Pub Date : 2025-10-28DOI: 10.1016/j.jtbi.2025.112291
Jacob M. Jepson , Leah R. Band
In the seedling, sucrose synthesised within the leaves is transported via the phloem throughout the plant for growth and maintenance. Sucrose allocation between the root and shoot thus determines their relative growth; however, our understanding of how phloem characteristics affects sucrose allocation remains incomplete. In this paper, we develop and analyse a mathematical model that describes phloem sucrose transport in the Arabidopsis thaliana seedling, from a source region in a leaf to a sink region in either the root or shoot. Motivated by experimental observations in Arabidopsis seedlings, we assume sucrose unloading occurs via both bulk flow and diffusion. Moreover, we extend previous models by assuming that the phloem water and sucrose are unloaded via two different microscopic channels traversing the phloem boundary (plasmodesmata and aquaporins), the density of which vary along the phloem. Numerical solutions of our mathematical model predict that differences between the plasmodesmatal fluxes in the root or shoot (which are controlled by plasmodesmatal number and aperture) are the dominant mechanism controlling root-shoot sucrose allocation. We predict that while the sucrose concentration external to the phloem affects the relative diffusive and advective unloading, it has limited affect on sucrose allocation. Furthermore, we predict that negative pressure gradients external to the phloem (due to the xylem, for example) can inhibit sucrose allocation to the root. However, the model predicts that the Arabidopsis thaliana seedling modelled here can alleviate this effect by increasing the plasmodesmatal conductivity within the root.
{"title":"Sucrose transport to the root and shoot in the seedling phloem","authors":"Jacob M. Jepson , Leah R. Band","doi":"10.1016/j.jtbi.2025.112291","DOIUrl":"10.1016/j.jtbi.2025.112291","url":null,"abstract":"<div><div>In the seedling, sucrose synthesised within the leaves is transported via the phloem throughout the plant for growth and maintenance. Sucrose allocation between the root and shoot thus determines their relative growth; however, our understanding of how phloem characteristics affects sucrose allocation remains incomplete. In this paper, we develop and analyse a mathematical model that describes phloem sucrose transport in the <em>Arabidopsis thaliana</em> seedling, from a source region in a leaf to a sink region in either the root or shoot. Motivated by experimental observations in <em>Arabidopsis</em> seedlings, we assume sucrose unloading occurs via both bulk flow and diffusion. Moreover, we extend previous models by assuming that the phloem water and sucrose are unloaded via two different microscopic channels traversing the phloem boundary (plasmodesmata and aquaporins), the density of which vary along the phloem. Numerical solutions of our mathematical model predict that differences between the plasmodesmatal fluxes in the root or shoot (which are controlled by plasmodesmatal number and aperture) are the dominant mechanism controlling root-shoot sucrose allocation. We predict that while the sucrose concentration external to the phloem affects the relative diffusive and advective unloading, it has limited affect on sucrose allocation. Furthermore, we predict that negative pressure gradients external to the phloem (due to the xylem, for example) can inhibit sucrose allocation to the root. However, the model predicts that the <em>Arabidopsis thaliana</em> seedling modelled here can alleviate this effect by increasing the plasmodesmatal conductivity within the root.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112291"},"PeriodicalIF":2.0,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145410824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-24DOI: 10.1016/j.jtbi.2025.112292
Áron Kertész, Gábor Horváth
In nature there occur various pipe structures with a triangle cross-section. An ancient example is the thin-walled triangular wing bones of extinct Pteranodon flying reptiles. Recent examples include many plant species with triangular hollow stems. However, the most widespread plant stem cross-section is circular. What can be the advantage of triangular stems over cylindrical ones, or vice versa? We provide here a novel theoretical framework for understanding the mechanical superiority of triangular plant stems to cylindrical ones. The second moment of inertia I of the cross-section determines the resistance of plant stems to stresses induced by wind-load and gravitation, because a larger I results in a greater mechanical resistance. Based on I, a study has shown a particular advantage of square cross-sections over circular ones under certain geometrical parameter configurations. Using the analytical methods of this earlier study, we calculate and compare here the rotation-invariant second moments of inertia Itriangle and Icircle of plant stems with regular (equilateral) triangle and circle cross-sections of the same surface area. We determine those configurations of the ratio k of the inner and outer dimensions and ratio Q of the outer dimensions of the triangle and circle, for which Itriangle is larger than Icircle. If Itriangle > Icircle, then triangular stems are mechanically more resistant than cylindrical stems, which provides a definite advantage of the former over the latter.
