Pub Date : 2025-11-07DOI: 10.1016/j.jtbi.2025.112303
Zhao Song , Chen Shen , The Anh Han
Non-binding communication is common in daily life and crucial for fostering cooperation, even though it has no direct payoff consequences. However, despite robust empirical evidence, its evolutionary basis remains poorly understood. Here, we develop a game-theoretic model in which individuals can signal an intention to cooperate before playing a Donation game. Strategies differ in how they respond to these signals, ranging from unconditional to conditional types, with the latter incurring a cognitive cost for deliberation. Through evolutionary analysis, we show that non-binding communication alone cannot sustain cooperation in well-mixed, anonymous populations, consistent with empirical observations. In contrast, structured populations support the emergence of cooperation, with conditional cooperators acting as catalysts that protect unconditional cooperators through context-dependent patterns of cyclic dominance. These findings offer an evolutionary explanation for how non-binding communication promotes cooperation and provide a modelling framework for exploring its effects in diverse social settings.
{"title":"Network reciprocity turns cheap talk into a force for cooperation","authors":"Zhao Song , Chen Shen , The Anh Han","doi":"10.1016/j.jtbi.2025.112303","DOIUrl":"10.1016/j.jtbi.2025.112303","url":null,"abstract":"<div><div>Non-binding communication is common in daily life and crucial for fostering cooperation, even though it has no direct payoff consequences. However, despite robust empirical evidence, its evolutionary basis remains poorly understood. Here, we develop a game-theoretic model in which individuals can signal an intention to cooperate before playing a Donation game. Strategies differ in how they respond to these signals, ranging from unconditional to conditional types, with the latter incurring a cognitive cost for deliberation. Through evolutionary analysis, we show that non-binding communication alone cannot sustain cooperation in well-mixed, anonymous populations, consistent with empirical observations. In contrast, structured populations support the emergence of cooperation, with conditional cooperators acting as catalysts that protect unconditional cooperators through context-dependent patterns of cyclic dominance. These findings offer an evolutionary explanation for how non-binding communication promotes cooperation and provide a modelling framework for exploring its effects in diverse social settings.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112303"},"PeriodicalIF":2.0,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145474952","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 : 2025-11-07DOI: 10.1016/j.jtbi.2025.112285
Linhe Zhu , Le He , Haoyan Sha , Shuling Shen
Spatial heterogeneity and population migration may affect transmission threshold and the asymptotic behavior of epidemic transmission near the steady state. To investigate this issue, an epidemic transmission model with nonlinear natural growth mechanism and linear migration mechanism based on multi-patch structure is established. First, we study the findings related to the equilibrium state of the system and the transmission threshold, proving the uniqueness and the existence of epidemic-free equilibrium points, the existence of positive equilibrium points under certain conditions and the non-existence of mixed equilibrium points. Meanwhile, we discuss the asymptotic behavior of various types of equilibrium points and define the global basic reproduction number and the local basic reproduction number, demonstrating some of their unequal relationships. Further, we also consider the impact of the blocking mechanism on the patch model, illustrating that the epidemic disappears or persists in single patch under certain conditions. Finally, we carry out the numerical simulation analysis of our system. The results suggest that the epidemic may form a certain oscillatory pattern in space and there are multiple positive equilibrium points for the system. At the same time, the blocking mechanism may lead to different types of equilibrium states in different patches, but it is not effective in reducing the total number of infected individuals and the convergence time of the system.
