Pub Date : 2026-04-07Epub Date: 2025-12-03DOI: 10.1016/j.jtbi.2025.112329
Isobel R Abell, Thao P Le, Jennifer A Flegg, Christopher M Baker
Varroa destructor is a significant European honeybee pest, impacting agricultural industries globally. Since arriving in 2022, Australia faces the possibility that Varroa will become established in European honeybee colonies nationally. Australia initially pursued a strategy of testing and subsequently eliminating hives infested with Varroa. These management efforts raise interesting questions about the interplay between hive testing and elimination, and the spread of Varroa between hives. This study uses mathematical modelling to investigate how combined hive testing and elimination strategies impact the spread of Varroa through a network of European honeybee hives. We develop a model of both within-hive reproduction of Varroa and hive testing, and between-hive movement of Varroa on a network of hives. This model is used to assess the impact of various testing and hive elimination strategies on the total number of hives eliminated on the network of hives. Each model simulation starts with a single infested hive, and from this we observed one of two dynamics: either the infestation is caught before spreading, or Varroa spreads extensively through the network before being caught by testing. Within our model we implement two common hive testing methods - sugar shake and alcohol testing. A shared limitation of these testing methods is that they can only detect mites in a specific stage of their lifecycle. As such, testing is not only dependent on how many Varroa mites are in a hive, but also on what lifecycle stage the mites are in at the time of testing. By varying testing and movement parameters, we see that this testing limitation greatly impacts the number of hives eliminated in various scenarios. Furthermore, testing earlier, or testing more frequently, does not guarantee a smaller invasion. Our model results suggest irregular testing schedules, e.g. testing multiple times in close succession rather than just once in a given timeframe, may help overcome the limitations of common hive testing strategies.
{"title":"Modelling the spread and management of Varroa destructor in naive european honeybee populations.","authors":"Isobel R Abell, Thao P Le, Jennifer A Flegg, Christopher M Baker","doi":"10.1016/j.jtbi.2025.112329","DOIUrl":"10.1016/j.jtbi.2025.112329","url":null,"abstract":"<p><p>Varroa destructor is a significant European honeybee pest, impacting agricultural industries globally. Since arriving in 2022, Australia faces the possibility that Varroa will become established in European honeybee colonies nationally. Australia initially pursued a strategy of testing and subsequently eliminating hives infested with Varroa. These management efforts raise interesting questions about the interplay between hive testing and elimination, and the spread of Varroa between hives. This study uses mathematical modelling to investigate how combined hive testing and elimination strategies impact the spread of Varroa through a network of European honeybee hives. We develop a model of both within-hive reproduction of Varroa and hive testing, and between-hive movement of Varroa on a network of hives. This model is used to assess the impact of various testing and hive elimination strategies on the total number of hives eliminated on the network of hives. Each model simulation starts with a single infested hive, and from this we observed one of two dynamics: either the infestation is caught before spreading, or Varroa spreads extensively through the network before being caught by testing. Within our model we implement two common hive testing methods - sugar shake and alcohol testing. A shared limitation of these testing methods is that they can only detect mites in a specific stage of their lifecycle. As such, testing is not only dependent on how many Varroa mites are in a hive, but also on what lifecycle stage the mites are in at the time of testing. By varying testing and movement parameters, we see that this testing limitation greatly impacts the number of hives eliminated in various scenarios. Furthermore, testing earlier, or testing more frequently, does not guarantee a smaller invasion. Our model results suggest irregular testing schedules, e.g. testing multiple times in close succession rather than just once in a given timeframe, may help overcome the limitations of common hive testing strategies.</p>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":" ","pages":"112329"},"PeriodicalIF":2.0,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688186","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 : 2026-02-06DOI: 10.1016/j.jtbi.2026.112397
Houda Fahim, Mohammed Guedda, Nour Eddine Alaa
In this study, we revisit the Canham-Helfrich energy to analytically determine the equilibrium configurations of the red blood cell (RBC). By extending the work of Au and Wan Au and Wan (2003), we establish a sufficient analytical condition ensuring the existence of the biconcave equilibrium shape. This result provides a rigorous complement to previous asymptotic arguments, clarifying the mechanical balance underlying RBC morphology. Moreover, the analytical derivation of the equilibrium shape function from the Helfrich energy naturally reproduces the empirical contour equation proposed by Evans and Fung Evans and Fung (1972). This demonstrates that their experimental results can be obtained via the energy-minimization framework, thereby linking experimental observations with a consistent theoretical foundation. The present results provide both a mathematical completion and a physical unification of previous models, confirming that the biconcave RBC geometry arises as an equilibrium configuration governed by simple curvature constraints.
