BiosystemsPub Date : 2025-10-22DOI: 10.1016/j.biosystems.2025.105630
Shouwei Li , Bo Peng , Baochen Li , Yan Shi
{"title":"Cooperation in structured populations via coupled reputation and learning: A spatial evolutionary game approach","authors":"Shouwei Li , Bo Peng , Baochen Li , Yan Shi","doi":"10.1016/j.biosystems.2025.105630","DOIUrl":"10.1016/j.biosystems.2025.105630","url":null,"abstract":"<div><div>This study presents an agent-based model to investigate cooperation dynamics in spatial evolutionary games by integrating memory-based reputation tracking with heterogeneous adaptive learning. Agents interact on a lattice network and update their strategies based on both neighbors’ historical cooperation rates and payoff differences, governed by a modified Fermi rule with individual sensitivity parameters. Simulation results demonstrate that this dual-layered mechanism sustains cooperation even under strong defection incentives and limited interaction ranges. The model also reveals how memory length and learning heterogeneity jointly influence spatial cooperation patterns and strategy diversity. These findings offer new insights into decentralized mechanisms that promote cooperation in structured populations, with implications for evolutionary biology, distributed systems, and behavioral economics.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105630"},"PeriodicalIF":1.9,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145365332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-16DOI: 10.1016/j.biosystems.2025.105620
Nalini Devi K. , Srinivasa G.
{"title":"Spectral bounds for Sombor and Sombor energy indices: A graph-theoretic study of neurotransmitter molecular networks","authors":"Nalini Devi K. , Srinivasa G.","doi":"10.1016/j.biosystems.2025.105620","DOIUrl":"10.1016/j.biosystems.2025.105620","url":null,"abstract":"<div><div>This paper applies the recently introduced Sombor index and its spectral extension, the Sombor energy, to model and analyze the structural complexity of neurotransmitter molecular graphs. Let <span><math><mi>G</mi></math></span> denote a molecular graph whose vertices and edges correspond to atoms and covalent bonds, respectively. For each <span><math><mi>G</mi></math></span>, we compute <span><math><mrow><mi>S</mi><mi>O</mi><mrow><mo>(</mo><mi>G</mi><mo>)</mo></mrow></mrow></math></span> and <span><math><mrow><mi>S</mi><mi>O</mi><mi>E</mi><mrow><mo>(</mo><mi>G</mi><mo>)</mo></mrow></mrow></math></span>, and derive degree-based, spectral-radius, and Frobenius-norm bounds to quantify molecular irregularity. Unlike traditional indices such as Zagreb or Wiener, Sombor descriptors incorporate both degree heterogeneity and geometric weighting, offering refined sensitivity to branching and aromaticity. Comparative analysis across inhibitory (glycine, GABA) and excitatory or modulatory (dopamine, serotonin, norepinephrine) neurotransmitters reveals that higher Sombor measures correspond to greater structural and functional complexity. These results confirm that Sombor-based descriptors capture biologically interpretable differences in molecular organization. The study thereby extends spectral graph theory to neurochemical systems, providing a quantitative framework for cheminformatics, drug design, and functional classification of neurotransmitters.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105620"},"PeriodicalIF":1.9,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-14DOI: 10.1016/j.biosystems.2025.105618
P.G. Tello , S. Kauffman
{"title":"When Maxwell’s Demon leaves the room","authors":"P.G. Tello , S. Kauffman","doi":"10.1016/j.biosystems.2025.105618","DOIUrl":"10.1016/j.biosystems.2025.105618","url":null,"abstract":"<div><div>This work revisits the Maxwell Demon paradigm to explore its implications for evolutionary dynamics from an information-theoretic perspective. By removing the Demon as an intentional agent, we reinterpret the emergence of order as a natural outcome of physical laws combined with stochastic processes. Using models inspired by information theory, such as binary and Z-channels, we show how random fluctuations (e.g., stochastic resonance) can decrease entropy, generate mutual information, and induce non-ergodicity. These dynamics highlight the role of memory and correlation as emergent features of purely physical interactions without recourse to purposeful agency. In this framework, evolutionary exaptations, rather than sole adaptations, emerge as key drivers of biological evolution. Finally, we connect our analysis with recent contributions on agency and memory, underscoring the relevance of informational concepts for understanding the purposeless yet structured dynamics of evolutionary processes.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105618"},"PeriodicalIF":1.9,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145309894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-13DOI: 10.1016/j.biosystems.2025.105615
Luca Zamboni