{"title":"Stability and threshold analysis of a class of epidemic models in a multi-patch environment","authors":"Linhe Zhu , Le He , Haoyan Sha , Shuling Shen","doi":"10.1016/j.jtbi.2025.112285","DOIUrl":"10.1016/j.jtbi.2025.112285","url":null,"abstract":"<div><div>Spatial heterogeneity and population migration may affect transmission threshold and the asymptotic behavior of epidemic transmission near the steady state. To investigate this issue, an epidemic transmission model with nonlinear natural growth mechanism and linear migration mechanism based on multi-patch structure is established. First, we study the findings related to the equilibrium state of the system and the transmission threshold, proving the uniqueness and the existence of epidemic-free equilibrium points, the existence of positive equilibrium points under certain conditions and the non-existence of mixed equilibrium points. Meanwhile, we discuss the asymptotic behavior of various types of equilibrium points and define the global basic reproduction number and the local basic reproduction number, demonstrating some of their unequal relationships. Further, we also consider the impact of the blocking mechanism on the patch model, illustrating that the epidemic disappears or persists in single patch under certain conditions. Finally, we carry out the numerical simulation analysis of our system. The results suggest that the epidemic may form a certain oscillatory pattern in space and there are multiple positive equilibrium points for the system. At the same time, the blocking mechanism may lead to different types of equilibrium states in different patches, but it is not effective in reducing the total number of infected individuals and the convergence time of the system.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"618 ","pages":"Article 112285"},"PeriodicalIF":2.0,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145477166","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 : 2025-11-07DOI: 10.1016/j.jtbi.2025.112315
Juseong Kim , Kwang Su Kim , Ayato Takada , Yusuke Asai , Shingo Iwami , Seung-Woo Son , Mi Jin Lee
Ebola and Marburg viruses are highly pathogenic filoviruses that cause severe hemorrhagic fever in humans, with case fatality rates reaching approximately 50 %. These viruses pose significant public health challenges owing to their potential for large-scale outbreaks. A key step in their infection process is the interaction between the Niemann-Pick C1 (NPC1) protein on host cells and the viral glycoprotein (GP), which is responsible for viral entry into cells. Genetic variations in NPC1 caused by single nucleotide polymorphisms (SNPs) can lead to amino acid substitutions, potentially altering the efficiency of viral entry. To better understand this process, we developed an agent-based model (ABM) to simulate viral plaque growth with spatial resolution beyond traditional models. By applying this model, we quantified how naturally occurring SNPs at GP-binding interface of NPC1, such as D508N, P424A, and S425L, reduced entry efficiency of both Ebola and Marburg viruses. Notably, the P424A substitution led to a 53 % reduction in Ebola virus entry efficiency compared to the wild-type. Our findings highlight the potential of computational modeling to uncover the impact of genetic variations on viral infections and provide insights that may inform therapeutic strategies against these deadly viruses.
{"title":"Evaluating the impact of NPC1 single nucleotide polymorphisms on entry efficiency of filoviruses in vitro: Agent-based model approach","authors":"Juseong Kim , Kwang Su Kim , Ayato Takada , Yusuke Asai , Shingo Iwami , Seung-Woo Son , Mi Jin Lee","doi":"10.1016/j.jtbi.2025.112315","DOIUrl":"10.1016/j.jtbi.2025.112315","url":null,"abstract":"<div><div>Ebola and Marburg viruses are highly pathogenic filoviruses that cause severe hemorrhagic fever in humans, with case fatality rates reaching approximately 50 %. These viruses pose significant public health challenges owing to their potential for large-scale outbreaks. A key step in their infection process is the interaction between the Niemann-Pick C1 (NPC1) protein on host cells and the viral glycoprotein (GP), which is responsible for viral entry into cells. Genetic variations in NPC1 caused by single nucleotide polymorphisms (SNPs) can lead to amino acid substitutions, potentially altering the efficiency of viral entry. To better understand this process, we developed an agent-based model (ABM) to simulate viral plaque growth with spatial resolution beyond traditional models. By applying this model, we quantified how naturally occurring SNPs at GP-binding interface of NPC1, such as D508N, P424A, and S425L, reduced entry efficiency of both Ebola and Marburg viruses. Notably, the P424A substitution led to a 53 % reduction in Ebola virus entry efficiency compared to the wild-type. Our findings highlight the potential of computational modeling to uncover the impact of genetic variations on viral infections and provide insights that may inform therapeutic strategies against these deadly viruses.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"618 ","pages":"Article 112315"},"PeriodicalIF":2.0,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145483539","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}
