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Exploring the constituent mechanisms of hepatitis: a dynamical systems approach. 探索肝炎的组成机制:动力系统方法。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2023-03-13 DOI: 10.1093/imammb/dqac013
Joanne L Dunster, Jonathan M Gibbins, Martin R Nelson

Hepatitis is the term used to describe inflammation in the liver. It is associated with a high rate of mortality, but the underlying disease mechanisms are not completely understood and treatment options are limited. We present a mathematical model of hepatitis that captures the complex interactions between hepatocytes (liver cells), hepatic stellate cells (cells in the liver that produce hepatitis-associated fibrosis) and the immune components that mediate inflammation. The model is in the form of a system of ordinary differential equations. We use numerical techniques and bifurcation analysis to characterize and elucidate the physiological mechanisms that dominate liver injury and its outcome to a healthy or unhealthy, chronic state. This study reveals the complex interactions between the multiple cell types and mediators involved in this complex disease and highlights potential problems in targeting inflammation in the liver therapeutically.

肝炎是用来描述肝脏炎症的术语。它与高死亡率有关,但潜在的疾病机制尚不完全清楚,治疗方案有限。我们提出了一个肝炎的数学模型,该模型捕获了肝细胞(肝细胞)、肝星状细胞(肝脏中产生肝炎相关纤维化的细胞)和介导炎症的免疫成分之间复杂的相互作用。该模型是常微分方程组的形式。我们使用数值技术和分岔分析来表征和阐明主导肝损伤及其健康或不健康慢性状态的生理机制。这项研究揭示了参与这种复杂疾病的多种细胞类型和介质之间的复杂相互作用,并强调了靶向肝脏炎症治疗的潜在问题。
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引用次数: 1
Computer simulation of surgical interventions for the treatment of refractory pulmonary hypertension. 难治性肺动脉高压手术干预的计算机模拟。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2023-03-13 DOI: 10.1093/imammb/dqac011
Seong Woo Han, Charles Puelz, Craig G Rusin, Daniel J Penny, Ryan Coleman, Charles S Peskin

This paper describes computer models of three interventions used for treating refractory pulmonary hypertension (RPH). These procedures create either an atrial septal defect, a ventricular septal defect or, in the case of a Potts shunt, a patent ductus arteriosus. The aim in all three cases is to generate a right-to-left shunt, allowing for either pressure or volume unloading of the right side of the heart in the setting of right ventricular failure, while maintaining cardiac output. These shunts are created, however, at the expense of introducing de-oxygenated blood into the systemic circulation, thereby lowering the systemic arterial oxygen saturation. The models developed in this paper are based on compartmental descriptions of human hemodynamics and oxygen transport. An important parameter included in our models is the cross-sectional area of the surgically created defect. Numerical simulations are performed to compare different interventions and various shunt sizes and to assess their impact on hemodynamic variables and oxygen saturations. We also create a model for exercise and use it to study exercise tolerance in simulated pre-intervention and post-intervention RPH patients.

本文描述了用于治疗难治性肺动脉高压(RPH)的三种干预措施的计算机模型。这些手术要么造成房间隔缺损,要么造成室间隔缺损,或者,在波茨分流术的情况下,造成动脉导管未闭。这三个病例的目的都是产生一个从右到左的分流,在右心室衰竭的情况下,允许心脏右侧的压力或容量卸载,同时保持心输出量。然而,这些分流术是以将缺氧血液引入体循环为代价的,从而降低了全身动脉氧饱和度。本文建立的模型是基于人体血流动力学和氧运输的区隔描述。我们的模型中包含的一个重要参数是手术产生的缺陷的横截面积。通过数值模拟来比较不同的干预措施和不同的分流尺寸,并评估其对血流动力学变量和血氧饱和度的影响。我们还创建了一个运动模型,并使用它来研究模拟干预前和干预后RPH患者的运动耐量。
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引用次数: 1
Predicting elimination of evolving virus variants. 预测消除不断进化的病毒变体。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-12-02 DOI: 10.1093/imammb/dqac012
Elliott Hughes, Rachelle Binny, Shaun Hendy, Alex James

As the SARS-CoV-2 virus spreads around the world new variants are appearing regularly. Although some countries have achieved very swift and successful vaccination campaigns, on a global scale the vast majority of the population is unvaccinated and new variants are proving more resistant to the current set of vaccines. We present a simple model of disease spread, which includes the evolution of new variants of a novel virus and varying vaccine effectiveness to these new strains. We show that rapid vaccine updates to target new strains are more effective than slow updates and containing spread through non-pharmaceutical interventions is vital while these vaccines are delivered. Finally, when measuring the key model inputs, e.g. the rate at which new mutations and variants of concern emerge, is difficult we show how an observable model output, the number of new variants that have been seen, is strongly correlated with the probability the virus is eliminated.

