Alessandro Mastrofini, Eva Karlöf, Ulf Hedin, Christian T Gasser, Michele Marino
{"title":"Modulating vascular stresses through homeostatic remodelling: a multi-patient analysis of atherosclerotic carotid biomechanics.","authors":"Alessandro Mastrofini, Eva Karlöf, Ulf Hedin, Christian T Gasser, Michele Marino","doi":"10.1098/rsif.2025.0313","DOIUrl":"10.1098/rsif.2025.0313","url":null,"abstract":"<p><p>The biomechanical behaviour of vascular tissues is influenced by the presence of residual stresses, yet their role in vascular adaptation to pathological conditions remains largely unexplored. These residual stresses may arise within the vessel wall as a result of growth and remodelling (G&R) processes governed by the principles of tensional homeostasis. This study extends our previous work by refining a computational workflow that integrates homeostasis-driven G&R into patient-specific carotid geometries. Key advancements include adopting a total Lagrangian framework to handle complex geometries, introducing novel post-processing metrics for improved comparisons and conducting statistical analyses to assess G&R's impact on biomechanical evaluations of atherosclerotic vessels. These improvements enabled the analysis of a cohort of 18 cases, incorporating patient-specific geometries and pathological tissue distributions reconstructed from clinical imaging data. Results suggest that G&R generally reduces peak stress, though its effectiveness depends on plaque morphology and tissue composition. High calcification leads to localized stress concentrations, limiting remodelling, whereas matrix-rich regions promote stress homogenization. At the cohort level, findings underscore the need for patient-specific analyses in plaque risk evaluation, reinforcing the importance of personalized biomechanical modelling in assessing atherosclerotic disease and guiding clinical decision-making.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250313"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lucila Gisele Alvarez Zuzek, Laura Ferrarotti, Bruno Lepri, Riccardo Gallotti
{"title":"Predicting human cooperation: sensitizing drift-diffusion model to interaction and external stimuli.","authors":"Lucila Gisele Alvarez Zuzek, Laura Ferrarotti, Bruno Lepri, Riccardo Gallotti","doi":"10.1098/rsif.2025.0168","DOIUrl":"10.1098/rsif.2025.0168","url":null,"abstract":"<p><p>Human cooperation arises naturally and is essential for the development of successful societies. This study aims to identify which aspects of the interaction influence societal cooperation and defection. Specifically, we investigate human cooperation within the framework of the Multiplayer Iterated Prisoner's Dilemma game, modelling the decision-making process by using the drift-diffusion model (DDM). We propose a novel Bayesian model for the evolution of the DDM parameters, based on the nature of interactions experienced with other players. This approach enables us to predict the evolution of the expected rate of cooperation within the population. We successfully validate our model using an unseen test dataset-separated from the training one-and apply it to explore three strategic scenarios known from previous research to affect cooperation: (i) manipulation of co-players, (ii) the use of rewards and punishments, and (iii) time pressure. Our model successfully explains the test dataset and behaves consistently with established findings in the literature on human behaviour in these simulated scenarios. These results support the potential of our model as a foundational tool for developing and testing strategies that foster cooperation, improving our ability to study, understand and intervene in scenarios where individual and collective interests conflict.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250168"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Physical traits of supercompetitors in cell competition.","authors":"Logan C Carpenter, Shiladitya Banerjee","doi":"10.1098/rsif.2025.0638","DOIUrl":"10.1098/rsif.2025.0638","url":null,"abstract":"<p><p>Cell competition is a fitness control mechanism in tissues, where less fit cells are eliminated to maintain tissue homeostasis. Two primary mechanisms of cell competition have been identified: contact-dependent apoptosis and mechanical stress-induced competition. While both operate in tissues, their combined impact on population dynamics is unclear. Here, we present a cell-based computational model that integrates cellular mechanics with proliferation, contact-induced apoptosis and mechanically triggered