{"title":"Comparing the biomechanics of triangular and cylindrical plant stems: When are triangular hollow structures mechanically superior to cylindrical ones?","authors":"Áron Kertész, Gábor Horváth","doi":"10.1016/j.jtbi.2025.112292","DOIUrl":"10.1016/j.jtbi.2025.112292","url":null,"abstract":"<div><div>In nature there occur various pipe structures with a triangle cross-section. An ancient example is the thin-walled triangular wing bones of extinct <em>Pteranodon</em> flying reptiles. Recent examples include many plant species with triangular hollow stems. However, the most widespread plant stem cross-section is circular. What can be the advantage of triangular stems over cylindrical ones, or <em>vice versa</em>? We provide here a novel theoretical framework for understanding the mechanical superiority of triangular plant stems to cylindrical ones. The second moment of inertia <em>I</em> of the cross-section determines the resistance of plant stems to stresses induced by wind-load and gravitation, because a larger <em>I</em> results in a greater mechanical resistance. Based on <em>I</em>, a study has shown a particular advantage of square cross-sections over circular ones under certain geometrical parameter configurations. Using the analytical methods of this earlier study, we calculate and compare here the rotation-invariant second moments of inertia <em>I</em><sub>triangle</sub> and <em>I</em><sub>circle</sub> of plant stems with regular (equilateral) triangle and circle cross-sections of the same surface area. We determine those configurations of the ratio <em>k</em> of the inner and outer dimensions and ratio <em>Q</em> of the outer dimensions of the triangle and circle, for which <em>I</em><sub>triangle</sub> is larger than <em>I</em><sub>circle</sub>. If <em>I</em><sub>triangle</sub> > <em>I</em><sub>circle</sub>, then triangular stems are mechanically more resistant than cylindrical stems, which provides a definite advantage of the former over the latter.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112292"},"PeriodicalIF":2.0,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145425357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-17DOI: 10.1016/j.jtbi.2025.112286
Michael Napoli , Rifat Sipahi , Maurizio Porfiri
Thirty years of research into activity rhythms of ant colonies have contributed an improved understanding of this fascinating form of collective behavior. Yet, little is known about how the colony size influences the intensity and tempo of the rhythms. Here, we address this knowledge gap through a two-pronged approach, combining the re-evaluation of published experimental observations on California ant, Temnothorax rudis, with the formulation of a novel mathematical model. From the analysis of published data, we discover that the period of the activity bursts is nearly independent of the colony size, while the number of ants activated during the bursts scales hypometrically with the colony size. In search of the biological mechanisms underpinning this evidence, we put forward a compartmental model consisting of three classes: active, inactive, and refractory ants. The study of the resulting system of nonlinear delay-differential equations explains the emergence of activity rhythms as stable limit cycles. The period of these limit cycles is controlled by the refractory delay for the resting phase, independently of the colony size, but their amplitude allometrically varies with the colony size due to social deactivation. During activity rhythms, ants spontaneously deactivate when socially interacting with active individuals.