随着SARS-CoV-2病毒在世界各地的传播,新的变种经常出现。虽然一些国家已经非常迅速和成功地开展了疫苗接种运动,但在全球范围内,绝大多数人口未接种疫苗,而且新的变种对现有的疫苗具有更强的抵抗力。我们提出了一个简单的疾病传播模型,其中包括一种新病毒的新变种的进化和对这些新毒株的不同疫苗有效性。我们表明,针对新菌株的快速疫苗更新比缓慢更新更有效,并且在提供这些疫苗时,通过非药物干预措施遏制传播至关重要。最后,当难以测量关键模型输入时,例如新突变和引起关注的变体出现的速度时,我们展示了可观察到的模型输出,即已观察到的新变体的数量,如何与病毒被消除的可能性密切相关。
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引用次数: 0
Estimating decay curves of neutralizing antibodies to SARS-CoV-2 infection. 估计SARS-CoV-2感染中和抗体的衰减曲线。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-12-02 DOI: 10.1093/imammb/dqac008
Elliot Poehler, Liam Gibson, Audrey Lustig, Nicole J Moreland, Reuben McGregor, Alex James

Estimating the longevity of an individual's immune response to the SARS-Cov-2 virus is vital for future planning, particularly of vaccine requirements. Neutralizing antibodies (Nabs) are increasingly being recognized as a correlate of protection and while there are many studies that follow the response of a cohort of people, each study alone is not enough to predict the long-term response. Studies use different assays to measure Nabs, making them hard to combine. We present a modelling method that can combine multiple datasets and can be updated as more detailed data becomes available. Combining data from seven published datasets we predict that the NAb decay has two phases, an initial fast but short-lived decay period followed by a longer term and slower decay period.

估计个体对SARS-Cov-2病毒免疫反应的持续时间对于未来规划,特别是疫苗需求至关重要。中和抗体(nab)越来越被认为是一种相关的保护,尽管有许多研究跟踪了一群人的反应,但每项研究都不足以预测长期反应。研究使用不同的分析方法来测量nab,这使得它们很难结合起来。我们提出了一种建模方法,可以结合多个数据集,并可以随着更详细的数据变得可用而更新。结合七个已发表的数据集的数据,我们预测NAb衰变有两个阶段,一个最初的快速但短暂的衰变期,然后是一个较长且较慢的衰变期。
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引用次数: 4
How quickly does a wound heal? Bayesian calibration of a mathematical model of venous leg ulcer healing. 伤口愈合得多快?贝叶斯校正腿部静脉溃疡愈合的数学模型。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-12-02 DOI: 10.1093/imammb/dqac007
Adriana Zanca, James M Osborne, Sophie G Zaloumis, Carolina D Weller, Jennifer A Flegg

Chronic wounds, such as venous leg ulcers, are difficult to treat and can reduce the quality of life for patients. Clinical trials have been conducted to identify the most effective venous leg ulcer treatments and the clinical factors that may indicate whether a wound will successfully heal. More recently, mathematical modelling has been used to gain insight into biological factors that may affect treatment success but are difficult to measure clinically, such as the rate of oxygen flow into wounded tissue. In this work, we calibrate an existing mathematical model using a Bayesian approach with clinical data for individual patients to explore which clinical factors may impact the rate of wound healing for individuals. Although the model describes group-level behaviour well, it is not able to capture individual-level responses in all cases. From the individual-level analysis, we propose distributions for coefficients of clinical factors in a linear regression model, but ultimately find that it is difficult to draw conclusions about which factors lead to faster wound healing based on the existing model and data. This work highlights the challenges of using Bayesian methods to calibrate partial differential equation models to individual patient clinical data. However, the methods used in this work may be modified and extended to calibrate spatiotemporal mathematical models to multiple data sets, such as clinical trials with several patients, to extract additional information from the model and answer outstanding biological questions.