The circadian clock maintains a period close to 24 hours across a broad range of temperatures, achieving stability through temperature compensation of different period lengths. While PSEUDO-RESPONSE REGULATOR7 (PRR7) and PRR9 have established roles in temperature compensation, TIMING OF CAB EXPRESSION 1 (TOC1, also known as PRR1) are specifically essential for this process at low temperatures. However, their function under high-temperature conditions remains unknown. In this study, we develop a tomato circadian clock model incorporating continuous light and temperature inputs to better approximate natural environmental conditions. Our kernel modeling demonstrates that TOC1 serves as the primary regulator of LHY. Simulations under continuous light conditions yield transcriptional profiles that aligned more closely with experimental data than those using abrupt light transitions. We further examine system dynamics under both isolated light inputs and combined light-temperature conditions. Under constant light, reduced degradation rates of TOC1 perturb circadian homeostasis, inducing both monostable and multistable states. Temperature-mediated regulation of TOC1 degradation enzymes means that decreased mRNA degradation destabilizes the system. Diminished degradation rates of core circadian components can lead to arrhythmicity, while reduced gene degradation shortens the diurnal period and causes phase advances. In integrated light-temperature cycles, the clock maintains robust stability across physiological temperature ranges, with minimal impact from degradation rate variations, exhibiting remarkable robustness of the model.
{"title":"Modeling the circadian period and phase shifts in tomatoes: low degradation-driven oscillator dynamics under continuous light and temperature","authors":"Ting Huang , Xiong You , Federico Frascoli , Tonghua Zhang","doi":"10.1016/j.jtbi.2025.112309","DOIUrl":"10.1016/j.jtbi.2025.112309","url":null,"abstract":"<div><div>The circadian clock maintains a period close to 24 hours across a broad range of temperatures, achieving stability through temperature compensation of different period lengths. While <em>PSEUDO-RESPONSE REGULATOR7</em> (<em>PRR7</em>) and <em>PRR9</em> have established roles in temperature compensation, TIMING OF CAB EXPRESSION 1 (TOC1, also known as PRR1) are specifically essential for this process at low temperatures. However, their function under high-temperature conditions remains unknown. In this study, we develop a tomato circadian clock model incorporating continuous light and temperature inputs to better approximate natural environmental conditions. Our kernel modeling demonstrates that <em>TOC1</em> serves as the primary regulator of <em>LHY</em>. Simulations under continuous light conditions yield transcriptional profiles that aligned more closely with experimental data than those using abrupt light transitions. We further examine system dynamics under both isolated light inputs and combined light-temperature conditions. Under constant light, reduced degradation rates of TOC1 perturb circadian homeostasis, inducing both monostable and multistable states. Temperature-mediated regulation of TOC1 degradation enzymes means that decreased mRNA degradation destabilizes the system. Diminished degradation rates of core circadian components can lead to arrhythmicity, while reduced gene degradation shortens the diurnal period and causes phase advances. In integrated light-temperature cycles, the clock maintains robust stability across physiological temperature ranges, with minimal impact from degradation rate variations, exhibiting remarkable robustness of the model.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112309"},"PeriodicalIF":2.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145460687","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 : 2025-11-04DOI: 10.1016/j.jtbi.2025.112305
Quang Anh Le , Seung Ki Baek
A social norm defines what is good and what is bad in social contexts, as well as what to do based on such assessments. A stable social norm should be maintained against errors committed by its players. In addition, individuals may have different probabilities of errors in following the norm, and a social norm would be unstable if it benefited those who do not follow the norm carefully. In this work, we show that Simple Standing, which has been known to resist errors and mutants successfully, actually exhibits threshold behavior. That is, in a population of individuals playing the donation game according to Simple Standing, the residents can suppress the invasion of mutants with higher error proneness only if the residents’ own error proneness is sufficiently low. Otherwise, the population will be invaded by mutants that commit assessment errors more frequently, and a series of such invasions will eventually undermine the existing social norm. This study suggests that the stability analysis of a social norm may have a different picture if the probability of error itself is regarded as an individual attribute.