{"title":"The role of colony size on activity rhythms of ants","authors":"Michael Napoli , Rifat Sipahi , Maurizio Porfiri","doi":"10.1016/j.jtbi.2025.112286","DOIUrl":"10.1016/j.jtbi.2025.112286","url":null,"abstract":"<div><div>Thirty years of research into activity rhythms of ant colonies have contributed an improved understanding of this fascinating form of collective behavior. Yet, little is known about how the colony size influences the intensity and tempo of the rhythms. Here, we address this knowledge gap through a two-pronged approach, combining the re-evaluation of published experimental observations on California ant, <em>Temnothorax rudis</em>, with the formulation of a novel mathematical model. From the analysis of published data, we discover that the period of the activity bursts is nearly independent of the colony size, while the number of ants activated during the bursts scales hypometrically with the colony size. In search of the biological mechanisms underpinning this evidence, we put forward a compartmental model consisting of three classes: active, inactive, and refractory ants. The study of the resulting system of nonlinear delay-differential equations explains the emergence of activity rhythms as stable limit cycles. The period of these limit cycles is controlled by the refractory delay for the resting phase, independently of the colony size, but their amplitude allometrically varies with the colony size due to social deactivation. During activity rhythms, ants spontaneously deactivate when socially interacting with active individuals.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112286"},"PeriodicalIF":2.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145330676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-17DOI: 10.1016/j.jtbi.2025.112300
Jian-Zhong Gao , Feng Zhang , Derek W. Dunn , Hao Wang , K.Charlotte Jandér , Rui-Wu Wang
A fundamental problem in ecology is to understand how mutualisms remain stable. The density-dependent regulations within interacting species potentially impact the persistence of these interspecific relationships. Yet few studies explore such intraspecific regulations’ role in stabilizing mutualisms. In addition, partner species often gain unequal benefits in mutualisms. To what extent such an interspecific asymmetry affects the stability of mutualisms is also poorly understood. We here developed a dynamic model for the asymmetric interaction between plants and their pollinators in nursery mutualisms, considering the intraspecific competition of each mutualist. We found that (i) a mutualism can be stabilized only if both mutualists are subject to the regulation of intraspecific competition; (ii) stabilizing the system also requires that the degree of asymmetry in benefits between mutualists must be limited to a range of ‘tolerance’, which narrows as intraspecific competition increases and even fades away with strong competition within both mutualistic species; (iii) when intraspecific competition within a species increases, the tolerant range is compressed from the side beneficial for it, with thus its partner species gaining relatively more benefit allocation; (iv) if the plant-pollinator interaction initiates from a small host plant population, these host plants must offer pollinators high levels of benefits, that can be subsequently reduced to favor plants once the mutualism has been successfully established. The agreement of empirical data to theoretical predictions suggests model reliability. These results highlight the role of intraspecific competition and the degree of benefit asymmetry between host plants and symbionts in stabilizing mutualisms.
{"title":"Intraspecific competition can stabilize asymmetric nursery pollination mutualisms","authors":"Jian-Zhong Gao , Feng Zhang , Derek W. Dunn , Hao Wang , K.Charlotte Jandér , Rui-Wu Wang","doi":"10.1016/j.jtbi.2025.112300","DOIUrl":"10.1016/j.jtbi.2025.112300","url":null,"abstract":"<div><div>A fundamental problem in ecology is to understand how mutualisms remain stable. The density-dependent regulations within interacting species potentially impact the persistence of these interspecific relationships. Yet few studies explore such intraspecific regulations’ role in stabilizing mutualisms. In addition, partner species often gain unequal benefits in mutualisms. To what extent such an interspecific asymmetry affects the stability of mutualisms is also poorly understood. We here developed a dynamic model for the asymmetric interaction between plants and their pollinators in nursery mutualisms, considering the intraspecific competition of each mutualist. We found that (i) a mutualism can be stabilized only if both mutualists are subject to the regulation of intraspecific competition; (ii) stabilizing the system also requires that the degree of asymmetry in benefits between mutualists must be limited to a range of ‘tolerance’, which narrows as intraspecific competition increases and even fades away with strong competition within both mutualistic species; (iii) when intraspecific competition within a species increases, the tolerant range is compressed from the side beneficial for it, with thus its partner species gaining relatively more benefit allocation; (iv) if the plant-pollinator interaction initiates from a small host plant population, these host plants must offer pollinators high levels of benefits, that can be subsequently reduced to favor plants once the mutualism has been successfully established. The agreement of empirical data to theoretical predictions suggests model reliability. These results highlight the role of intraspecific competition and the degree of benefit asymmetry between host plants and symbionts in stabilizing mutualisms.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112300"},"PeriodicalIF":2.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145330722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-16DOI: 10.1016/j.jtbi.2025.112299
Haruto Tomizuka , Yuuya Tachiki
Batesian mimicry is adopted by palatable prey species (mimics) to avoid predator attack by resembling unpalatable species (models). Despite numerous studies on this phenomenon, several aspects of its evolution remain unclear. One of the key questions is whether mimics can exist allopatrically from their models. Classical theory suggests that mimics should typically exist sympatrically with their models because the protection afforded to mimics relies on predators learning to associate the model’s phenotype with unpalatability. However, several studies have reported mimics that live outside the distribution range of their models. This phenomenon is called “mimics without models”. Although various hypotheses have been proposed to explain mimics without models, these hypotheses have been independently developed based on either ecological or evolutionary perspectives. In this study, we adopted eco-evolutionary dynamics, a framework that simultaneously addresses both ecological and evolutionary processes, aiming for an integrated understanding of these hypotheses. We identified that mimics without models occurred when specific conditions are satisfied by the six parameters, including carrying capacities, migration rate of mimics, migration rate of predators, and the evolution rate of mimic phenotype. As an important finding, the migration of predators should be restricted under eco-evolutionary feedback, which differed from previous predictions that considered population and evolutionary dynamics independently.
