A Model Based on Cellular Automata to Simulate Epidemic Diseases

Rey, Ángel Martín del; White, Sara Hoya; Sánchez, Gerardo Rodríguez

doi:10.1007/11861201_36

Cited by 14 publications

(7 citation statements)

References 12 publications

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“…Network theory and cellular automaton models (del Rey et al 2006) might also be useful in exploring possible patchiness and lack of spatial homogeneity of the probability of the spread of WNS. If limited data are available, individual‐based simulation models may be useful (e.g., Kindlmann & Burel 2008; Lookingbill et al 2010).…”

Section: Knowledge Gapsmentioning

confidence: 99%

Investigating and Managing the Rapid Emergence of White-Nose Syndrome, a Novel, Fatal, Infectious Disease of Hibernating Bats

Foley

Clifford

Castle

et al. 2011

Conservation Biology

110

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White-nose syndrome (WNS) is a fatal disease of bats that hibernate. The etiologic agent of WNS is the fungus Geomyces destructans, which infects the skin and wing membranes. Over 1 million bats in six species in eastern North America have died from WNS since 2006, and as a result several species of bats may become endangered or extinct. Information is lacking on the pathogenesis of G. destructans and WNS, WNS transmission and maintenance, individual and site factors that contribute to the probability of an outbreak of WNS, and spatial dynamics of WNS spread in North America. We considered how descriptive and analytical epidemiology could be used to fill these information gaps, including a four-step (modified) outbreak investigation, application of a set of criteria (Hill's) for assessing causation, compartment models of disease dynamics, and spatial modeling. We cataloged and critiqued adaptive-management options that have been either previously proposed for WNS or were helpful in addressing other emerging diseases of wild animals. These include an ongoing program of prospective surveillance of bats and hibernacula for WNS, treatment of individual bats, increasing population resistance to WNS (through vaccines, immunomodulators, or other methods), improving probability of survival from starvation and dehydration associated with WNS, modifying hibernacula environments to eliminate G. destructans, culling individuals or populations, controlling anthropogenic spread of WNS, conserving genetic diversity of bats, and educating the public about bats and bat conservation issues associated with WNS.

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Section: Knowledge Gapsmentioning

confidence: 99%

Investigating and Managing the Rapid Emergence of White-Nose Syndrome, a Novel, Fatal, Infectious Disease of Hibernating Bats

Foley

Clifford

Castle

et al. 2011

Conservation Biology

110

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“…We use CA model where the finite set of states

can be observed in the cellular two-dimensional space

, with

rows and

columns iterated by

and

, respectively. The CA system is defined by tuple

, where

is a function of the Moore neighborhood( del Rey et al, 2006 , Delorme, 1999 ) with a distance of one and

is a local transition function

cell at the

instant of time. Fig.1 shows the example of a state of an

–th cell at the time

described by equations where

is the whole population of the

cell,

and

are respectively numbers of susceptible and recovered individuals and

and

are the numbers of exposed and infective individuals in a

–th day of the given stage of an infection, where

and

are the periods of exposed and infective stages in days.…”

Section: Numerical Epidemic Modelmentioning

confidence: 99%

Numerical simulation of the novel coronavirus spreading

Mędrek

Pastuszak

2021

Expert Systems with Applications

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The COVID-19 virus outbreak has affected most of the world in 2020. This paper deals with artificial intelligence (AI) methods that can address the problem of predicting scale, dynamics and sensitivity of the outbreak to preventive actions undertaken with a view to combatting the epidemic. In our study, we developed a cellular automata (CA) model for simulating the COVID-19 disease spreading. The enhanced infectious disease dynamics (Susceptible, Exposed, Infectious, and Recovered) model was applied to estimate the epidemic trends in Poland, France, and Spain. We introduced new parameters into the simulation framework which reflect the statistically confirmed dependencies such as age-dependent death probability, a different definition of the contact rate and enhanced parameters reflecting population mobility. To estimate key epidemiological measures and to predict possible dynamics of the disease, we juxtaposed crucial CA framework parameters to the reported COVID-19 values, e.g. length of infection, mortality rates and the reproduction number. Moreover, we used real population density and age structures of the studied epidemic populations. The model presented allows for the examination of the effectiveness of preventive actions and their impact on the spreading rate and the duration of the disease. It also shows the influence of structure and behavior of the populations studied on key epidemic parameters, such as mortality and infection rates. Although our results are critically dependent on the assumptions underpinning our model and there is considerable uncertainty associated with the outbreaks at such an early epidemic stage, the obtained simulation results seem to be in general agreement with the observed behavior of the real COVID-19 disease, and our numerical framework can be effectively used to analyze the dynamics and efficacy of epidemic containment methods.