{"title":"Threshold behavior of a social norm in response to error proneness","authors":"Quang Anh Le , Seung Ki Baek","doi":"10.1016/j.jtbi.2025.112305","DOIUrl":"10.1016/j.jtbi.2025.112305","url":null,"abstract":"<div><div>A social norm defines what is good and what is bad in social contexts, as well as what to do based on such assessments. A stable social norm should be maintained against errors committed by its players. In addition, individuals may have different probabilities of errors in following the norm, and a social norm would be unstable if it benefited those who do not follow the norm carefully. In this work, we show that Simple Standing, which has been known to resist errors and mutants successfully, actually exhibits threshold behavior. That is, in a population of individuals playing the donation game according to Simple Standing, the residents can suppress the invasion of mutants with higher error proneness only if the residents’ own error proneness is sufficiently low. Otherwise, the population will be invaded by mutants that commit assessment errors more frequently, and a series of such invasions will eventually undermine the existing social norm. This study suggests that the stability analysis of a social norm may have a different picture if the probability of error itself is regarded as an individual attribute.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112305"},"PeriodicalIF":2.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145460631","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 : 2025-11-02DOI: 10.1016/j.jtbi.2025.112301
Michael T. Gorczyca
Many behavioral, molecular, and physiological phenomena oscillate on an approximately 24-h cycle, or display a circadian rhythm. One phenomenon of particular interest is gene expression, as multiple studies have identified associations between the oscillations in gene expression levels and a person’s health. A challenge in identifying these associations for a population is that the circadian rhythm is unique to each person. Specifically, the times at which a gene’s expression levels peak and trough are based on a person’s internal circadian clock, and each person’s internal circadian clock time is uniquely offset relative to the 24-h day-night cycle time. If each person’s offset is not taken into account when estimating the parameters of a population-level cosinor model, which is commonly used to represent how gene expression levels oscillate, then the population-level amplitude parameter estimate for this model could be erroneously attenuated. This attenuation bias would increase the likelihood of falsely concluding that a gene’s expression levels do not oscillate. While laboratory tests can mitigate attenuation bias by determining each person’s offset, these laboratory tests are often expensive to perform. To address attenuation bias without performing laboratory tests, we propose a new method for estimating the parameters of a population-level cosinor model using longitudinal data from multiple genes and people. First, the parameters of a population-level cosinor model are estimated for each gene without considering each person’s offset. Second, the parameters of an individual-level cosinor model are estimated for each person and each gene. Third, a data-driven offset is computed for each person using the parameter estimates of these models. Fourth, the parameters of a new population-level cosinor model are estimated for each gene incorporating these data-driven offsets. Simulation studies show that this method mitigates attenuation bias in population-level amplitude parameter estimates and in hypothesis test statistics that are computed to determine whether or not a gene’s expression levels oscillate. Application of this method on data from three different studies demonstrates that this method consistently produces population-level parameter estimates and hypothesis test statistics that closely match those obtained when each person’s offset is determined from laboratory tests.