{"title":"Eco-evolutionary metapopulation dynamics of Batesian mimicry: Conditions for mimics without models","authors":"Haruto Tomizuka , Yuuya Tachiki","doi":"10.1016/j.jtbi.2025.112299","DOIUrl":"10.1016/j.jtbi.2025.112299","url":null,"abstract":"<div><div>Batesian mimicry is adopted by palatable prey species (mimics) to avoid predator attack by resembling unpalatable species (models). Despite numerous studies on this phenomenon, several aspects of its evolution remain unclear. One of the key questions is whether mimics can exist allopatrically from their models. Classical theory suggests that mimics should typically exist sympatrically with their models because the protection afforded to mimics relies on predators learning to associate the model’s phenotype with unpalatability. However, several studies have reported mimics that live outside the distribution range of their models. This phenomenon is called “mimics without models”. Although various hypotheses have been proposed to explain mimics without models, these hypotheses have been independently developed based on either ecological or evolutionary perspectives. In this study, we adopted eco-evolutionary dynamics, a framework that simultaneously addresses both ecological and evolutionary processes, aiming for an integrated understanding of these hypotheses. We identified that mimics without models occurred when specific conditions are satisfied by the six parameters, including carrying capacities, migration rate of mimics, migration rate of predators, and the evolution rate of mimic phenotype. As an important finding, the migration of predators should be restricted under eco-evolutionary feedback, which differed from previous predictions that considered population and evolutionary dynamics independently.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112299"},"PeriodicalIF":2.0,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-15DOI: 10.1016/j.jtbi.2025.112288
Wissam El Hajj , Nader El Khatib , Vitaly Volpert
Inflammation is a fundamental component of immune response, triggered by harmful stimuli to protect tissues, promote healing, and restore homeostasis. This process unfolds in distinct stages: initiation, amplification, and resolution. The transition from the amplification phase to resolution is crucial for restoring tissue homeostasis, and failure to achieve this transition can lead to chronic inflammation and the development of various diseases. Despite its importance, the biological mechanisms governing this transition remain insufficiently understood.
In this work, we develop a mathematical model to explore the interplay between pro- and anti-inflammatory mediators in inflammation resolution. The model consists of a delayed integro-differential reaction-diffusion system that captures the spatial and temporal evolution of inflammation within tissue. Specifically, the model tracks the concentrations of uninflamed cells, inflamed cells, and pro-inflammatory mediators (classically activated macrophages and pro-inflammatory cytokines), as well as anti-inflammatory mediators (alternatively activated macrophages, tissue-resident macrophages (TRM), and anti-inflammatory cytokines).
Mathematical analysis reveals several distinct states of inflammation propagation, highlighting conditions under which inflammation either resolves or transitions to chronic states. A particular focus is placed on the dynamic roles of both tissue-resident and circulating macrophages, demonstrating how these immune cells influence inflammation outcomes. Numerical simulations illustrate potential pathways toward inflammation resolution and offer biological interpretations that could inform therapeutic strategies targeting chronic inflammation.