{"title":"The threat of asymptomatic carriers and the benefits of testing","authors":"Luca Zamboni","doi":"10.1016/j.biosystems.2025.105615","DOIUrl":"10.1016/j.biosystems.2025.105615","url":null,"abstract":"<div><div>I present a model of infectious disease transmission with asymptomatic carriers, social distancing, and diagnostic testing. First, I study the impact of asymptomatic carriers on the spread of an infectious disease in the absence of testing, to determine when their presence increases the overall prevalence of symptomatic infection and hence unhealthy agents. Then, I consider mass testing and isolation policies to identify and isolate asymptomatic carriers, and incorporate them into my model. I establish that diagnostic testing successfully reduces steady state disease prevalence. I then explore the implications of testing accuracy, explicitly studying the impact of false positive and false negative test results. I find that reducing the rate of false negatives is unambiguously beneficial, since it improves the identification and isolation of asymptomatic carriers. In contrast, reducing the rate of false positives can be detrimental: by limiting the unintended isolation of susceptible individuals, lower rates of false positives reduce the overall level of social distancing in the population and increase disease spread. Hence, I demonstrate how, under certain conditions, false positive results can improve social welfare.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105615"},"PeriodicalIF":1.9,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145304079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-11DOI: 10.1016/j.biosystems.2025.105610
Kevin Hudnall
{"title":"Information and the living tree of life A theory of measurement grounded in biology.","authors":"Kevin Hudnall","doi":"10.1016/j.biosystems.2025.105610","DOIUrl":"https://doi.org/10.1016/j.biosystems.2025.105610","url":null,"abstract":"<p><p>We extend a formal framework that previously derived time from the multifractal structure of biological lineages (Hudnall & D'Souza, 2025). That work showed that time itself is multifractal - not a universal background dimension, but an observer-dependent geometry. Here we develop the corresponding theory of measurement: showing that a multifractal conception of time not only permits measurement, but grounds it more rigorously in the structure of biology. The tree of life is modeled as the outcome of stochastic, convex branching, and we show how information-theoretic and fractal measures render its multifractal geometry into measurable, observer-relative time intervals. At the core is a dilation equation that expresses relative time elapse between entities as dimensionless ratios. Operational standards such as the SI second remain valid, but our framework makes explicit their lineage-dependence. This framework unifies measurement theory with biological form, preserves full compatibility with established science, and provides a biologically grounded theory of observation. It enables comparative analyses of duration and kinematics across lineages, with predictions that are directly open to experimental validation.</p>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":" ","pages":"105610"},"PeriodicalIF":1.9,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145287622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-11DOI: 10.1016/j.biosystems.2025.105608
Ian Todd
{"title":"The limits of falsifiability: Dimensionality, measurement thresholds, and the sub-Landauer domain in biological systems","authors":"Ian Todd","doi":"10.1016/j.biosystems.2025.105608","DOIUrl":"10.1016/j.biosystems.2025.105608","url":null,"abstract":"<div><div>Karl Popper’s falsifiability criterion assumes that scientific hypotheses can be reduced to binary tests. We show this assumption is <em>scale-dependent</em> and can <em>saturate</em> in high-dimensional biological systems operating near physical measurement limits, especially near criticality. In neural networks, much relevant information exists as patterns below the Landauer threshold for irreversible bit recording—signals too weak for individual neurons to detect but detectable when pooled across populations. These sub-threshold patterns cannot be projected into binary outcomes without destroying their causal structure. We develop a framework connecting dimensionality, thermodynamic measurement limits, and biological epistemology, showing that Popperian logic represents a special case applicable only to low-dimensional systems with strong signals. Our analysis has implications for neuroscience, where aspects of conscious processing may in part depend on sub-threshold coherence patterns that resist binary measurement, motivating a shift from single-case hypothesis tests to multi-scale, ensemble-based inference. The framework extends to other complex biological systems including ecological networks, protein folding dynamics, and evolutionary processes where causal relationships exist as irreducible multi-dimensional structures operating below classical measurement thresholds.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105608"},"PeriodicalIF":1.9,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145287667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-11DOI: 10.1016/j.biosystems.2025.105616
J. Menezes , R. Menezes , S. Batista , E. Rangel
{"title":"Antagonistic coinfection in rock–paper–scissors models during concurrent epidemics","authors":"J. Menezes , R. Menezes , S. Batista , E. Rangel","doi":"10.1016/j.biosystems.2025.105616","DOIUrl":"10.1016/j.biosystems.2025.105616","url":null,"abstract":"<div><div>We investigate the dynamics of dual disease epidemics within the spatial rock–paper–scissors model. In this framework, individuals from all species are equally susceptible to infection by two distinct pathogens transmitted via person-to-person contact. We assume antagonistic mortality, where the simultaneous occurrence of coinfection reduces the probability of host mortality due to complications arising from either coexisting disease. Specifically, we explore two scenarios: global antagonism, where the presence of one pathogen inhibits the progression of the other in coinfected hosts, and uneven antagonism, where only one pathogen affects the development of the other. Using stochastic simulations, we show that the characteristic length scale of the spatial patterns emerging from random initial conditions diminishes as antagonism becomes more significant. We find that antagonism enhances species population growth and reduces the average probability of healthy organisms becoming infected. Additionally, introducing individuals’ mobility restrictions significantly decreases both organisms’ infection risk and selection pressures. Our results demonstrate that combining mobility restrictions with antagonistic coinfection can increase organisms’ life expectancy by up to 54%. Our findings show that integrating antagonistic coinfection and mobility restriction strategies into ecological models may provide insights into designing interventions for managing concurrent epidemics in complex systems.