arXiv subjects

Grzegorz A. Rempała

Publications and source records attributed to Grzegorz A. Rempała.

6 recordsLinked to original sources

arXiv2026

Coloured Epidemic Models: Functional Law of Large Numbers and Propagation of Chaos

In this paper, we study a stochastic Susceptible-Infected-Removed (SIR) model where the infection and the recovery rates depend on individual covariates for susceptibility and infectiousness of the infector and the infectee. Such models allow explicit nonlinearity in the incidence term. They are also important from a practical perspective, as they allow for the incorporation of individual heterogeneity into the epidemic process. Statistical estimates for crucial epidemiological parameters, such as the basic reproduction number, herd immunity threshold, could be vastly different, and even biased, when the population heterogeneity is ignored in the mathematical model. We describe our epidemic model as an Interacting Particle System (IPS) of Stochastic Differential Equations (SDEs) driven by Poisson Random Measures. Our main mathematical contributions are a Functional Law of Large Numbers (FLLN), which approximates the empirical random measure of the IPS by means of a deterministic measure-valued function, and the propagation of chaos phenomenon, which establishes asymptotic independence of the particles as the population size goes to infinity with an explicit construction of McKean--Vlasov type Kac's ``nonlinear process''. We also briefly mention how the propagation of chaos phenomenon leads to a product-form likelihood function, which forms the basis of the so-called Dynamic Survival Analysis (DSA) method for parameter inference based on sparse data.

math.PR↗

arXiv2021

Functional Central Limit Theorem For Susceptible-Infected Process On Configuration Model Graphs

We study a stochastic compartmental susceptible-infected (SI) epidemic process on a configuration model random graph with a given degree distribution over a finite time interval $[0,T],$ for some $ T>0$. In this setting, we split the population of graph nodes into two compartments, namely, $S$ and $I$, denoting the susceptible and infected nodes, respectively. In addition to the sizes of these two compartments, we study counts of $SI$-edges (those connecting a susceptible and an infected node) and $SS$-edges (those connecting two susceptible nodes). We describe the dynamical process in terms of these counts and present a functional central limit theorem (FCLT) for them, a scaling limit of the dynamical process as $n$, the number of nodes in the random graph, grows to infinity. To be precise, we show that these counts, when appropriately scaled, converge weakly to a continuous Gaussian vector martingale process the usual Skorohod space of real 3-dimensional vector-valued \cadlag\, functions on $[0,T]$ endowed with the Skorohod topology. We assume certain technical requirements for this purpose. We discuss applications of our FCLT in percolation theory (from a non-equilibrium statistical mechanics point of view), and in computer science in the context of spread of computer viruses. We also provide simulation results for some common degree distributions.

math.PR↗

arXiv2018

The large graph limit of a stochastic epidemic model on a dynamic multilayer network

We consider an SIR-type (Susceptible $\to$ Infected $\to$ Recovered) stochastic epidemic process with multiple modes of transmission on a contact network. The network is given by a random graph following a multilayer configuration model where edges in different layers correspond to potentially infectious contacts of different types. We assume that the graph structure evolves in response to the epidemic via activation or deactivation of edges. We derive a large graph limit theorem that gives a system of ordinary differential equations (ODEs) describing the evolution of quantities of interest, such as the proportions of infected and susceptible vertices, as the number of nodes tends to infinity. Analysis of the limiting system elucidates how the coupling of edge activation and deactivation to infection status affects disease dynamics, as illustrated by a two-layer network example with edge types corresponding to community and healthcare contacts. Our theorem extends some earlier results deriving the deterministic limit of stochastic SIR processes on static, single-layer configuration model graphs. We also describe precisely the conditions for equivalence between our limiting ODEs and the systems obtained via pair approximation, which are widely used in the epidemiological and ecological literature to approximate disease dynamics on networks. Potential applications include modeling Ebola dynamics in West Africa, which was the motivation for this study.

q-bio.PE↗

arXiv2017

Quasi-steady-state approximations derived from the stochastic model of enzyme kinetics

In this paper we derive several quasi steady-state approximations (QSSAs) to the stochastic reaction network describing the Michaelis-Menten enzyme kinetics. We show how the different assumptions about chemical species abundance and reaction rates lead to the standard QSSA (sQSSA), the total QSSA (tQSSA), and the reverse QSSA (rQSSA) approximations. These three QSSAs have been widely studied in the literature in deterministic ordinary differential equation (ODE) settings and several sets of conditions for their validity have been proposed. By using multiscaling techniques introduced in Kang (and Kurtz 2013) and Ball et al. (2006) we show that these conditions for deterministic QSSAs largely agree with the ones for QSSAs in the large volume limits of the underlying stochastic enzyme kinetic network.

q-bio.MN↗

arXiv2016

Double asymptotics for the chi-square statistic

We consider distributional limit of the Pearson chi-square statistic when the number of classes m increases with the sample size n in such way that $n/\sqrt{m} \to λ$. Under mild moment conditions, the limit is Gaussian for $λ = \infty$, Poisson for finite $λ > 0$, and degenerate for $λ = 0$.

math.PR↗

arXiv2015

Limit Theorems for Empirical Rényi Entropy and Divergence with Applications to Molecular Diversity Analysis

Quantitative methods for studying biodiversity have been traditionally rooted in the classical theory of finite frequency tables analysis. However, with the help of modern experimental tools, like high throughput sequencing, we now begin to unlock the outstanding diversity of genomic data in plants and animals reflective of the long evolutionary history of our planet. This molecular data often defies the classical frequency/contingency tables assumptions and seems to require sparse tables with very large number of categories and highly unbalanced cell counts, e.g., following heavy tailed distributions (for instance, power laws). Motivated by the molecular diversity studies, we propose here a frequency-based framework for biodiversity analysis in the asymptotic regime where the number of categories grows with sample size (an infinite contingency table). Our approach is rooted in information theory and based on the Gaussian limit results for the effective number of species (the Hill numbers) and the empirical Renyi entropy and divergence. We argue that when applied to molecular biodiversity analysis our methods can properly account for the complicated data frequency patterns on one hand and the practical sample size limitations on the other. We illustrate this principle with two specific RNA sequencing examples: a comparative study of T-cell receptor populations and a validation of some preselected molecular hepatocellular carcinoma (HCC) markers.

stat.ME↗