在这项研究中,我们重新审视canham - helrich能量来分析确定红细胞(RBC)的平衡构型。通过推广Au和Wan(2003)的工作,我们建立了保证双凹平衡形状存在的充分分析条件。这一结果为之前的渐近论证提供了严格的补充,阐明了红细胞形态下的机械平衡。此外,由helrich能量解析推导出的平衡形状函数自然再现了Evans and Fung(1972)提出的经验轮廓方程。这表明他们的实验结果可以通过能量最小化框架获得,从而将实验观察与一致的理论基础联系起来。目前的结果提供了先前模型的数学完成和物理统一,证实了双凹RBC几何结构是由简单曲率约束控制的平衡构型。
{"title":"Equilibrium red blood shape configurations to Canham-Hilfrich energy: Analytical study.","authors":"Houda Fahim, Mohammed Guedda, Nour Eddine Alaa","doi":"10.1016/j.jtbi.2026.112397","DOIUrl":"https://doi.org/10.1016/j.jtbi.2026.112397","url":null,"abstract":"<p><p>In this study, we revisit the Canham-Helfrich energy to analytically determine the equilibrium configurations of the red blood cell (RBC). By extending the work of Au and Wan Au and Wan (2003), we establish a sufficient analytical condition ensuring the existence of the biconcave equilibrium shape. This result provides a rigorous complement to previous asymptotic arguments, clarifying the mechanical balance underlying RBC morphology. Moreover, the analytical derivation of the equilibrium shape function from the Helfrich energy naturally reproduces the empirical contour equation proposed by Evans and Fung Evans and Fung (1972). This demonstrates that their experimental results can be obtained via the energy-minimization framework, thereby linking experimental observations with a consistent theoretical foundation. The present results provide both a mathematical completion and a physical unification of previous models, confirming that the biconcave RBC geometry arises as an equilibrium configuration governed by simple curvature constraints.</p>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":" ","pages":"112397"},"PeriodicalIF":2.0,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146144299","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 : 2026-02-04DOI: 10.1016/j.jtbi.2026.112396
Cristina Koprinski, Georgio Hawi, Peter S Kim
Ovarian cancer is the deadliest gynaecological cancer and the fourth leading cause of cancer deaths in women. High-grade serous ovarian cancer (HGSOC) accounts for 75% of cases, and chemotherapy resistance and relapse occur in 85% of patients, leading to a 5-year survival of 45%. Currently, the literature lacks comprehensive immunobiological models of HGSOC, and developing such models could provide critical insights into the disease's underlying mechanisms and interactions within the tumour microenvironment. We address this by constructing an immunobiological model using delay differential equations and then optimise chemotherapy regimens to maximise efficacy, minimise toxicity, and improve treatment efficiency for first-line treatment. The model consists of two compartments, the tumour site and tumour-draining lymph node, with immune processes such as dendritic cell (DC) maturation, T cell priming and proliferation, and cytokine interactions modelled. Parameter values are estimated using experimental data from ovarian cancer tissue samples as well as the TCGA OV database. The results indicate that low-dose, more frequent chemotherapy provides comparable results to the standard regimen with a lower toxicity, and alternative dosing strategies with rest weeks can allow patients to recover from the toxic side effects of chemotherapy.