慢性伤口,如腿部静脉溃疡,很难治疗,并可能降低患者的生活质量。临床试验已经进行,以确定最有效的静脉腿溃疡治疗和临床因素,可能表明伤口是否会成功愈合。最近,数学模型已被用于深入了解可能影响治疗成功但难以在临床上测量的生物学因素,例如氧气流入受伤组织的速率。在这项工作中,我们使用贝叶斯方法与个体患者的临床数据校准现有的数学模型,以探索哪些临床因素可能影响个体的伤口愈合率。尽管该模型很好地描述了群体层面的行为,但它无法在所有情况下捕捉到个人层面的反应。从个体层面分析,我们提出了线性回归模型中临床因素系数的分布,但最终发现基于现有的模型和数据很难得出哪些因素导致伤口愈合更快的结论。这项工作强调了使用贝叶斯方法校准偏微分方程模型以个体患者临床数据的挑战。然而,这项工作中使用的方法可能会被修改和扩展,以校准时空数学模型到多个数据集,例如多个患者的临床试验,以从模型中提取额外的信息并回答突出的生物学问题。
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引用次数: 1
Multi-scale modelling of nanoparticle delivery and heat transport in vascularised tumours. 血管化肿瘤中纳米颗粒传递和热传递的多尺度建模。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-12-02 DOI: 10.1093/imammb/dqac009
Tahani Al Sariri, Raimondo Penta

We focus on modelling of cancer hyperthermia driven by the application of the magnetic field to iron oxide nanoparticles. We assume that the particles are interacting with the tumour environment by extravasating from the vessels into the interstitial space. We start from Darcy's and Stokes' problems in the interstitial and fluid vessels compartments. Advection-diffusion of nanoparticles takes place in both compartments (as well as uptake in the tumour interstitium), and a heat source proportional to the concentration of nanoparticles drives heat diffusion and convection in the system. The system under consideration is intrinsically multi-scale. The distance between adjacent vessels (the micro-scale) is much smaller than the average tumour size (the macro-scale). We then apply the asymptotic homogenisation technique to retain the influence of the micro-structure on the tissue scale distribution of heat and particles. We derive a new system of homogenised partial differential equations (PDEs) describing blood transport, delivery of nanoparticles and heat transport. The new model comprises a double Darcy's law, coupled with two double advection-diffusion-reaction systems of PDEs describing fluid, particles and heat transport and mass, drug and heat exchange. The role of the micro-structure is encoded in the coefficients of the model, which are to be computed solving appropriate periodic problems. We show that the heat distribution is impaired by increasing vessels' tortuosity and that regularization of the micro-vessels can produce a significant increase (1-2 degrees) in the maximum temperature. We quantify the impact of modifying the properties of the magnetic field depending on the vessels' tortuosity.

我们专注于模拟由氧化铁纳米粒子磁场驱动的癌症热疗。我们假设这些颗粒通过从血管外渗进入间隙与肿瘤环境相互作用。我们从达西和斯托克斯关于间质和液体血管室的问题开始。纳米颗粒的平流扩散发生在两个腔室中(以及肿瘤间质的吸收),与纳米颗粒浓度成正比的热源驱动系统中的热扩散和对流。所考虑的系统本质上是多尺度的。邻近血管之间的距离(微观尺度)远小于肿瘤的平均大小(宏观尺度)。然后,我们应用渐近均质化技术来保留微观结构对热量和粒子的组织尺度分布的影响。我们推导了一种新的均质偏微分方程(PDEs)系统,描述血液运输、纳米颗粒输送和热运输。新模型包括一个双达西定律,以及描述流体、颗粒和热传递以及质量、药物和热交换的两个PDEs双平流-扩散-反应系统。微观结构的作用被编码在模型的系数中,这些系数是通过求解适当的周期问题来计算的。我们发现,增加血管的弯曲度会损害热分布,微血管的正则化会使最高温度显著升高(1-2度)。我们量化了根据血管弯曲度改变磁场特性的影响。
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引用次数: 3
On a tumor growth model with brain lactate kinetics. 基于脑乳酸动力学的肿瘤生长模型。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-12-02 DOI: 10.1093/imammb/dqac010
Laurence Cherfils, Stefania Gatti, Carole Guillevin, Alain Miranville, Rémy Guillevin

Our aim in this paper is to study a mathematical model for high grade gliomas, taking into account lactates kinetics, as well as chemotherapy and antiangiogenic treatment. In particular, we prove the existence and uniqueness of biologically relevant solutions. We also perform numerical simulations based on different therapeutical situations that can be found in the literature. These simulations are consistent with what is expected in these situations.

