{"title":"Forecasting the changes between endemic and epidemic phases of a contagious disease, with the example of COVID-19.","authors":"Jacques Demongeot, Pierre Magal, Kayode Oshinubi","doi":"10.1093/imammb/dqae012","DOIUrl":"10.1093/imammb/dqae012","url":null,"abstract":"<p><strong>Background: </strong>Predicting the endemic/epidemic transition during the temporal evolution of a contagious disease.</p><p><strong>Methods: </strong>Indicators for detecting the transition endemic/epidemic, with four scalars to be compared, are calculated from the daily reported news cases: coefficient of variation, skewness, kurtosis and entropy. The indicators selected are related to the shape of the empirical distribution of the new cases observed over 14 days. This duration has been chosen to smooth out the effect of weekends when fewer new cases are registered. For finding a forecasting variable, we have used the principal component analysis (PCA), whose first principal component (a linear combination of the selected indicators) explains a large part of the observed variance and can then be used as a predictor of the phenomenon studied (here the occurrence of an epidemic wave).</p><p><strong>Results: </strong>A score has been built from the four proposed indicators using the PCA, which allows an acceptable level of forecasting performance by giving a realistic retro-predicted date for the rupture of the stationary endemic model corresponding to the entrance in the epidemic exponential growth phase. This score is applied to the retro-prediction of the limits of the different phases of the COVID-19 outbreak in successive endemic/epidemic transitions for three countries, France, India and Japan.</p><p><strong>Conclusion: </strong>We provided a new forecasting method for predicting an epidemic wave occurring after an endemic phase for a contagious disease.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"98-112"},"PeriodicalIF":0.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142010169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Henri Berestycki, Jean-Michel Roquejoffre, Luca Rossi
{"title":"Biological invasions and epidemics with nonlocal diffusion along a line.","authors":"Henri Berestycki, Jean-Michel Roquejoffre, Luca Rossi","doi":"10.1093/imammb/dqae014","DOIUrl":"10.1093/imammb/dqae014","url":null,"abstract":"<p><p>To James D. Murray, with our admiration. The goal of this work is to understand and quantify how a line with nonlocal diffusion given by an integral enhances a reaction-diffusion process occurring in the surrounding plane. This is part of a long-term programme where we aim at modelling, in a mathematically rigorous way, the effect of transportation networks on the speed of biological invasions or propagation of epidemics. We prove the existence of a global propagation speed and characterize in terms of the parameters of the system the situations where such a speed is boosted by the presence of the line. In the course of the study we also uncover unexpected regularity properties of the model. On the quantitative side, the two main parameters are the intensity of the diffusion kernel and the characteristic size of its support. One outcome of this work is that the propagation speed will significantly be enhanced even if only one of the two is large, thus broadening the picture that we have already drawn in our previous works on the subject, with local diffusion modelled by a standard Laplacian. We further investigate the role of the other parameters, enlightening some subtle effects due to the interplay between the diffusion in the half plane and that on the line. Lastly, in the context of propagation of epidemics, we also discuss the model where, instead of a diffusion, displacement on the line comes from a pure transport term.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"4-37"},"PeriodicalIF":0.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of diffusivity of amyloid beta monomers on the formation of senile plaques.","authors":"Andrey V Kuznetsov","doi":"10.1093/imammb/dqae019","DOIUrl":"10.1093/imammb/dqae019","url":null,"abstract":"<p><p>Alzheimer's disease (AD) presents a perplexing question: why does its development span decades, even though individual amyloid beta (Aβ) deposits (senile plaques) can form rapidly in as little as 24 hours, as recent publications suggest? This study investigated whether the formation of senile plaques can be limited by factors other than polymerization kinetics alone. Instead, their formation may be limited by the diffusion-driven supply of Aβ monomers, along with the rate at which the monomers are produced from amyloid precursor protein and the rate at which Aβ monomers undergo degradation. A mathematical model incorporating the nucleation and autocatalytic process (via the Finke-Watzky model), as well as Aβ monomer diffusion, was proposed. The obtained system of partial differential equations was solved numerically, and a simplified version was investigated analytically. The computational results predicted that it takes approximately 7 years for Aβ aggregates to reach a neurotoxic concentration of 50 μM. Additionally, a sensitivity analysis was performed to examine how the diffusivity of Aβ monomers and their production rate impact the concentration of Aβ aggregates.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"346-362"},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Avishek Mukherjee, Navid Mohammad Mirzaei, Pak-Wing Fok
