426 research outputs found
Can exercise affect immune function to increase susceptibility to infection?
Multiple studies in humans and animals have demonstrated the profound impact that exercise can have on the immune system. There is a general consensus that regular bouts of short-lasting (i.e. up to 45 minutes) moderate intensity exercise is beneficial for host immune defense, particularly in older adults and people with chronic diseases. In contrast, infection burden is reported to be high among high performance athletes and second only to injury for the number of training days lost during preparation for major sporting events. This has shaped the common view that arduous exercise (i.e. those activities practiced by high performance athletes/ military personnel that greatly exceed recommended physical activity guidelines) can suppress immunity and increase infection risk. However, the idea that exercise per se can suppress immunity and increase infection risk independently of the many other factors (e.g. anxiety, sleep disruption, travel, exposure, nutritional deficits, environmental extremes, etc.) experienced by these populations has recently been challenged. The purpose of this debate article was to solicit opposing arguments centered around this fundamental question in the exercise immunology field: can exercise affect immune function to increase susceptibility to infection. Issues that were contested between the debating groups include: (i) whether or not athletes are more susceptible to infection (mainly of the upper respiratory tract) than the general population; (ii) whether exercise per se is capable of altering immunity to increase infection risk independently of the multiple factors that activate shared immune pathways and are unique to the study populations involved; (iii) the usefulness of certain biomarkers and the interpretation of in vitro and in vivo data to monitor immune health in those who perform arduous exercise; and (iv) the quality of scientific evidence that has been used to substantiate claims for and against the potential negative effects of arduous exercise on immunity and infection risk. A key point of agreement between the groups is that infection susceptibility has a multifactorial underpinning. An issue that remains to be resolved is whether exercise per se is a causative factor of increased infection risk in athletes. This article should provide impetus for more empirical research to unravel the complex questions that surround this contentious issue in the field of exercise immunology
A General Model of Dynamics on Networks with Graph Automorphism Lumping
In this paper we introduce a general Markov chain model of dynamical processes on networks. In this model, nodes in the network can adopt a finite number of states and transitions can occur that involve multiple nodes changing state at once. The rules that govern transitions only depend on measures related to the state and structure of the network and not on the particular nodes involved. We prove that symmetries of the network can be used to lump equivalent states in state-space. We illustrate how several examples of well-known dynamical processes on networks correspond to particular cases of our general model. This work connects a wide range of models specified in terms of node-based dynamical rules to their exact continuous-time Markov chain formulation
Slightly generalized Generalized Contagion: Unifying simple models of biological and social spreading
We motivate and explore the basic features of generalized contagion, a model
mechanism that unifies fundamental models of biological and social contagion.
Generalized contagion builds on the elementary observation that spreading and
contagion of all kinds involve some form of system memory. We discuss the three
main classes of systems that generalized contagion affords, resembling: simple
biological contagion; critical mass contagion of social phenomena; and an
intermediate, and explosive, vanishing critical mass contagion. We also present
a simple explanation of the global spreading condition in the context of a
small seed of infected individuals.Comment: 8 pages, 5 figures; chapter to appear in "Spreading Dynamics in
Social Systems"; Eds. Sune Lehmann and Yong-Yeol Ahn, Springer Natur
Network segregation in a model of misinformation and fact checking
Misinformation under the form of rumor, hoaxes, and conspiracy theories
spreads on social media at alarming rates. One hypothesis is that, since social
media are shaped by homophily, belief in misinformation may be more likely to
thrive on those social circles that are segregated from the rest of the
network. One possible antidote is fact checking which, in some cases, is known
to stop rumors from spreading further. However, fact checking may also backfire
and reinforce the belief in a hoax. Here we take into account the combination
of network segregation, finite memory and attention, and fact-checking efforts.