我们的目的是在本文中研究高级别胶质瘤的数学模型,考虑到乳酸动力学,以及化疗和抗血管生成治疗。特别地,我们证明了生物相关解的存在性和唯一性。我们还根据文献中发现的不同治疗情况进行数值模拟。这些模拟与在这些情况下的预期是一致的。
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引用次数: 1
Modelling the spreading of the SARS-CoV-2 in presence of the lockdown and quarantine measures by a kinetic-type reactions approach. 通过动力学型反应方法模拟在封锁和隔离措施下SARS-CoV-2的传播。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-06-11 DOI: 10.1093/imammb/dqab017
Giorgio Sonnino, Philippe Peeters, Pasquale Nardone

We propose a realistic model for the evolution of the COVID-19 pandemic subject to the lockdown and quarantine measures, which takes into account the timedelay for recovery or death processes. The dynamic equations for the entire process are derived by adopting a kinetic-type reactions approach. More specifically, the lockdown and the quarantine measures are modelled by some kind of inhibitor reactions where susceptible and infected individuals can be trapped into inactive states. The dynamics for the recovered people is obtained by accounting people who are only traced back to hospitalized infected people. To get the evolution equation we take inspiration from the Michaelis Menten's enzyme-substrate reaction model (the so-called MM reaction) where the enzyme is associated to the available hospital beds, the substrate to the infected people, and the product to the recovered people, respectively. In other words, everything happens as if the hospitals beds act as a catalyzer in the hospital recovery process. Of course, in our case, the reverse MM reaction has no sense in our case and, consequently, the kinetic constant is equal to zero. Finally, the ordinary differential equations (ODEs) for people tested positive to COVID-19 is simply modelled by the following kinetic scheme $S+IRightarrow 2I$ with $IRightarrow R$ or $IRightarrow D$, with $S$, $I$, $R$ and $D$ denoting the compartments susceptible, infected, recovered and deceased people, respectively. The resulting kinetic-type equations provide the ODEs, for elementary reaction steps, describing the number of the infected people, the total number of the recovered people previously hospitalized, subject to the lockdown and the quarantine measure and the total number of deaths. The model foresees also the second wave of infection by coronavirus. The tests carried out on real data for Belgium, France and Germany confirmed the correctness of our model.