{"title":"Optimising Chemotherapy for Advanced High-Grade Serous Ovarian Cancer via Delay-Differential Equations.","authors":"Cristina Koprinski, Georgio Hawi, Peter S Kim","doi":"10.1016/j.jtbi.2026.112396","DOIUrl":"https://doi.org/10.1016/j.jtbi.2026.112396","url":null,"abstract":"<p><p>Ovarian cancer is the deadliest gynaecological cancer and the fourth leading cause of cancer deaths in women. High-grade serous ovarian cancer (HGSOC) accounts for 75% of cases, and chemotherapy resistance and relapse occur in 85% of patients, leading to a 5-year survival of 45%. Currently, the literature lacks comprehensive immunobiological models of HGSOC, and developing such models could provide critical insights into the disease's underlying mechanisms and interactions within the tumour microenvironment. We address this by constructing an immunobiological model using delay differential equations and then optimise chemotherapy regimens to maximise efficacy, minimise toxicity, and improve treatment efficiency for first-line treatment. The model consists of two compartments, the tumour site and tumour-draining lymph node, with immune processes such as dendritic cell (DC) maturation, T cell priming and proliferation, and cytokine interactions modelled. Parameter values are estimated using experimental data from ovarian cancer tissue samples as well as the TCGA OV database. The results indicate that low-dose, more frequent chemotherapy provides comparable results to the standard regimen with a lower toxicity, and alternative dosing strategies with rest weeks can allow patients to recover from the toxic side effects of chemotherapy.</p>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":" ","pages":"112396"},"PeriodicalIF":2.0,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133508","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 : 2026-02-03DOI: 10.1016/j.jtbi.2026.112394
Jonatan T Kaare-Rasmussen, A Raine Detmer, Eleanor M Caves, Holly V Moeller
Cleaner shrimp engage in a mutualistic relationship with reef fish, providing cleaning services in exchange for nutritional benefits. These shrimp inhabit stationary sea anemones, forming "cleaning stations" that rely on mobile fish clients to locate and revisit them. To investigate how fish movement behaviors influence the spatial distribution of cleaning stations, we developed an individual-based model that explicitly incorporates both stochastic fish movement and two forms of directed fish movement strategies: taxis (i.e. gradient-following) and memory-based movement. Our results reveal that directed movement, whether through taxis or memory, promotes the formation of spatially clustered cleaning stations, but only when the range of directed movement outweighs the homogenizing effects of random dispersal. Specifically, memory-based clustering requires the memory range to exceed dispersal distance, while taxis-based clustering emerges even with taxis-based movement ranges exceeded by dispersal distance. By parameterizing the model with empirical data on client fish visitation frequencies, we further show that reefs dominated by "Choosy" fish (those willing to travel farther for preferred stations) exhibit stronger station clustering compared to reefs with "Resident" fish (territorial species with limited movement). These findings highlight how client behavior shapes the spatial ecology of cleaning mutualisms, with implications for understanding partner encounter dynamics in other species interactions.
{"title":"Seeking Service: How Client Behavior Determines Cleaning Station Clustering.","authors":"Jonatan T Kaare-Rasmussen, A Raine Detmer, Eleanor M Caves, Holly V Moeller","doi":"10.1016/j.jtbi.2026.112394","DOIUrl":"https://doi.org/10.1016/j.jtbi.2026.112394","url":null,"abstract":"<p><p>Cleaner shrimp engage in a mutualistic relationship with reef fish, providing cleaning services in exchange for nutritional benefits. These shrimp inhabit stationary sea anemones, forming \"cleaning stations\" that rely on mobile fish clients to locate and revisit them. To investigate how fish movement behaviors influence the spatial distribution of cleaning stations, we developed an individual-based model that explicitly incorporates both stochastic fish movement and two forms of directed fish movement strategies: taxis (i.e. gradient-following) and memory-based movement. Our results reveal that directed movement, whether through taxis or memory, promotes the formation of spatially clustered cleaning stations, but only when the range of directed movement outweighs the homogenizing effects of random dispersal. Specifically, memory-based clustering requires the memory range to exceed dispersal distance, while taxis-based clustering emerges even with taxis-based movement ranges exceeded by dispersal distance. By parameterizing the model with empirical data on client fish visitation frequencies, we further show that reefs dominated by \"Choosy\" fish (those willing to travel farther for preferred stations) exhibit stronger station clustering compared to reefs with \"Resident\" fish (territorial species with limited movement). These findings highlight how client behavior shapes the spatial ecology of cleaning mutualisms, with implications for understanding partner encounter dynamics in other species interactions.</p>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":" ","pages":"112394"},"PeriodicalIF":2.0,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146127470","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}