We consider a compartmental model of two interacting epidemic processes over a
network that is segregated between gullible and skeptic users. Extensive
simulation and mean-field analysis show that a more segregated network
facilitates the spread of a hoax only at low forgetting rates, but has no
effect when agents forget at faster rates. This finding may inform the
development of mitigation techniques and overall inform on the risks of
uncontrolled misinformation online
Beyond clustering: mean-field dynamics on networks with arbitrary subgraph composition
Clustering is the propensity of nodes that share a common neighbour to be connected. It is ubiquitous in many networks but poses many modelling challenges. Clustering typically manifests itself by a higher than expected frequency of triangles, and this has led to the principle of constructing networks from such building blocks. This approach has been generalised to networks being constructed from a set of more exotic subgraphs. As long as these are fully connected, it is then possible to derive mean-field models that approximate epidemic dynamics well. However, there are virtually no results for non-fully connected subgraphs. In this paper, we provide a general and automated approach to deriving a set of ordinary differential equations, or mean-field model, that describes, to a high degree of accuracy, the expected values of system-level quantities, such as the prevalence of infection. Our approach offers a previously unattainable degree of control over the arrangement of subgraphs and network characteristics such as classical node degree, variance and clustering. The combination of these features makes it possible to generate families of networks with different subgraph compositions while keeping classical network metrics constant. Using our approach, we show that higher-order structure realised either through the introduction of loops of different sizes or by generating networks based on different subgraphs but with identical degree distribution and clustering, leads to non-negligible differences in epidemic dynamics
Exact analysis of summary statistics for continuous-time discrete-state Markov processes on networks using graph-automorphism lumping
We propose a unified framework to represent a wide range of continuous-time discrete-state Markov processes on networks, and show how many network dynamics models in the literature can be represented in this unified framework. We show how a particular sub-set of these models, referred to here as single-vertex-transition (SVT) processes, lead to the analysis of quasi-birth-and-death (QBD) processes in the theory of continuous-time Markov chains. We illustrate how to analyse a number of summary statistics for these processes, such as absorption probabilities and first-passage times. We extend the graph-automorphism lumping approach [Kiss, Miller, Simon, Mathematics of Epidemics on Networks, 2017; Simon, Taylor, Kiss, J. Math. Bio. 62(4), 2011], by providing a matrix-oriented representation of this technique, and show how it can be applied to a very wide range of dynamical processes on networks. This approach can be used not only to solve the master equation of the system, but also to analyse the summary statistics of interest. We also show the interplay between the graph-automorphism lumping approach and the QBD structures when dealing with SVT processes. Finally, we illustrate our theoretical results with examples from the areas of opinion dynamics and mathematical epidemiology
Rate Equations for Graphs
In this paper, we combine ideas from two different scientific traditions: 1)
graph transformation systems (GTSs) stemming from the theory of formal
languages and concurrency, and 2) mean field approximations (MFAs), a
collection of approximation techniques ubiquitous in the study of complex
dynamics. Using existing tools from algebraic graph rewriting, as well as new
ones, we build a framework which generates rate equations for stochastic GTSs
and from which one can derive MFAs of any order (no longer limited to the
humanly computable). The procedure for deriving rate equations and their
approximations can be automated. An implementation and example models are
available online at https://rhz.github.io/fragger. We apply our techniques and
tools to derive an expression for the mean velocity of a two-legged walker
protein on DNA.Comment: to be presented at the 18th International Conference on Computational
Methods in Systems Biology (CMSB 2020
Epidemics on contact networks: a general stochastic approach
Dynamics on networks is considered from the perspective of Markov stochastic
processes. We partially describe the state of the system through network motifs
and infer any missing data using the available information. This versatile
approach is especially well adapted for modelling spreading processes and/or
population dynamics. In particular, the generality of our systematic framework
and the fact that its assumptions are explicitly stated suggests that it could
be used as a common ground for comparing existing epidemics models too complex
for direct comparison, such as agent-based computer simulations. We provide
many examples for the special cases of susceptible-infectious-susceptible (SIS)
and susceptible-infectious-removed (SIR) dynamics (e.g., epidemics propagation)
and we observe multiple situations where accurate results may be obtained at
low computational cost. Our perspective reveals a subtle balance between the
complex requirements of a realistic model and its basic assumptions.Comment: Main document: 16 pages, 7 figures. Electronic Supplementary Material
(included): 6 pages, 1 tabl
Local variation of hashtag spike trains and popularity in Twitter
We draw a parallel between hashtag time series and neuron spike trains. In
each case, the process presents complex dynamic patterns including temporal
correlations, burstiness, and all other types of nonstationarity. We propose
the adoption of the so-called local variation in order to uncover salient
dynamics, while properly detrending for the time-dependent features of a
signal. The methodology is tested on both real and randomized hashtag spike
trains, and identifies that popular hashtags present regular and so less bursty
behavior, suggesting its potential use for predicting online popularity in
social media.Comment: 7 pages, 7 figure
Consistent approximation of epidemic dynamics on degree-heterogeneous clustered networks
Realistic human contact networks capable of spreading infectious disease, for example studied in social contact surveys, exhibit both significant degree heterogeneity and clustering, both of which greatly affect epidemic dynamics. To understand the joint effects of these two network properties on epidemic dynamics, the effective degree model of Lindquist et al. [28] is reformulated with a new moment closure to apply to highly clustered networks. A simulation study comparing alternative ODE models and stochastic simulations is performed for SIR (Susceptible–Infected–Removed) epidemic dynamics, including a test for the conjectured error behaviour in [40], providing evidence that this novel model can be a more accurate approximation to epidemic dynamics on complex networks than existing approaches
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