{"title":"Genesis of intimal thickening due to hemodynamical shear stresses.","authors":"Avishek Mukherjee, Navid Mohammad Mirzaei, Pak-Wing Fok","doi":"10.1093/imammb/dqae018","DOIUrl":"10.1093/imammb/dqae018","url":null,"abstract":"<p><p>This paper investigates intimal growth in arteries, induced by hemodynamical shear stress, through finite element simulation using the FEniCS computational environment. In our model, the growth of the intima depends on cross-section geometry and shear stress. In this work, the arterial wall is modeled as three distinct layers: the intima, the media and the adventitia, each with different mechanical properties. We assume that the cross-section of the vessel does not change in the axial direction. We further assume that the blood flow is steady, non-turbulent and unidirectional. Blood flow induces shear stress on the endothelium and stimulates the release of platelet derived growth factor (PDGF) which drives the growth. We simulate intimal growth for three distinct arterial cross section geometries. We show that the qualitative nature of intimal thickening varies depending on arterial geometry. For cross section geometries that are annular, the growth of the intima is uniform in the angular direction, and the endothelium stays circular as the intima grows. For non-annular cross section geometries, the intima grows more quickly where it is thicker, and shear stress and intimal thickening are negatively correlated with the distance from the flow center, where the flow velocity is maximal. Over time, the maxima and minima of the curvature increase and decrease, respectively, the PDGF concentration increases and the lumen becomes more polygonal. The model provides a framework for coupling hemodynamics simulations to mathematical descriptions of atherosclerosis, both of which have been modeled separately in great detail.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"363-381"},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S J Franks, J L Dunster, S R Carding, J M Lord, M Hewison, P C Calder, J R King
{"title":"Modelling the influence of vitamin D and probiotic supplementation on the microbiome and immune response.","authors":"S J Franks, J L Dunster, S R Carding, J M Lord, M Hewison, P C Calder, J R King","doi":"10.1093/imammb/dqae017","DOIUrl":"10.1093/imammb/dqae017","url":null,"abstract":"<p><p>The intestinal microbiota play a critical role in human health and disease, maintaining metabolic and immune/inflammatory health, synthesizing essential vitamins and amino acids and maintaining intestinal barrier integrity. The aim of this paper is to develop a mathematical model to describe the complex interactions between the microbiota, vitamin D/vitamin D receptor (VDR) pathway, epithelial barrier and immune response in order to understand better the effects of supplementation with probiotics and vitamin D. This is motivated by emerging data indicating the beneficial effects of vitamin D and probiotics individually and when combined. We propose a system of ordinary differential equations determining the time evolution of intestinal bacterial populations, concentration of the VDR:1,25(OH)$_{2}$D complex in epithelial and immune cells, the epithelial barrier and the immune response. The model shows that administration of probiotics and/or vitamin D upregulates the VDR complex, which enhances barrier function and protects against intestinal inflammation. The model also suggests co-supplementation to be superior to individual supplements. We explore the effects of inflammation on the populations of commensal and pathogenic bacteria and the vitamin D/VDR pathway and discuss the value of gathering additional experimental data motivated by the modelling insights.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"304-345"},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Polymer-interface-tissue model to estimate leachable release from medical devices.","authors":"Martin L Tanaka, David M Saylor, Robert M Elder","doi":"10.1093/imammb/dqae020","DOIUrl":"10.1093/imammb/dqae020","url":null,"abstract":"<p><p>The ability to predict clinically relevant exposure to potentially hazardous compounds that can leach from polymeric components can help reduce testing needed to evaluate the biocompatibility of medical devices. In this manuscript, we compare two physics-based exposure models: 1) a simple, one-component model that assumes the only barrier to leaching is the migration of the compound through the polymer matrix and 2) a more clinically relevant, two-component model that also considers partitioning across the polymer-tissue interface and migration in the tissue away from the interface. Using data from the literature, the variation of the model parameters with key material properties were established, enabling the models to be applied to a wide range of combinations of leachable compound, polymer matrix and tissue type. Exposure predictions based on the models suggest that the models are indistinguishable over much of the range of clinically relevant scenarios. However, for systems with low partitioning and/or slow tissue diffusion, the two-component model predicted up to three orders of magnitude less mass release over the same time period. Thus, despite the added complexity, in some scenarios it can be beneficial to use the two-component model to provide more clinically relevant estimates of exposure to leachable substances from implanted devices.