Metastasis remains the decisive event in most solid cancers, yet the mathematical tools we use to describe it are still largely tied to tumor size. In the curent work, we recast metastatic spread in terms of tumor age and generational ancestry, turning an implicit notion into the main organizing principle of the model. Building on the classical Iwata-Kawasaki-Shigesada (IKS) framework, we construct a transformation from size to age and derive a hierarchy of integral equations indexed by metastatic generation. Our reformulation yields closed-form expressions for first-generation metastases and simple one-dimensional recursive integrals for higher generations, avoiding direct numerical solution of the original size-structured partial differential equation (PDE) with its nonlocal boundary condition. Using Gompertzian growth and power-law metastatic emission, we show that the age-generation model reproduces IKS predictions over clinically relevant time scales while offering improved numerical stability and interpretability. The generational decomposition reveals a robust pattern: lesions seeded directly from the primary dominate early in the disease course, whereas successively younger generations, emitted by existing metastases, come to dominate the total lesion count at small sizes, leaving older generations to occupy the macroscopic tail of the distribution. Introducing an explicit detection threshold naturally separates a small number of radiologically visible macrometastases from a much larger, unseen pool of micrometastases. Together, these results provide a transparent and computationally efficient framework that links primary-tumor growth, metastatic seeding across generations, and the hidden microscopic burden that underlies clinical presentation.
{"title":"Age and Generation-Based Model of Metastatic Cancer: From Micrometastases to Macrometastases.","authors":"Panagiotis Gavriliadis, Georgios Lolas, Themis Matsoukas","doi":"10.1016/j.jtbi.2026.112392","DOIUrl":"https://doi.org/10.1016/j.jtbi.2026.112392","url":null,"abstract":"<p><p>Metastasis remains the decisive event in most solid cancers, yet the mathematical tools we use to describe it are still largely tied to tumor size. In the curent work, we recast metastatic spread in terms of tumor age and generational ancestry, turning an implicit notion into the main organizing principle of the model. Building on the classical Iwata-Kawasaki-Shigesada (IKS) framework, we construct a transformation from size to age and derive a hierarchy of integral equations indexed by metastatic generation. Our reformulation yields closed-form expressions for first-generation metastases and simple one-dimensional recursive integrals for higher generations, avoiding direct numerical solution of the original size-structured partial differential equation (PDE) with its nonlocal boundary condition. Using Gompertzian growth and power-law metastatic emission, we show that the age-generation model reproduces IKS predictions over clinically relevant time scales while offering improved numerical stability and interpretability. The generational decomposition reveals a robust pattern: lesions seeded directly from the primary dominate early in the disease course, whereas successively younger generations, emitted by existing metastases, come to dominate the total lesion count at small sizes, leaving older generations to occupy the macroscopic tail of the distribution. Introducing an explicit detection threshold naturally separates a small number of radiologically visible macrometastases from a much larger, unseen pool of micrometastases. Together, these results provide a transparent and computationally efficient framework that links primary-tumor growth, metastatic seeding across generations, and the hidden microscopic burden that underlies clinical presentation.</p>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":" ","pages":"112392"},"PeriodicalIF":2.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115033","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 : 2026-01-29DOI: 10.1016/j.jtbi.2026.112391
Antonio F Miguel
The global ecological dominance of angiosperms represents a major evolutionary success. This study suggests that their ascendance is not due to a single trait but to a deeply integrated hydraulic design that maximizes performance and resilience. A model is developed, and based on the constructal law, the leaf vascular architecture of three major plant lineages, angiosperms, gymnosperms, and ferns is compared. The model evaluates performance based on two foundational parameters: the branching exponent which accounts for the supply efficiency, and the vein placement ratio, which controls water distribution. The results demonstrate that the angiosperm architecture is superior across all modeled metrics. This design minimizes the energetic cost of water transport, ensures uniform water distribution, and enables rapid hydraulic responsiveness. Significantly, the model reveals that this profound efficiency generates a bioenergetic surplus that funds a resilient, redundant vascular network. This fault-tolerant design provides a decisive advantage against physical damage, ensuring that high photosynthetic capacity is a sustained reality rather than a fragile state. It is this synergistic system that provides a quantitative explanation for the enduring global supremacy of angiosperms.
