CT-based geometry analysis and finite element models of the human and ovine bronchial tree

2004 ◽  
Vol 97 (6) ◽  
pp. 2310-2321 ◽  
Author(s):  
Merryn H. Tawhai ◽  
Peter Hunter ◽  
Juerg Tschirren ◽  
Joseph Reinhardt ◽  
Geoffrey McLennan ◽  
...  

The interpretation of experimental results from functional medical imaging is complicated by intersubject and interspecies differences in airway geometry. The application of computational models in understanding the significance of these differences requires methods for generation of subject-specific geometric models of the bronchial airway tree. In the current study, curvilinear airway centerline and diameter models have been fitted to human and ovine bronchial trees using detailed data segmented from multidetector row X-ray-computed tomography scans. The trees have been extended to model the entire conducting airway system by using a volume-filling algorithm to generate airway centerline locations within detailed volume descriptions of the lungs or lobes. Analysis of the geometry of the scan-based and model-based airways has verified their consistency with measures from previous anatomic studies and has provided new anatomic data for the ovine bronchial tree. With the use of an identical parameter set, the volume-filling algorithm has produced airway trees with branching asymmetry appropriate for the human and ovine lung, demonstrating the dependence of the method on the shape of the lung or lobe volume. The modeling approach that has been developed can be applied to any level of detail of the airway tree and into any volume shape for the lung; hence it can be used directly for different individuals or animals and for any number of scan-based airways. The resulting models are subject-specific computational meshes with anatomically consistent geometry, suitable for application in simulation studies.

2020 ◽  
Vol 36 ◽  
pp. 101460
Author(s):  
Christian Gobert ◽  
Andelle Kudzal ◽  
Jennifer Sietins ◽  
Clara Mock ◽  
Jessica Sun ◽  
...  

2019 ◽  
pp. 1-13 ◽  
Author(s):  
John Metzcar ◽  
Yafei Wang ◽  
Randy Heiland ◽  
Paul Macklin

Cancer biology involves complex, dynamic interactions between cancer cells and their tissue microenvironments. Single-cell effects are critical drivers of clinical progression. Chemical and mechanical communication between tumor and stromal cells can co-opt normal physiologic processes to promote growth and invasion. Cancer cell heterogeneity increases cancer’s ability to test strategies to adapt to microenvironmental stresses. Hypoxia and treatment can select for cancer stem cells and drive invasion and resistance. Cell-based computational models (also known as discrete models, agent-based models, or individual-based models) simulate individual cells as they interact in virtual tissues, which allows us to explore how single-cell behaviors lead to the dynamics we observe and work to control in cancer systems. In this review, we introduce the broad range of techniques available for cell-based computational modeling. The approaches can range from highly detailed models of just a few cells and their morphologies to millions of simpler cells in three-dimensional tissues. Modeling individual cells allows us to directly translate biologic observations into simulation rules. In many cases, individual cell agents include molecular-scale models. Most models also simulate the transport of oxygen, drugs, and growth factors, which allow us to link cancer development to microenvironmental conditions. We illustrate these methods with examples drawn from cancer hypoxia, angiogenesis, invasion, stem cells, and immunosurveillance. An ecosystem of interoperable cell-based simulation tools is emerging at a time when cloud computing resources make software easier to access and supercomputing resources make large-scale simulation studies possible. As the field develops, we anticipate that high-throughput simulation studies will allow us to rapidly explore the space of biologic possibilities, prescreen new therapeutic strategies, and even re-engineer tumor and stromal cells to bring cancer systems under control.


2020 ◽  
Author(s):  
Carl A. Whitfield ◽  
Peter Latimer ◽  
Alex Horsley ◽  
Jim M. Wild ◽  
Guilhem J. Collier ◽  
...  

AbstractThis paper introduces a linear operator for the purposes of quantifying the spectral properties of transport within resistive trees, such as airflow in lung airway networks. The operator, which we call the Maury matrix, acts only on the terminal nodes of the tree and is equivalent to the adjacency matrix of a complete graph summarising the relationships between all pairs of terminal nodes. We show that the eigenmodes of the Maury operator have a direct physical interpretation as the relaxation, or resistive, modes of the network. We apply these findings to both idealised and image-based models of ventilation in lung airway trees and show that the spectral properties of the Maury matrix characterise the flow asymmetry in these networks more concisely than the Laplacian modes, and that eigenvector centrality in the Maury spectrum is closely related to the phenomenon of ventilation heterogeneity caused by airway narrowing or obstruction. This method has applications in dimensionality reduction in simulations of lung mechanics, as well as for characterisation of models of the airway tree derived from medical images.


Author(s):  
Kavinaya C ◽  
Ashuthoshkumar L

Computation of knee modeling is a subject-specific techniquethatdefining the zero-load measurements of the cruciate and indemnity ligaments.The dynamic knee simulator was used to test the three carcass knees. The carcass knees also experiencedphysicalsachet of motion testing to discovery their inactivesort of motion in order to regulate the zero-load measurements for everymuscle bundle. Compotation multibody knee representations were shaped for each knee and classical kinematics were likened to investigational kinematics for a replicated walk series. Simple-minded non-linear mechanisminhibition elements were used to characterize cruciate and deposited particles in musclepackages in the knee representations. This learningoriginate that knee kinematics was enormously sensitive to changing of the zero-load measurement. The domino effects also recommendoptimum methods for describing each of the muscle bundle zero-load measurements, irrespective of the subject. These consequencesvalidate the significance ofthe zero-load length when modeling the knee united and verify that physicalcloak of motion dimensions can be usedto determine the passive range of motion of the knee joint. It is also supposed that the method defined here forresponsible zero-load measurement can be used for in vitro or in vivo subject-specific computational models.