apoptosis to investigate competition between two distinct cell types. Using this framework, we systematically examine how differences in physical traits-such as stiffness, adhesion and crowding sensitivity-govern competitive outcomes. Our results show that apoptosis rates alone are insufficient to predict cell fate; differences in proliferation and contact inhibition play equally important, context-dependent roles. Notably, we find that increased cell stiffness can confer a fitness advantage, enabling stiffer cells to outcompete softer neighbours. However, cells with reduced stiffness can become 'soft' supercompetitors if they exhibit faster growth and lower sensitivity to crowding. We also demonstrate that colony size critically influences competition: a minimum size is required for mutant expansion, below which elimination becomes stochastic. This stochastic clearance is driven by a protrusive instability in the interface between two cells that promotes invasion of the supercompetitors.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250638"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael Pan, Fatemeh Malekipour, Peter Pivonka, Ashleigh V Morrice-West, Jennifer A Flegg, R Chris Whitton, Peta L Hitchens
{"title":"A mathematical model of metacarpal subchondral bone adaptation, microdamage and repair in racehorses.","authors":"Michael Pan, Fatemeh Malekipour, Peter Pivonka, Ashleigh V Morrice-West, Jennifer A Flegg, R Chris Whitton, Peta L Hitchens","doi":"10.1098/rsif.2025.0297","DOIUrl":"10.1098/rsif.2025.0297","url":null,"abstract":"<p><p>Fractures of the distal limb in Thoroughbred racehorses primarily occur because of accumulation of bone microdamage from high-intensity training. Mathematical models of subchondral bone adaptation of the third metacarpal lateral condyles are capable of approximating existing data for Thoroughbred racehorses in training or at rest. To improve upon previous models, we added a dynamic resorption rate and microdamage accumulation and repair processes. Our ordinary differential equation model simulates the coupled processes of bone adaptation and microdamage accumulation, and is calibrated to data on racehorses in training and rest. Sensitivity analyses of our model suggest that joint loads and distances covered per day are among the most significant parameters for predicting microdamage accumulated during training. We also use the model to compare the impact of incrementally increasing training programmes as horses enter training from a period of rest, and maintenance workloads of horses that are race fit on bone adaptation. We find that high-speed training accounts for the majority of damage to the bone. Furthermore, for horses in race training, the estimated rates of bone repair are unable to offset the rate of damage accumulation under a typical Australian racing campaign, highlighting the need for regular rest from training.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250297"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kamal Dingle, Pascal Hagolani, Roland Zimm, Muhammad Umar, Samantha O'Sullivan, Ard Louis
{"title":"Bounding phenotype transition probabilities via conditional complexity.","authors":"Kamal Dingle, Pascal Hagolani, Roland Zimm, Muhammad Umar, Samantha O'Sullivan, Ard Louis","doi":"10.1098/rsif.2024.0916","DOIUrl":"10.1098/rsif.2024.0916","url":null,"abstract":"<p><p>By linking genetic sequences to phenotypic traits, genotype-phenotype maps represent a key layer in biological organization. Their structure modulates the effects of genetic mutations which can contribute to shaping evolutionary outcomes. Recent work based on algorithmic information theory introduced an upper bound on the likelihood of a random genetic mutation causing a transition between two phenotypes, using only the conditional complexity between them. Here we evaluate how well this bound works for a range of genotype-phenotype maps, including a differential equation model for circadian rhythm, a matrix-multiplication model of gene regulatory networks, a developmental model of tooth morphologies for ringed seals, a polyomino-tile shape model of biological self-assembly, and the hydrophobic/polar (HP) lattice protein model. By assessing three levels of predictive performance, we find that the bound provides meaningful estimates of phenotype transition probabilities across these complex systems. These results suggest that transition probabilities can be predicted to some degree directly from the phenotypes themselves, without needing detailed knowledge of the underlying genotype-phenotype map.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20240916"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mario Castro, Rafael Vida, Javier Galeano, Jose A Cuesta