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“…As far as μ is concerned, however, we attempt a first rough estimate based on deductions derived from cellular fluid mechanics [104], and on available data for transport through TNTs [20].…”

Section: The Modelmentioning

confidence: 99%

A New Hypothesis of Pathogenesis Based on the Divorce between Mitochondria and their Host Cells: Possible Relevance for Alzheimers Disease

Lf¹,

Guidolin

Baluška³

et al. 2010

CAR

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On the basis of not only the endosymbiotic theory of eukaryotic cell organization and evolution but also of observations of transcellular communication via Tunneling NanoTubes (TNTs), the hypothesis is put forward that when mitochondria, which were once independently living prokaryote-like organisms, are subjected to detrimental genetic, toxic, or environmental conditions, including age-related endogenous factors, they can regress towards their original independent state. At that point, they can become potentially pathogenic intruders within their eukaryotic host cell. Because of the protoplasmic disequilibrium caused by an altered, or mutated, mitochondral population, certain host cells with a minimal capacity for self-renewal, such as dopaminergic neurons, risk a loss of function and degenerate. It is also proposed that altered mitochondria, as well as their mutated mtDNA, can migrate, via TNTs, into adjacent cells. In this way, neurodegenerative states are propagated between cells (glia and/or neurons) of the Central Nervous System (CNS) and that this leads to conditions such as Alzheimer's and Parkinson's disease. This proposal finds indirect support from observations on rotenone-poisoned glioblastoma cells which have been co-cultured with non-poisoned cells. Immunocytochemical techniques revealed that mitochondria, moving along the TNTs, migrated from the poisoned cells towards the healthy cells. It has also been demonstrated by means of immunocytochemistry that, in glioblastoma cell cultures, Amyloid Precursor Protein (APP) is present in TNTs, hence it may migrate from one cell to neighbouring cells. This datum may be of high relevance for a better understanding of Alzheimer's Disease (AD) since molecular, cellular, and animal model studies have revealed that the formation of amyloid beta (Abeta) and other derivatives of the APP are key pathogenic factors in AD, causing mitochondrial dysfunction, free radical generation, oxidative damage, and inflammation. Furthermore, the present data demonstrate the presence of alpha-synuclein (alpha-syn) within TNTs, hence a similar pathogenic mechanism to the one surmised for AD, but centred on alpha-syn rather than on Abeta, may play a role in Parkinson's Disease (PD). As a matter of fact, alpha-syn can enter mitochondria and interact with complex I causing respiratory deficiency and increased oxygen free radical production. In agreement with this view, it has been demonstrated that, in comparison with normal subjects, PD patients show a significant accumulation of alpha-syn at Substantia Nigra and Striatal level, predominantly associated with the inner mitochondrial membrane,. These observations suggest that potentially neuropathogenic proteins, such as Abeta and alpha-syn, can not only diffuse via the extracellular space but also move from cell to cell also via TNTs where they can cause mitochondrial damage and cell degeneration. A mathematical model (see Appendix) is proposed to simulate the pathogenic consequences of the migration of altered mitochondria and/or of ...

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A Model Based on Cellular Automata to Simulate Epidemic Diseases

Cited by 14 publications

References 12 publications

Investigating and Managing the Rapid Emergence of White-Nose Syndrome, a Novel, Fatal, Infectious Disease of Hibernating Bats

Investigating and Managing the Rapid Emergence of White-Nose Syndrome, a Novel, Fatal, Infectious Disease of Hibernating Bats

Numerical simulation of the novel coronavirus spreading

A New Hypothesis of Pathogenesis Based on the Divorce between Mitochondria and their Host Cells: Possible Relevance for Alzheimers Disease

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