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105616"},"PeriodicalIF":1.9,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-11DOI: 10.1016/j.biosystems.2025.105617
Carey Witkov
{"title":"A hybrid phase-synchronization framework for rotary motors: Discrete dynamics in ATP synthase and continuous dynamics in the bacterial flagellar motor","authors":"Carey Witkov","doi":"10.1016/j.biosystems.2025.105617","DOIUrl":"10.1016/j.biosystems.2025.105617","url":null,"abstract":"<div><div>ATP synthase functions as a dual-rotor molecular motor, with the F<span><math><msub><mrow></mrow><mrow><mn>0</mn></mrow></msub></math></span> and F<span><math><msub><mrow></mrow><mrow><mn>1</mn></mrow></msub></math></span> units stepping in mismatched increments, yet achieving near 100% chemomechanical efficiency of the F<span><math><msub><mrow></mrow><mrow><mn>1</mn></mrow></msub></math></span> motor under near-reversible conditions. This raises the question of how stable phase synchronization is maintained despite such symmetry mismatch. We address this problem by modeling ATP synthase as a driven oscillator system in which the central elastic stalk acts as a torsional filter, transmitting and modulating torque. We propose a hybrid synchronization model that integrates continuous and discrete dynamics, governed by a torsional energy-dependent mixing parameter that determines interpolation between limits. The resulting single hybrid phase synchronization equation captures both gradual continuous phase drift and discrete pulsed entrainment. This framework reproduces key experimental features, including stable synchronization, intermittent slip events in ATP synthase, and recovery dynamics under varying loads, and offers testable predictions. In the discrete limit, the model specializes to a van Slooten-type pulse map that accords with the well-established 120° stepping of F<span><math><msub><mrow></mrow><mrow><mn>1</mn></mrow></msub></math></span>-ATPase; in the continuous limit, it reduces to an Adler-type equation appropriate for the near-constant-torque behavior of the bacterial flagellar motor. This framing unifies two historically separate descriptions without requiring a literal mode change within a single molecule and clarifies how elastic energy can interpolate between limits via the mixing parameter <span><math><mrow><mi>σ</mi><mrow><mo>(</mo><mi>E</mi><mo>)</mo></mrow></mrow></math></span>. The hybrid model proposes that ATP synthase and the bacterial flagellar motor exploit elastic filtering and energy-regulated regime interpolation between limits to achieve robust rotational coordination, providing new insights into the dynamics of biological rotary motors.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105617"},"PeriodicalIF":1.9,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145287714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-10DOI: 10.1016/j.biosystems.2025.105619
Aleck H. Alexopoulos
{"title":"Corrigendum to “Pandemic preparedness and new model developments for airborne diseases transmitting via aerosols” [BioSystems 255 (2025) 105532]","authors":"Aleck H. Alexopoulos","doi":"10.1016/j.biosystems.2025.105619","DOIUrl":"10.1016/j.biosystems.2025.105619","url":null,"abstract":"","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"257 ","pages":"Article 105619"},"PeriodicalIF":1.9,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiosystemsPub Date : 2025-10-10DOI: 10.1016/j.biosystems.2025.105621
Thomas Lissek
{"title":"Maladaptation diseases as disorders of intraorganismal individuation","authors":"Thomas Lissek","doi":"10.1016/j.biosystems.2025.105621","DOIUrl":"10.1016/j.biosystems.2025.105621","url":null,"abstract":"<div><div>The present work introduces the hypothesis that various human maladaptation diseases including addiction, cancer, autoimmunity, fibrosis, depression, chronic pain and post-traumatic stress disorder share a universal functional pattern in that they are caused by defects in goal state integration of physiological subsystems into whole-organism goal states and by the resulting emergence of new levels of individuality within the organism. In this framework, a general mechanism in ontogenetic maladaptation is the intraorganismal individuation of subsystems via physiological adaptation mechanisms, which results in these systems becoming uncoupled from the rest of the organism and developing disproportional autonomy at the cost of whole organism health. A central mechanism for mediating continued dysfunction in these disorders is the formation and maintenance of maladaptive memories. A potential universal therapeutic principle for maladaptation disorders is to provide physiological integration pressure to force subsystems to integrate back into the functional organization of the whole organism.</div></div>","PeriodicalId":50730,"journal":{"name":"Biosystems","volume":"258 ","pages":"Article 105621"},"PeriodicalIF":1.9,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}