{"title":"A mixed-effects cosinor modelling framework for circadian gene expression","authors":"Michael T. Gorczyca","doi":"10.1016/j.jtbi.2025.112301","DOIUrl":"10.1016/j.jtbi.2025.112301","url":null,"abstract":"<div><div>Many behavioral, molecular, and physiological phenomena oscillate on an approximately 24-h cycle, or display a circadian rhythm. One phenomenon of particular interest is gene expression, as multiple studies have identified associations between the oscillations in gene expression levels and a person’s health. A challenge in identifying these associations for a population is that the circadian rhythm is unique to each person. Specifically, the times at which a gene’s expression levels peak and trough are based on a person’s internal circadian clock, and each person’s internal circadian clock time is uniquely offset relative to the 24-h day-night cycle time. If each person’s offset is not taken into account when estimating the parameters of a population-level cosinor model, which is commonly used to represent how gene expression levels oscillate, then the population-level amplitude parameter estimate for this model could be erroneously attenuated. This attenuation bias would increase the likelihood of falsely concluding that a gene’s expression levels do not oscillate. While laboratory tests can mitigate attenuation bias by determining each person’s offset, these laboratory tests are often expensive to perform. To address attenuation bias without performing laboratory tests, we propose a new method for estimating the parameters of a population-level cosinor model using longitudinal data from multiple genes and people. First, the parameters of a population-level cosinor model are estimated for each gene without considering each person’s offset. Second, the parameters of an individual-level cosinor model are estimated for each person and each gene. Third, a data-driven offset is computed for each person using the parameter estimates of these models. Fourth, the parameters of a new population-level cosinor model are estimated for each gene incorporating these data-driven offsets. Simulation studies show that this method mitigates attenuation bias in population-level amplitude parameter estimates and in hypothesis test statistics that are computed to determine whether or not a gene’s expression levels oscillate. Application of this method on data from three different studies demonstrates that this method consistently produces population-level parameter estimates and hypothesis test statistics that closely match those obtained when each person’s offset is determined from laboratory tests.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112301"},"PeriodicalIF":2.0,"publicationDate":"2025-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145446408","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 : 2025-10-31DOI: 10.1016/j.jtbi.2025.112302
Santana Mondal , Ludek Berec , Subhas Khajanchi
The predator-prey interaction is likely the most studied relationship in ecology. Predator consumption rate is modulated by more efficient hunting of prey by predators or, conversely, by more efficient hiding from predators by prey. Here, we study predator and prey adaptations in these traits using a common modeling framework, consisting of juvenile prey, adult prey, and an unstructured predator. What distinguishes the cases with predator and prey adaptations is the trade-offs. While more efficient predator hunting is assumed to be negatively correlated to its mortality rate (hunting trade-off), more efficient prey hiding is assumed to reduce prey reproduction (hiding trade-off). Natural selection benefits predators with high hunting efficiency if the hunting trade-off is strongly concave. For prey hiding efficiency, concave trade-offs give rise to a continuously stable strategy, whereas evolutionary branching is observed for convex trade-offs. In the latter case, the distance separating two branches on the evolutionary tree grows with increasing prey maturation rate; one branch eventually develops toward maximal hiding efficiency and minimal reproduction rate, while the other branch evolves towards minimal hiding efficiency and maximal reproduction rate. The concave trade-off thus serves a dual function in prey and predator evolution. For prey-hiding evolution, it increases prey protection. For predator-hunting evolution, it decreases hunting efficiency and thus promotes prey protection, too. Thus, the trade-off form proves to be a crucial determinant of evolutionary outcomes.
{"title":"Evolution of hunting efficiency of predator and hiding efficiency of prey in a stage-structured prey-predator model","authors":"Santana Mondal , Ludek Berec , Subhas Khajanchi","doi":"10.1016/j.jtbi.2025.112302","DOIUrl":"10.1016/j.jtbi.2025.112302","url":null,"abstract":"<div><div>The predator-prey interaction is likely the most studied relationship in ecology. Predator consumption rate is modulated by more efficient hunting of prey by predators or, conversely, by more efficient hiding from predators by prey. Here, we study predator and prey adaptations in these traits using a common modeling framework, consisting of juvenile prey, adult prey, and an unstructured predator. What distinguishes the cases with predator and prey adaptations is the trade-offs. While more efficient predator hunting is assumed to be negatively correlated to its mortality rate (hunting trade-off), more efficient prey hiding is assumed to reduce prey reproduction (hiding trade-off). Natural selection benefits predators with high hunting efficiency if the hunting trade-off is strongly concave. For prey hiding efficiency, concave trade-offs give rise to a continuously stable strategy, whereas evolutionary branching is observed for convex trade-offs. In the latter case, the distance separating two branches on the evolutionary tree grows with increasing prey maturation rate; one branch eventually develops toward maximal hiding efficiency and minimal reproduction rate, while the other branch evolves towards minimal hiding efficiency and maximal reproduction rate. The concave trade-off thus serves a dual function in prey and predator evolution. For prey-hiding evolution, it increases prey protection. For predator-hunting evolution, it decreases hunting efficiency and thus promotes prey protection, too. Thus, the trade-off form proves to be a crucial determinant of evolutionary outcomes.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112302"},"PeriodicalIF":2.0,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433050","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 : 2025-10-30DOI: 10.1016/j.jtbi.2025.112306
Deepak K Pattanaik , Nachieketa K Sharma , Vasudevan Lakshminarayanan
Background
The development of an oxidative stress model has been used to explain the decrease in the ERG’s a-wave amplitude in the presence of iron ions. Reactive oxygen species (ROS), which are produced by iron ions, are thought to reduce photoreceptor hyperpolarization. In Retinitis Pigmentosa (RP), oxygen builds up inside the cells of the rods, where superoxide radicals are produced. This provides an explanation for the decrease in scotopic a-wave amplitude in RP patients.