{"title":"Scarce data, noisy inferences and overfitting: the hidden flaws in ecological dynamics modelling.","authors":"Mario Castro, Rafael Vida, Javier Galeano, Jose A Cuesta","doi":"10.1098/rsif.2025.0183","DOIUrl":"10.1098/rsif.2025.0183","url":null,"abstract":"<p><p>Metagenomic data has significantly advanced microbiome research by employing ecological models, particularly in personalized medicine. The generalized Lotka-Volterra (gLV) model is commonly used to understand microbial interactions and predict ecosystem dynamics. However, gLV models often fail to capture complex interactions, especially when data are limited or noisy. This study critically assesses the effectiveness of gLV and similar models using Bayesian inference and a model reduction method based on information theory. We found that ecological data often leads to non-interpretability and overfitting due to limited information, noisy data and parameter sloppiness. Our results highlight the need for simpler models that align with the available data and propose a distribution-based approach to better capture ecosystem diversity, stability and competition. These findings challenge current bottom-up ecological modelling practices and aim to shift the focus towards a statistical mechanics view of ecology based on distributions of parameters.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250183"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12505159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jian Jiang, Long Chen, Lu Ke, Bozheng Dou, Yueying Zhu, Yazhou Shi, Huahai Qiu, Ben-Gong Zhang, Tianshou Zhou, Guo-Wei Wei
{"title":"Machine learning predictions from unpredictable chaos.","authors":"Jian Jiang, Long Chen, Lu Ke, Bozheng Dou, Yueying Zhu, Yazhou Shi, Huahai Qiu, Ben-Gong Zhang, Tianshou Zhou, Guo-Wei Wei","doi":"10.1098/rsif.2025.0441","DOIUrl":"10.1098/rsif.2025.0441","url":null,"abstract":"<p><p>Chaos is omnipresent in nature, and its understanding provides enormous social and economic benefits. However, the unpredictability of chaotic systems is a textbook concept due to their sensitivity to initial conditions, aperiodic behaviour, fractal dimensions, nonlinearity and strange attractors. In this work, we introduce, for the first time, chaotic learning, a novel multiscale topological paradigm that enables accurate predictions from chaotic systems. We show that seemingly random and unpredictable chaotic dynamics counterintuitively offer unprecedented quantitative predictions. Specifically, we devise multiscale topological Laplacians to embed real-world data into a family of interactive chaotic dynamical systems, modulate their dynamical behaviours and enable the accurate prediction of the input data. As a proof of concept, we consider 28 datasets from four categories of realistic problems: 10 brain waves, four benchmark protein datasets, 13 single-cell RNA sequencing datasets and an image dataset, as well as two distinct chaotic dynamical systems, namely the Lorenz and Rossler attractors. We demonstrate chaotic learning predictions of the physical properties from chaos. Our new chaotic learning paradigm profoundly changes the textbook perception of chaos and bridges topology, chaos and learning for the first time.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250441"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Stroke impairs the proactive control of dynamic balance during predictable treadmill accelerations.","authors":"Tara Cornwell, James Finley","doi":"10.1098/rsif.2025.0336","DOIUrl":"10.1098/rsif.2025.0336","url":null,"abstract":"<p><p>We maintain balance during gait using both proactive and reactive control strategies. Damage to the brain from a stroke impairs reactive balance, but little is known about how a stroke impacts proactive control during walking. Stroke-related impairments to proactive control could become targets for interventions designed to improve responses to predictable disturbances and reduce fall risk. Therefore, we determined whether proactive strategies during predictable treadmill accelerations differed between people post-stroke (<i>n</i> = 14) and people without stroke (<i>n</i> = 14). Both groups walked with accelerations at random (every one to five strides) and regular (every three strides) intervals. We quantified the effects of the perturbations as changes to the centre of mass (COM) speed and used mechanical leg work to quantify the proactive strategies to slow the COM. Participants without stroke reduced peak COM speed better than those with stroke when perturbations were regular (-0.016 m s<sup>-1</sup> versus +0.004 m s<sup>-1</sup>; <i>p</i> = 0.007). They also reduced positive leg work more during the perturbation step than the group post-stroke (-5.7% versus +2.5%; <i>p</i> = 0.003). One implication of these findings is that people post-stroke may be more susceptible to falls during predictable gait disturbances, and future work should identify the underlying impairments that cause these deficits.