{"title":"The evolutionary success of angiosperms: a foundation of bioenergetic surplus.","authors":"Antonio F Miguel","doi":"10.1016/j.jtbi.2026.112391","DOIUrl":"10.1016/j.jtbi.2026.112391","url":null,"abstract":"<p><p>The global ecological dominance of angiosperms represents a major evolutionary success. This study suggests that their ascendance is not due to a single trait but to a deeply integrated hydraulic design that maximizes performance and resilience. A model is developed, and based on the constructal law, the leaf vascular architecture of three major plant lineages, angiosperms, gymnosperms, and ferns is compared. The model evaluates performance based on two foundational parameters: the branching exponent which accounts for the supply efficiency, and the vein placement ratio, which controls water distribution. The results demonstrate that the angiosperm architecture is superior across all modeled metrics. This design minimizes the energetic cost of water transport, ensures uniform water distribution, and enables rapid hydraulic responsiveness. Significantly, the model reveals that this profound efficiency generates a bioenergetic surplus that funds a resilient, redundant vascular network. This fault-tolerant design provides a decisive advantage against physical damage, ensuring that high photosynthetic capacity is a sustained reality rather than a fragile state. It is this synergistic system that provides a quantitative explanation for the enduring global supremacy of angiosperms.</p>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":" ","pages":"112391"},"PeriodicalIF":2.0,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097630","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 : 2026-01-29DOI: 10.1016/j.jtbi.2026.112389
Natalia G. Lavalle , Jerónimo Miranda-Rodríguez , Emanuel Cura Costa , Augusto Borges , Oriol Viader-Llargués , Hernán López-Schier , Osvaldo Chara
Biological systems are never in equilibrium, yet they maintain stability in the face of continuous external disturbances. A prime example of this is organ regeneration, during which organs are reliably rebuilt through controlled cellular proliferation. In this study, we employ a cell-based computational modelling approach to investigate the proliferative response of an organ after injury. We developed a minimal two-dimensional Cellular Potts Model (CPM) using empirical data from regenerating neuromasts in larval zebrafish. Remarkably, the CPM both qualitatively and quantitatively recapitulates the regenerative response of neuromasts following laser-mediated cell ablation. Assuming that cell proliferation is locally regulated by a delayed switch, we discovered that mitotic activity ceases once the type-dependent number of neighbouring cells exceeds a deterministic critical threshold. An intriguing corollary of our findings is that a local negative feedback loop among identical cells may represent a general mechanism underlying organ-level proportional homeostasis.
{"title":"Local control of cellular proliferation underlies neuromast regeneration in zebrafish","authors":"Natalia G. Lavalle , Jerónimo Miranda-Rodríguez , Emanuel Cura Costa , Augusto Borges , Oriol Viader-Llargués , Hernán López-Schier , Osvaldo Chara","doi":"10.1016/j.jtbi.2026.112389","DOIUrl":"10.1016/j.jtbi.2026.112389","url":null,"abstract":"<div><div>Biological systems are never in equilibrium, yet they maintain stability in the face of continuous external disturbances. A prime example of this is organ regeneration, during which organs are reliably rebuilt through controlled cellular proliferation. In this study, we employ a cell-based computational modelling approach to investigate the proliferative response of an organ after injury. We developed a minimal two-dimensional Cellular Potts Model (CPM) using empirical data from regenerating neuromasts in larval zebrafish. Remarkably, the CPM both qualitatively and quantitatively recapitulates the regenerative response of neuromasts following laser-mediated cell ablation. Assuming that cell proliferation is locally regulated by a delayed switch, we discovered that mitotic activity ceases once the type-dependent number of neighbouring cells exceeds a deterministic critical threshold. An intriguing corollary of our findings is that a local negative feedback loop among identical cells may represent a general mechanism underlying organ-level proportional homeostasis.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"623 ","pages":"Article 112389"},"PeriodicalIF":2.0,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094835","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 : 2026-01-27DOI: 10.1016/j.jtbi.2026.112390
Denys Dutykh , Ramón Escobedo , Lee Spector
Social foraging exhibits unexpected features, such as the existence of a group size threshold above which hunting success is not improved, mainly because, above this threshold, additional individuals are free-riders that withhold effort. These observations have been supported by computational models of group hunting, which reveal a mechanism that causes hunting success to peak at small group sizes. In the model, hunters follow two simple rules: approach the prey until a safe distance is reached, and when closer to the prey than a critical avoidance distance, move away from other hunters. The mechanism is that the spatial configuration that the hunters adopt during the hunt is disrupted by the excessive number of participants. Direct observations of wolves (Canis lupus) in Yellowstone Park have shown that the group size threshold when hunting bison (Bison bison), their most formidable prey, is nearly three times greater than when hunting elk (Cervus elaphus). However, the relationship between prey type and the threshold pack size is complex and non-linear, driven by a feedback loop: hunting strategies are adjusted based on prey size and behaviour, which in turn affects the formation and effectiveness of the pack.
