumorwachstumsmodells. Wir leiten die entsprechende makroskopische Dynamik und berechnen die Tumorinvasionsgeschwindigkeit im Hinblick auf die Tumorzellenproliferation- und Migrationswerte. Darüber hinaus berechnen wir die Breite der invasiven Zone, wo die Mehrheit der mitotischer Aktivität konzentriert ist, und es wird festgestellt, dass diese proportional zu den Invasionsgeschwindigkeit ist. Mechanismen der Tumorinvasion Entstehung: Wir untersuchen Mechanismen, die für die Entstehung von Tumorinvasion im Verlauf des Krebs zuständig sind. Wir kommen zu dem Schluss, dass die Reaktion eines mikroskopischen intrazellulären Mechanismus (Migration/Proliferation Dichotomie) zu Sauerstoffmangel, d.h. Hypoxie, möglicheweise für den Übergang von einem gutartigen (proliferative) zu einer bösartigen (invasive) Tumor verantwortlich ist. Berechnung der in-vivo Tumorinvasion: Schließlich schlagen wir einen evolutionären Algorithmus vor, der die Parameter eines LGCA Modells von Tumorwachstum auf der Grundlage von medizinischen Daten des Patienten für mehrere Zeitpunkte (insbesondere die Magnet-Resonanz-und Diffusion Tensor Imaging Daten) ermöglicht. Diese Parameter erlauben Szenarien für einen klinisch relevanten Tumorwachstum für einen bestimmten Patienten zu reproduzieren, die eine Vorhersage des Tumorwachstums zu einem späteren Zeitpunkt möglich machen