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250336"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hélène Cecilia, Benjamin M Althouse, Sasha R Azar, Shannan L Rossi, Nikos Vasilakis, Kathryn A Hanley
{"title":"Inside-out: modelling the link between Zika virus viral dynamics within hosts and transmission to vectors across host species and virus strains.","authors":"Hélène Cecilia, Benjamin M Althouse, Sasha R Azar, Shannan L Rossi, Nikos Vasilakis, Kathryn A Hanley","doi":"10.1098/rsif.2025.0365","DOIUrl":"10.1098/rsif.2025.0365","url":null,"abstract":"<p><p>Epidemiological models of mosquito-borne virus transmission often lack accurate estimates of host-to-vector transmission probability. Here, we estimated this probability for two strains of Zika virus (ZIKV)-one sylvatic and one human-endemic-from two monkey species to <i>Aedes albopictus</i> mosquitoes using experimental infection data. Viral dynamics did not differ between monkey species, although one (cynomolgus macaque) is a native ZIKV host and the other (squirrel monkey) a novel host, but did differ between strains, with viremia for the human-endemic strain peaking later and lower than the sylvatic strain. Only the sylvatic strain was transmitted to mosquitoes. Within mosquitoes, anatomical barriers influence viral progression to salivary glands, complicating host infectiousness estimation. We quantified the probability of viral dissemination to the legs in <i>Ae. albopictus</i>, which increased with host viral load and was higher after feeding on squirrel monkeys than on cynomolgus macaques. We also found a positive relationship between virus titre in mosquito legs and virus detection in saliva after a 14-day extrinsic incubation period. Combining these factors, we found that squirrel monkeys were on average 1.5 times more infectious to <i>Ae. albopictus</i> than cynomolgus macaques. These estimates will help assess ZIKV's potential to establish an enzootic, sylvatic cycle in the Americas.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20250365"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Frank Bastian, Hassan Alkhayuon, Kieren Mulchrone, Micheal O'Riordain, Sebastian Maciej Wieczorek
{"title":"Cancer model with moving extinction threshold reproduces real cancer data.","authors":"Frank Bastian, Hassan Alkhayuon, Kieren Mulchrone, Micheal O'Riordain, Sebastian Maciej Wieczorek","doi":"10.1098/rsif.2024.0844","DOIUrl":"10.1098/rsif.2024.0844","url":null,"abstract":"<p><p>We propose a simple dynamic model of cancer development that captures carcinogenesis and subsequent cancer progression. A central idea of the model is to include the immune response to cancer, which leads to the emergence of an extinction threshold. We first identify the limitations of commonly used extinction threshold models from population biology in reproducing typical cancer progression. We then address these limitations by deriving a new model that incorporates: (i) random mutations of stem cells at a rate that increases with age and (ii) immune response whose strength may also vary over time. Our model accurately reproduces a wide range of real-world cancer data: the typical age-specific cumulative risk of most human cancers, the progression of breast cancer in mice and the unusual age-specific cumulative risk of breast cancer in women. In the last case, we model the different immune response at different phases of the menstrual cycle and menopausal treatment and show that this leads to a moving extinction threshold. This approach provides new insights into the effects of hormone replacement therapy and menstrual cycle length on breast cancer in women. More generally, it can be applied to a variety of other cancer scenarios where the immune response or other important factors vary over time.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 231","pages":"20240844"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}