This study explores how prey size influences the optimal pack size and vice versa. Our analysis confirms the non-linearity of this relationship. As the size and danger of the prey change, the optimal pack size does not follow a simple linear pattern. Instead, it reflects a more complex interaction, where both prey characteristics and wolf hunting strategies determine the most effective group size. This complexity arises from the need to balance the pressure exerted on the prey with the spatial arrangement of the pack. The feedback loop between hunting success and pack size illustrates how adaptations in hunting strategies lead to changes in pack organization, which then impact hunting success. This dynamic interaction underlines the need for models that account for these complex interactions to better understand and predict the behavior of wolf packs in different prey scenarios.
{"title":"Modeling how hunting strategies and pack size shape each other","authors":"Denys Dutykh , Ramón Escobedo , Lee Spector","doi":"10.1016/j.jtbi.2026.112390","DOIUrl":"10.1016/j.jtbi.2026.112390","url":null,"abstract":"<div><div>Social foraging exhibits unexpected features, such as the existence of a group size threshold above which hunting success is not improved, mainly because, above this threshold, additional individuals are free-riders that withhold effort. These observations have been supported by computational models of group hunting, which reveal a mechanism that causes hunting success to peak at small group sizes. In the model, hunters follow two simple rules: approach the prey until a safe distance is reached, and when closer to the prey than a critical avoidance distance, move away from other hunters. The mechanism is that the spatial configuration that the hunters adopt during the hunt is disrupted by the excessive number of participants. Direct observations of wolves (<em>Canis lupus</em>) in Yellowstone Park have shown that the group size threshold when hunting bison (<em>Bison bison</em>), their most formidable prey, is nearly three times greater than when hunting elk (<em>Cervus elaphus</em>). However, the relationship between prey type and the threshold pack size is complex and non-linear, driven by a feedback loop: hunting strategies are adjusted based on prey size and behaviour, which in turn affects the formation and effectiveness of the pack.</div><div>This study explores how prey size influences the optimal pack size and vice versa. Our analysis confirms the non-linearity of this relationship. As the size and danger of the prey change, the optimal pack size does not follow a simple linear pattern. Instead, it reflects a more complex interaction, where both prey characteristics and wolf hunting strategies determine the most effective group size. This complexity arises from the need to balance the pressure exerted on the prey with the spatial arrangement of the pack. The feedback loop between hunting success and pack size illustrates how adaptations in hunting strategies lead to changes in pack organization, which then impact hunting success. This dynamic interaction underlines the need for models that account for these complex interactions to better understand and predict the behavior of wolf packs in different prey scenarios.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"623 ","pages":"Article 112390"},"PeriodicalIF":2.0,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146088222","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 : 2026-01-24DOI: 10.1016/j.jtbi.2026.112388
Yue Deng , Mingjing Li , Jinzhi Lei
Understanding how microenvironmental heterogeneity influences tumor progression is essential for advancing both cancer biology and therapeutic strategies. In this study, we develop a cellular automata (CA) model to simulate tumor growth under varying microenvironmental conditions and genetic mutation rates, addressing a gap in existing studies that rarely integrate these two factors to explain tumor dynamics. The model explicitly incorporates the cellular heterogeneity of stem and non-stem cells, dynamic cell-cell interactions, and tumor-microenvironment crosstalk. Using computational simulations, we examine the synergistic effects of gene mutation rate, initial tumor burden, and microenvironmental state on tumor progression. Our results demonstrate that lowering the mutation rate significantly mitigates tumor expansion and preserves microenvironmental integrity. Interestingly, the initial tumor burden has a limited impact, whereas the initial condition of the microenvironment critically shapes tumor dynamics. A supportive microenvironment promotes proliferation and spatial invasion, while inhibitory conditions suppress tumor growth. These findings highlight the key role of microenvironmental modulation in tumor evolution and provide computational insights that may inform more effective cancer therapies.