Methods
The oxidative stress model is applied here since oxygen buildup produces ROS (superoxide radicals) that are comparable to those produced by iron ions. The loss of rod photoreceptors is a further consequence of ROS. A component denoting the fraction of rods present is incorporated into the formula for the a-wave voltage to account for the effect of rod deaths on amplitude.
Results
The ROS generated in RP eyes were able to draw calcium ions, increasing the calcium influx. The voltage vs. time graph can be determined with the aid of a factor that represents the percentage of rods present. The loss of rod photoreceptors and calcium ions both result in a decrease in the amplitude of the a-wave at any time t. The theoretical results compare well with experimental results.
Conclusion
Due to oxidative stress, which causes rod photoreceptors to die and cause tunnel vision and peripheral visual field loss, the decline in scotopic a-wave amplitude in RP patients’ eyes is explained.
{"title":"The effect of oxidative stress on the leading edge of the a-wave in retinitis pigmentosa","authors":"Deepak K Pattanaik , Nachieketa K Sharma , Vasudevan Lakshminarayanan","doi":"10.1016/j.jtbi.2025.112306","DOIUrl":"10.1016/j.jtbi.2025.112306","url":null,"abstract":"<div><h3>Background</h3><div>The development of an oxidative stress model has been used to explain the decrease in the ERG’s <em>a</em>-wave amplitude in the presence of iron ions. Reactive oxygen species (ROS), which are produced by iron ions, are thought to reduce photoreceptor hyperpolarization. In Retinitis Pigmentosa (RP), oxygen builds up inside the cells of the rods, where superoxide radicals are produced. This provides an explanation for the decrease in scotopic <em>a</em>-wave amplitude in RP patients.</div></div><div><h3>Methods</h3><div>The oxidative stress model is applied here since oxygen buildup produces ROS (superoxide radicals) that are comparable to those produced by iron ions. The loss of rod photoreceptors is a further consequence of ROS. A component denoting the fraction of rods present is incorporated into the formula for the <em>a</em>-wave voltage to account for the effect of rod deaths on amplitude.</div></div><div><h3>Results</h3><div>The ROS generated in RP eyes were able to draw calcium ions, increasing the calcium influx. The voltage vs. time graph can be determined with the aid of a factor that represents the percentage of rods present. The loss of rod photoreceptors and calcium ions both result in a decrease in the amplitude of the <em>a</em>-wave at any time <em>t</em>.<!--> <!-->The theoretical results compare well with experimental results.</div></div><div><h3>Conclusion</h3><div>Due to oxidative stress, which causes rod photoreceptors to die and cause tunnel vision and peripheral visual field loss, the decline in scotopic <em>a</em>-wave amplitude in RP patients’ eyes is explained.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"617 ","pages":"Article 112306"},"PeriodicalIF":2.0,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427203","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 : 2025-10-28DOI: 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.
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