我们为新冠肺炎大流行的演变提出了一个现实的模型,该模型受封锁和隔离措施的影响,其中考虑了恢复或死亡过程的时间延迟。采用动力学型反应方法导出了整个过程的动力学方程。更具体地说,封锁和隔离措施是由某种抑制剂反应模拟的,在这种反应中,易感和受感染的人可能会被困在不活跃的状态中。康复者的动态是通过统计只追溯到住院感染者的人数来获得的。为了得到进化方程,我们从Michaelis-Menten的酶-底物反应模型(所谓的MM反应)中获得灵感,其中酶分别与可用的病床、感染者的底物和康复者的产物有关。换言之,一切都发生在医院病床在医院恢复过程中起着催化剂的作用。当然,在我们的例子中,反MM反应在我们的情况下没有意义,因此,动力学常数等于零。最后,新冠肺炎检测呈阳性的人的常微分方程(ODEs)简单地通过以下动力学方案$S+IRightarrow 2I$建模,其中$IRigightarrow R$或$IRightarrow D$,其中$S$、$I$、$R$和$D$分别表示易感、感染、康复和死亡的人。由此产生的动力学类型方程为基本反应步骤提供了ODE,描述了受封锁和隔离措施影响的感染者人数、先前住院的康复者总数以及死亡总数。该模型还预测了冠状病毒的第二波感染。对比利时、法国和德国的实际数据进行的测试证实了我们模型的正确性。
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引用次数: 4
Modelling articular cartilage: the relative motion of two adjacent poroviscoelastic layers. 关节软骨的建模:两个相邻的孔粘弹性层的相对运动。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-06-09 DOI: 10.1093/imammb/dqac005
J. Whiteley, Cameron P. Brown, E. Gaffney
In skeletal joints two layers of adjacent cartilage are often in relative motion. The individual cartilage layers are often modelled as a poroviscoelastic material. To model the relative motion, noting the separation of scales between the pore level and the macroscale, a homogenization based on multiple scale asymptotic analysis has been used in this study to derive a macroscale model for the relative translation of two poroviscoelastic layers separated by a very thin layer of fluid. In particular the fluid layer thickness is essentially zero at the macroscale so that the two poroviscoelastic layers are effectively in contact and their interaction is captured in the derived model via a set of interfacial conditions, including a generalization of the Beavers-Joseph condition at the interface between a viscous fluid and a porous medium. In the simplifying context of a uniform geometry, constant fixed charge density, a Newtonian interstitial fluid and a viscoelastic scaffold, modelled via finite deformation theory, we present preliminary simulations that may be used to highlight predictions for how oscillatory relative movement of cartilage under load influences the peak force the cartilage experiences and the extent of the associated deformations. In addition to highlighting such cartilage mechanics, the systematic derivation of the macroscale models will enable the study of how nanoscale cartilage physics, such as the swelling pressure induced by fixed charges, manifests in cartilage mechanics at much higher lengthscales.
在骨关节中,相邻的两层软骨经常相对运动。单个软骨层通常被建模为多孔粘弹性材料。为了模拟相对运动,注意到孔隙水平和宏观尺度之间的尺度分离,本研究中使用了基于多尺度渐近分析的均匀化方法,推导了由非常薄的流体层隔开的两个孔粘弹性层的相对平移的宏观尺度模型。特别是流体层厚度在宏观尺度上基本上为零,因此两个孔粘弹性层有效地接触,它们的相互作用通过一组界面条件在推导模型中被捕获,包括在粘性流体和多孔介质之间的界面上的bevers - joseph条件的推广。在简化的背景下,均匀的几何形状,恒定的固定电荷密度,牛顿间隙流体和粘弹性支架,通过有限变形理论建模,我们提出了初步的模拟,可以用来突出预测软骨在载荷下的振荡相对运动如何影响软骨所经历的峰值力和相关变形的程度。除了强调这种软骨力学外,宏观尺度模型的系统推导将使研究纳米尺度软骨物理(如固定电荷引起的膨胀压力)如何在更高长度尺度的软骨力学中表现出来。
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引用次数: 0
A mathematical model to describe antibody-dependent enhancement and assess the effect of limiting cloning for plasma cells in heterologous secondary dengue infection. 一个数学模型来描述抗体依赖性增强和评估限制克隆对异源继发性登革热感染浆细胞的影响。
IF 1.1 4区 数学 Q4 BIOLOGY Pub Date : 2022-04-03 DOI: 10.1093/imammb/dqab021
Felipe Alves Rubio, Hyun Mo Yang
We propose a mathematical model to study the antibody-dependent enhancement (ADE) phenomenon. Here, we explore the interaction between macrophages, dengue virus and plasma cells, especially the effect of a limitation on plasma cell proliferation, which occurs due to immunological memory. The model has up to three equilibrium points: one virus-free equilibrium and two virus-presence equilibrium, depending on the value of two thresholds. We determine the existence regions for the model equilibrium points and their stability, a sensitivity analysis was performed in the model thresholds. Numerical simulations illustrate that ADE can occur even when the basic reproduction number is less than one.
我们提出了一个数学模型来研究抗体依赖性增强(ADE)现象。在这里,我们探讨巨噬细胞、登革热病毒和浆细胞之间的相互作用,特别是免疫记忆对浆细胞增殖的限制的影响。根据两个阈值的值,该模型最多有三个平衡点:一个无病毒平衡点和两个病毒存在平衡点。我们确定了模型平衡点及其稳定性的存在区域,并对模型阈值进行了敏感性分析。数值模拟表明,即使基本繁殖数小于1,ADE也会发生。
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引用次数: 2
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