2021 ◽  
Author(s):  
Mojgan Goftari ◽  
Chiahao Lu ◽  
Megan Schmidt ◽  
Remi Patriat ◽  
Tara Palnitkar ◽  
...  

Background: Deep brain stimulation (DBS) targeting the subthalamic nucleus (STN) often shows variable outcomes on treating gait dysfunction in Parkinson's disease (PD). Such variability may stem from which specific neuronal pathways are modulated by DBS and the extent to which those pathways are modulated relative to one another. Objective: Leveraging ultra-high-field (7T) imaging data and subject-specific computational models, this study investigated how activation of seven distinct pathways in and around STN, including the pallidopeduncular and pedunculopallidal pathways, affect step length at clinically-optimized STN-DBS settings. Methods: Personalized computational models were developed for 10 subjects with a clinical diagnosis of PD and with bilateral STN-DBS implants. Results: The subject-specific pathway activation models showed a significant positive association between activation of the pedunculopallidal pathway and increased step length, and negative association on step length with pallidopeduncular pathway and hyperdirect pathway activation. Conclusions: The STN region includes multiple pathways, including fibers of passage to and from the mesencephalic locomotor area. Future clinical optimization of STN-DBS should consider these fibers of passage in the context of treating parkinsonian gait.


Author(s):  
Tilo Winkler

Airway transmural pressure in healthy homogeneous lungs with dilated airways is approximately equal to the difference between intraluminal and pleural pressure. However, bronchoconstriction causes airway narrowing, parenchymal distortion, dynamic hyperinflation, and the emergence of ventilation defects (VDefs) affecting transmural pressure. This study aimed to investigate the changes in transmural pressure caused by bronchoconstriction in a bronchial tree. Transmural pressures before and during bronchoconstriction were estimated using an integrative computational model of bronchoconstriction. Briefly, this model incorporates a 12-generation symmetric bronchial tree, and the Anafi and Wilson model for the individual airways of the tree. Bronchoconstriction lead to the emergence of VDefs and a relative increase in peak transmural pressures of up to 84% compared to baseline. The highest increase in peak transmural pressure occurred in a central airway outside of VDefs, and the lowest increase was 27% in an airway within VDefs illustrating the heterogeneity in peak transmural pressures within a bronchial tree. Mechanisms contributing to the increase in peak transmural pressures include increased regional ventilation and dynamic hyperinflation both leading to increased alveolar pressures compared to baseline. Pressure differences between intraluminal and alveolar pressure increased driven by the increased airway resistance and its contribution to total transmural pressure reached up to 24%. In conclusion, peak transmural pressure in lungs with VDefs during bronchoconstriction can be substantially increased compared to dilated airways in healthy homogeneous lungs and is highly heterogeneous. Further insights will depend on the experimental studies taking these conditions into account.


2017 ◽  
Vol 44 (9) ◽  
pp. 4677-4686 ◽  
Author(s):  
George S. K. Fung ◽  
Luisa Ciuffo ◽  
Hiroshi Ashikaga ◽  
Katsuyuki Taguchi

2014 ◽  
Vol 117 (4) ◽  
pp. 353-362 ◽  
Author(s):  
D. Leary ◽  
T. Winkler ◽  
A. Braune ◽  
G. N. Maksym

Asymmetry and heterogeneity in the branching of the human bronchial tree are well documented, but their effects on bronchoconstriction and ventilation distribution in asthma are unclear. In a series of seminal studies, Venegas et al. have shown that bronchoconstriction may lead to self-organized patterns of patchy ventilation in a computational model that could explain areas of poor ventilation [ventilation defects (VDefs)] observed in positron emission tomography images during induced bronchoconstriction. To investigate effects of anatomic asymmetry on the emergence of VDefs we used the symmetric tree computational model that Venegas and Winkler developed using different trees, including an anatomic human airway tree provided by M. Tawhai (University of Auckland), a symmetric tree, and three trees with intermediate asymmetry (Venegas JG, Winkler T, Musch G, Vidal Melo MF, Layfield D, Tgavalekos N, Fischman AJ, Callahan RJ, Bellani G, Harris RS. Nature 434: 777–782, 2005 and Winkler T, Venegas JG. J Appl Physiol 103: 655–663, 2007). Ventilation patterns, lung resistance (RL), lung elastance (EL), and the entropy of the ventilation distribution were compared at different levels of airway smooth muscle activation. We found VDefs emerging in both symmetric and asymmetric trees, but VDef locations were largely persistent in asymmetric trees, and bronchoconstriction reached steady state sooner than in a symmetric tree. Interestingly, bronchoconstriction in the asymmetric tree resulted in lower RL (∼%50) and greater EL (∼%25). We found that VDefs were universally caused by airway instability, but asymmetry in airway branching led to local triggers for the self-organized patchiness in ventilation and resulted in persistent locations of VDefs. These findings help to explain the emergence and the persistence in location of VDefs found in imaging studies.


2017 ◽  
Vol 30 (6) ◽  
pp. 772-781 ◽  
Author(s):  
Lasse Wollatz ◽  
Steven J. Johnston ◽  
Peter M. Lackie ◽  
Simon J. Cox

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