{"title":"Local and systemic factors in the resolution of inflammation","authors":"Wissam El Hajj , Nader El Khatib , Vitaly Volpert","doi":"10.1016/j.jtbi.2025.112288","DOIUrl":"10.1016/j.jtbi.2025.112288","url":null,"abstract":"<div><div>Inflammation is a fundamental component of immune response, triggered by harmful stimuli to protect tissues, promote healing, and restore homeostasis. This process unfolds in distinct stages: initiation, amplification, and resolution. The transition from the amplification phase to resolution is crucial for restoring tissue homeostasis, and failure to achieve this transition can lead to chronic inflammation and the development of various diseases. Despite its importance, the biological mechanisms governing this transition remain insufficiently understood.</div><div>In this work, we develop a mathematical model to explore the interplay between pro- and anti-inflammatory mediators in inflammation resolution. The model consists of a delayed integro-differential reaction-diffusion system that captures the spatial and temporal evolution of inflammation within tissue. Specifically, the model tracks the concentrations of uninflamed cells, inflamed cells, and pro-inflammatory mediators (classically activated macrophages and pro-inflammatory cytokines), as well as anti-inflammatory mediators (alternatively activated macrophages, tissue-resident macrophages (TRM), and anti-inflammatory cytokines).</div><div>Mathematical analysis reveals several distinct states of inflammation propagation, highlighting conditions under which inflammation either resolves or transitions to chronic states. A particular focus is placed on the dynamic roles of both tissue-resident and circulating macrophages, demonstrating how these immune cells influence inflammation outcomes. Numerical simulations illustrate potential pathways toward inflammation resolution and offer biological interpretations that could inform therapeutic strategies targeting chronic inflammation.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112288"},"PeriodicalIF":2.0,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145310116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-15DOI: 10.1016/j.jtbi.2025.112287
Alessandra Cambi , Diane S. Lidke , Mariya Ptashnyk , Willemijn Smit , Stefanie Sonner
G protein-coupled receptors EP2 and EP4 are both activated by the lipid messenger Prostaglandin E2 (PGE2) and induce the intracellular production of cyclic AMP (cAMP), ultimately affecting gene expression. Changes in cellular responses to PGE2 can have important consequences on immunity and disease, yet a detailed understanding of the EP2-EP4 signaling network is lacking. EP2 and EP4 are often co-expressed in cells but their specific contribution to cAMP production is poorly understood. Experimental data have shown that cAMP levels differ depending on whether PGE2 triggers EP2 or EP4, or both. To better understand the underlying mechanisms and predict cellular responses to PGE2, we developed mathematical models for EP2 and EP4 cAMP signaling, including receptor crosstalk. The mathematical models qualitatively reproduce the experimentally observed cAMP levels and provide mechanistic insight into both the differences and commonalities in EP2/EP4 signaling. We found that ligand binding dynamics play a crucial role for both single-receptor signaling and inter-receptor crosstalk. Inhibition of PGE2 signaling via receptor antagonists is gaining increasing attention in tumor immunology. These mathematical models could therefore contribute to the design of more effective anti-tumor therapies targeting EP2 and EP4.
{"title":"Mathematical models for the EP2 and EP4 signaling pathways and their crosstalk","authors":"Alessandra Cambi , Diane S. Lidke , Mariya Ptashnyk , Willemijn Smit , Stefanie Sonner","doi":"10.1016/j.jtbi.2025.112287","DOIUrl":"10.1016/j.jtbi.2025.112287","url":null,"abstract":"<div><div>G protein-coupled receptors EP2 and EP4 are both activated by the lipid messenger Prostaglandin E2 (PGE2) and induce the intracellular production of cyclic AMP (cAMP), ultimately affecting gene expression. Changes in cellular responses to PGE2 can have important consequences on immunity and disease, yet a detailed understanding of the EP2-EP4 signaling network is lacking. EP2 and EP4 are often co-expressed in cells but their specific contribution to cAMP production is poorly understood. Experimental data have shown that cAMP levels differ depending on whether PGE2 triggers EP2 or EP4, or both. To better understand the underlying mechanisms and predict cellular responses to PGE2, we developed mathematical models for EP2 and EP4 cAMP signaling, including receptor crosstalk. The mathematical models qualitatively reproduce the experimentally observed cAMP levels and provide mechanistic insight into both the differences and commonalities in EP2/EP4 signaling. We found that ligand binding dynamics play a crucial role for both single-receptor signaling and inter-receptor crosstalk. Inhibition of PGE2 signaling via receptor antagonists is gaining increasing attention in tumor immunology. These mathematical models could therefore contribute to the design of more effective anti-tumor therapies targeting EP2 and EP4.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112287"},"PeriodicalIF":2.0,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-14DOI: 10.1016/j.jtbi.2025.112281
Saswati Biswas, Sudeshna Sinha