{"title":"Modeling tumor progression in heterogeneous microenvironments: A cellular automata approach","authors":"Yue Deng , Mingjing Li , Jinzhi Lei","doi":"10.1016/j.jtbi.2026.112388","DOIUrl":"10.1016/j.jtbi.2026.112388","url":null,"abstract":"<div><div>Understanding how microenvironmental heterogeneity influences tumor progression is essential for advancing both cancer biology and therapeutic strategies. In this study, we develop a cellular automata (CA) model to simulate tumor growth under varying microenvironmental conditions and genetic mutation rates, addressing a gap in existing studies that rarely integrate these two factors to explain tumor dynamics. The model explicitly incorporates the cellular heterogeneity of stem and non-stem cells, dynamic cell-cell interactions, and tumor-microenvironment crosstalk. Using computational simulations, we examine the synergistic effects of gene mutation rate, initial tumor burden, and microenvironmental state on tumor progression. Our results demonstrate that lowering the mutation rate significantly mitigates tumor expansion and preserves microenvironmental integrity. Interestingly, the initial tumor burden has a limited impact, whereas the initial condition of the microenvironment critically shapes tumor dynamics. A supportive microenvironment promotes proliferation and spatial invasion, while inhibitory conditions suppress tumor growth. These findings highlight the key role of microenvironmental modulation in tumor evolution and provide computational insights that may inform more effective cancer therapies.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"622 ","pages":"Article 112388"},"PeriodicalIF":2.0,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047329","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 : 2026-01-24DOI: 10.1016/j.jtbi.2026.112377
Philippe Dague
Modeling biological systems with Boolean networks (BNs) is a well-established approach that enables reasoning about the qualitative dynamics of such systems, such as gene and signaling networks. Several semantics for BNs, i.e., scheduling of component updates, have been proposed that can significantly affect the predicted dynamic behaviors. The synchronous and asynchronous ones are the most popular, but they fail to capture some of the behaviors observed in reality and accounted for by quantitative models. Recently, the most permissive semantics has been introduced, guaranteed not to miss any behavior achievable by a quantitative model following the same logic as the BN, and, in addition, significantly reducing the computational complexity of dynamical analysis. But this time, it appears too permissive and tolerates spurious behaviors in many real situations. After clarifying the relationships between existing semantics, we define the threshold semantics whose dynamic behaviors are all those given by a single threshold network, a subclass of multivalued networks, for any possible threshold map. The spurious behaviors are excluded by the threshold semantics, whose qualitative behaviors appear as a proper abstraction of real biological processes founded on activation and inhibition influences regulated by single thresholds whose values are unknown, which is generally the case. We show that threshold semantics is stricter (for reachability between Boolean configurations) than the cuttable extended semantics (called here linear semantics) and stricter than a given constrained version of the most permissive semantics. We then seek to operationalize this threshold semantics. For this, we equip the constrained version of the most permissive semantics with a system of symbolic constraints, attached to any given trajectory and verifiable by a satisfiability solver. The satisfiability of this set of constraints ensures the consistency of the formal threshold conditions associated with the transitions along the trajectory. It defines a new operational semantics at the level of trajectories. Then we prove that this semantics is equivalent to the threshold semantics. Finally, we prove that the computational complexity of this semantics is the same as that of classical semantics, i.e., PSPACE, and we state several conjectures for future work.
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