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"382-403"},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Beyond SIRD models: a novel dynamic model for epidemics, relating infected with entries to health care units and application for identification and restraining policy.","authors":"Christos Tsiliyannis","doi":"10.1093/imammb/dqae008","DOIUrl":"10.1093/imammb/dqae008","url":null,"abstract":"<p><p>Epidemic models of susceptibles, exposed, infected, recovered and deceased (SΕIRD) presume homogeneity, constant rates and fixed, bilinear structure. They produce short-range, single-peak responses, hardly attained under restrictive measures. Tuned via uncertain I,R,D data, they cannot faithfully represent long-range evolution. A robust epidemic model is presented that relates infected with the entry rate to health care units (HCUs) via population averages. Model uncertainty is circumvented by not presuming any specific model structure, or constant rates. The model is tuned via data of low uncertainty, by direct monitoring: (a) of entries to HCUs (accurately known, in contrast to delayed and non-reliable I,R,D data) and (b) of scaled model parameters, representing population averages. The model encompasses random propagation of infections, delayed, randomly distributed entries to HCUs and varying exodus of non-hospitalized, as disease severity subdues. It closely follows multi-pattern growth of epidemics with possible recurrency, viral strains and mutations, varying environmental conditions, immunity levels, control measures and efficacy thereof, including vaccination. The results enable real-time identification of infected and infection rate. They allow design of resilient, cost-effective policy in real time, targeting directly the key variable to be controlled (entries to HCUs) below current HCU capacity. As demonstrated in ex post case studies, the policy can lead to lower overall cost of epidemics, by balancing the trade-off between the social cost of infected and the economic contraction associated with social distancing and mobility restriction measures.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"192-224"},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142001625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inference on an interacting diffusion system with application to in vitro glioblastoma migration (publication template).","authors":"Gustav Lindwall, Philip Gerlee","doi":"10.1093/imammb/dqae010","DOIUrl":"10.1093/imammb/dqae010","url":null,"abstract":"<p><p>Glioblastoma multiforme is a highly aggressive form of brain cancer, with a median survival time for diagnosed patients of 15 months. Treatment of this cancer is typically a combination of radiation, chemotherapy and surgical removal of the tumour. However, the highly invasive and diffuse nature of glioblastoma makes surgical intrusions difficult, and the diffusive properties of glioblastoma are poorly understood. In this paper, we introduce a stochastic interacting particle system as a model of in vitro glioblastoma migration, along with a maximum likelihood-algorithm designed for inference using microscopy imaging data. The inference method is evaluated on in silico simulation of cancer cell migration, and then applied to a real data set. We find that the inference method performs with a high degree of accuracy on the in silico data, and achieve promising results given the in vitro data set.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"250-276"},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141972504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Selector of amino-acid scales set.","authors":"Anton Vrdoljak, Damir Vukičević","doi":"10.1093/imammb/dqae007","DOIUrl":"10.1093/imammb/dqae007","url":null,"abstract":"<p><p>Experimental and theoretical properties of amino acids as building blocks of peptides and proteins have been extensively researched. Each such method assigns a number to each amino acid, and one such assignment is called amino-acid scale. Their usage in bioinformatics to explain and predict behaviour of peptides and proteins is of essential value. The number of such scales is very large. There are more than a hundred scales related just to hydrophobicity. A large number of scales can be a computational burden for algorithms that try to define peptide descriptors combining several of these scales. Hence, it is of interest to construct a smaller, but still representative set of scales. Here, we present software that does this. We test it on the set of scales using a database constructed by Kawashima and collaborators and show that it is possible to significantly reduce the number of scales observed without losing much of the information. An algorithm is implemented in C#. As a result, we provide a smaller database that might be a very useful tool for the analyses and construction of new peptides. Another interesting application of this database would be to compare the artificial intelligence construction of peptides having as an input the complete Kawashima database and this reduced one. Obtaining in both cases similar results would give much credibility to the constructs of such AI algorithms.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"157-168"},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141560650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Infection spreading in tissue as a reaction-diffusion wave.","authors":"Saddam Hussain, Moitri Sen, Vitaly Volpert","doi":"10.1093/imammb/dqae009","DOIUrl":"10.1093/imammb/dqae009","url":null,"abstract":"<p><p>Viral infection develops in the organism due to virus replication inside infected cells and its transmission from infected to uninfected cells through the extracellular matrix or cell junctions. In this work, we model infection spreading in tissue with a delay reaction-diffusion system of equations for the concentrations of uninfected cells, infected cells and virus. We prove the wave existence, determine its speed of propagation and introduce a simplified one-equation model obtained from the complete model using a quasi-stationary approximation.</p>","PeriodicalId":94130,"journal":{"name":"Mathematical medicine and biology : a journal of the IMA","volume":" ","pages":"169-191"},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141622054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}