While ecosystems may experience sudden transitions to a degraded state under intensified exploitation, the impact of additional food provision in exploited patchy environments remains largely unexplored. This study investigates the trade-off between connectivity and resource allocation in mitigating tipping points that could lead to metacommunity-level population collapse. We first explore predator-prey dynamics within an isolated patch, investigating the effects of predator harvesting and additional food provision on population persistence. Our results reveal that, while additional food can rescue predators in scarcity, excessive provisioning may disrupt the trophic balance. Strategic harvesting helps mitigate this risk, but multistability across harvesting intensities complicates ecological management. Extending our analysis to a two-patch system with diffusive coupling, we find that a carefully calibrated food share ratio between patches is essential for long-term steady-state coexistence, with the required ratio modulated by coupling strength. However, beyond a critical dispersal threshold, stability can be maintained without strict adherence to a specific supply ratio. While dispersal aids in local predator rescue, higher flow can trigger a tipping point, resulting in catastrophic predator collapses across the metacommunity. Our findings reveal a potential rescue mechanism in which maintaining adequate food quality – ensuring uniformity across patches – is crucial to preventing abrupt population extinction, especially under strong connectivity. Overall, our study underscores the importance of integrating dispersal dynamics and the resource allocation mechanism in shaping ecosystem resilience, providing insight into strategies to mitigate population collapses in fragmented habitats.
{"title":"Strategic synergies: Dispersal and resource allocation in mitigating tipping cascades","authors":"Saswati Biswas, Sudeshna Sinha","doi":"10.1016/j.jtbi.2025.112281","DOIUrl":"10.1016/j.jtbi.2025.112281","url":null,"abstract":"<div><div>While ecosystems may experience sudden transitions to a degraded state under intensified exploitation, the impact of additional food provision in exploited patchy environments remains largely unexplored. This study investigates the trade-off between connectivity and resource allocation in mitigating tipping points that could lead to metacommunity-level population collapse. We first explore predator-prey dynamics within an isolated patch, investigating the effects of predator harvesting and additional food provision on population persistence. Our results reveal that, while additional food can rescue predators in scarcity, excessive provisioning may disrupt the trophic balance. Strategic harvesting helps mitigate this risk, but multistability across harvesting intensities complicates ecological management. Extending our analysis to a two-patch system with diffusive coupling, we find that a carefully calibrated food share ratio between patches is essential for long-term steady-state coexistence, with the required ratio modulated by coupling strength. However, beyond a critical dispersal threshold, stability can be maintained without strict adherence to a specific supply ratio. While dispersal aids in local predator rescue, higher flow can trigger a tipping point, resulting in catastrophic predator collapses across the metacommunity. Our findings reveal a potential rescue mechanism in which maintaining adequate food quality – ensuring uniformity across patches – is crucial to preventing abrupt population extinction, especially under strong connectivity. Overall, our study underscores the importance of integrating dispersal dynamics and the resource allocation mechanism in shaping ecosystem resilience, providing insight into strategies to mitigate population collapses in fragmented habitats.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112281"},"PeriodicalIF":2.0,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145309863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-14DOI: 10.1016/j.jtbi.2025.112282
Leonid Bunimovich , Athulya Ram
The paper continues the study of the phenomenon of local immunodeficiency in viral cross-immunoreactivity networks, with a focus on the roles and interactions between central and persistent viral variants. As usual, only the state of stable (i.e. observable) local immunodeficiency is analyzed. First, we show that a single central viral variant has an upper limit for the number of persistent viral variants that it can support. Our findings reveal that in viral cross-immunoreactivity networks, central viruses act essentially autonomously from each other. Namely, connections between central viruses change neither their qualitative roles nor the quantitative values of the strengths of their connections in the cross-immunoreactivity networks. In other words, each central virus does exactly the same actions, and has the same strengths with or without specific structural features such as central viruses. This indicates that local immunodeficiency can arise purely from the network structure. However, having more central viruses allows to keep the sizes of populations of persistent viruses at higher levels. Likewise, the strength of the immune response against any central virus remains at the same constant level regardless of how many persistent viruses this central virus supports (i.e. shields from the immune response of the host’s immune system). It is also shown that viruses strongly compete with each other in order to become persistent in the state of stable local immunodeficiency. We also present an (quite unexpected) example of a cross-immunoreactivity network with stable local immunodeficiency that only consists of persistent viral variants, which shows that persistent viruses may demonstrate a kind of self-consistency.
{"title":"Antigenic cooperation in viral populations: Maximal load on viruses and self-sufficiency of persistent viruses","authors":"Leonid Bunimovich , Athulya Ram","doi":"10.1016/j.jtbi.2025.112282","DOIUrl":"10.1016/j.jtbi.2025.112282","url":null,"abstract":"<div><div>The paper continues the study of the phenomenon of local immunodeficiency in viral cross-immunoreactivity networks, with a focus on the roles and interactions between central and persistent viral variants. As usual, only the state of stable (i.e. observable) local immunodeficiency is analyzed. First, we show that a single central viral variant has an upper limit for the number of persistent viral variants that it can support. Our findings reveal that in viral cross-immunoreactivity networks, central viruses act essentially autonomously from each other. Namely, connections between central viruses change neither their qualitative roles nor the quantitative values of the strengths of their connections in the cross-immunoreactivity networks. In other words, each central virus does exactly the same actions, and has the same strengths with or without specific structural features such as central viruses. This indicates that local immunodeficiency can arise purely from the network structure. However, having more central viruses allows to keep the sizes of populations of persistent viruses at higher levels. Likewise, the strength of the immune response against any central virus remains at the same constant level regardless of how many persistent viruses this central virus supports (i.e. shields from the immune response of the host’s immune system). It is also shown that viruses strongly compete with each other in order to become persistent in the state of stable local immunodeficiency. We also present an (quite unexpected) example of a cross-immunoreactivity network with stable local immunodeficiency that only consists of persistent viral variants, which shows that persistent viruses may demonstrate a kind of self-consistency.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112282"},"PeriodicalIF":2.0,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145310056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-07Epub Date: 2025-08-05DOI: 10.1016/j.jtbi.2025.112231
Georgio Hawi, Peter S Kim, Peter P Lee
Colorectal cancer (CRC) poses a major public health challenge due to its increasing prevalence, particularly among younger populations. Microsatellite instability-high (MSI-H) CRC and deficient mismatch repair (dMMR) CRC constitute 15 % of all CRC and exhibit remarkable responsiveness to immunotherapy, especially with PD-1 inhibitors. Despite this, there is a significant need to optimise immunotherapeutic regimens to maximise clinical efficacy and patient quality of life. To address this, we employ a novel framework driven by delay integro-differential equations to model the interactions among cancer cells, immune cells, and immune checkpoints in locally advanced MSI-H/dMMR CRC (laMCRC). Several of these components are being modelled deterministically for the first time in cancer, paving the way for a deeper understanding of the complex underlying immune dynamics. We consider two compartments: the tumour site and the tumour-draining lymph node, incorporating phenomena such as dendritic cell (DC) migration, T cell proliferation, and CD8+ T cell exhaustion and reinvigoration. Parameter values and initial conditions are derived from experimental data, integrating various pharmacokinetic, bioanalytical, and radiographic studies, along with deconvolution of bulk RNA-sequencing data from the TCGA COADREAD and GSE26571 datasets. We finally optimised neoadjuvant treatment with pembrolizumab, a widely used PD-1 inhibitor, to balance efficacy, efficiency, and toxicity in laMCRC patients. We mechanistically analysed factors influencing treatment success and improved upon currently FDA-approved therapeutic regimens for metastatic MSI-H/dMMR CRC, demonstrating that a single medium-to-high dose of pembrolizumab may be sufficient for effective tumour eradication while being efficient, safe and practical.
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