Growth description for vessel wall adaptation: a thick-walled mixture model of abdominal aortic aneurysm evolution

(1) Background: Vascular tissue seems to adapt towards stable homeostatic mechanical conditions, however, failure of reaching homeostasis may result in pathologies. Current vascular tissue adaptation models use many ad hoc assumptions, the implications of which are far from being fully understood; (2) Methods: The present study investigates the plausibility of different growth kinematics in modeling Abdominal Aortic Aneurysm (AAA) evolution in time. A structurally motivated constitutive description for the vessel wall is coupled to multi-constituent tissue growth descriptions; Constituent deposition preserved either the constituent’s density or its volume, and Isotropic Volume Growth (IVG), in-Plane Volume Growth (PVG), in-Thickness Volume Growth (TVG) and No Volume Growth (NVG) describe the kinematics of the growing vessel wall. The sensitivity of key modeling parameters is explored, and predictions are assessed for their plausibility; (3) Results: AAA development based on TVG and NVG kinematics provided not only quantitatively, but also qualitatively different results compared to IVG and PVG kinematics. Specifically, for IVG and PVG kinematics, increasing collagen mass production accelerated AAA expansion which seems counterintuitive. In addition, TVG and NVG kinematics showed less sensitivity to the initial constituent volume fractions, than predictions based on IVG and PVG; (4) Conclusions: The choice of tissue growth kinematics is of crucial importance when modeling AAA growth. Much more interdisciplinary experimental work is required to develop and validate vascular tissue adaption models, before such models can be of any practical use

GEREJA KRISTEN JAWA UNGARAN

Tugas Akhir ini dilatarbelakangi oleh kebutuhan jemaat Gereja Kristen Jawa Ungaran di dalam melaksanakan ibadah rutin dan pelayananan gereja. Permasalahan yang diangkat untuk dicari solusi desainnya adalah sebagai berikut : 1) Berapa besaran ruang yang diperlukan agar kegiatan ibadah dan pelayanan jemaat Gereja Kristen Jawa Ungaran dapat terfasilitasi, 2) Apa standar-standar yang harus dipenuhi di dalam menentukan ruang ibadah dan fasilitas pelayanan di Gereja Kristen Jawa Ungaran, 3) Bagaimana Gereja Kristen Jawa Ungaran dapat menerapkan arsitektur Jawa sebagai perwujudan komunitas jemaat Kristen Jawa di dalam gereja. Penekanan desain pada Gereja Kristen Jawa Ungaran ini adalah arsitektur yang bernafaskan kebudayaan Jawa. Gereja dengan arsitektur kebudayaan Jawa memberikan identitas khusus pada Gereja Kristen Jawa, membedakan gereja ini dengan gereja-gereja lain di kota Ungaran, serta memberikan suasana yang cocok dengan ibadah jemaat Gereja Kristen Jawa Ungaran. Kajian diawali dengan mempelajari pengertian dari agama Kristen, pengertian gereja Kristen, sejarah Gereja Kristen Jawa, pelaku dan pelayanan liturgi gereja, dan istilah-istilah yang sering digunakan di dalam gereja. Setelah itu dilakukan pendataan standar-standar di dalam membangun sebuah gereja. Dilakukan juga tinjauan mengenai lokasi di Ungaran menurut karakter geografis dan budayanya. Menggabungkan antara budaya Jawa dengan nilai kekristenan tetapi tetap mampu memberikan solusi dalam permasalahan kebutuhan jemaat yang ada merupakan tantangan tersendiri. Akhirnya, seluruh kajian dituangkan dalam bentuk program ruang dan konsep-konsep perancangan yang diaplikasikan ke dalam desain yang dipresentasikan ke dalam bentuk gambar-gambar arsitektur

A theoretical model of inflammation- and mechanotransduction- driven asthmatic airway remodelling

Inflammation, airway hyper-responsiveness and airway remodelling are well-established hallmarks of asthma, but their inter-relationships remain elusive. In order to obtain a better understanding of their inter-dependence, we develop a mechanochemical morphoelastic model of the airway wall accounting for local volume changes in airway smooth muscle (ASM) and extracellular matrix in response to transient inflammatory or contractile agonist challenges. We use constrained mixture theory, together with a multiplicative decomposition of growth from the elastic deformation, to model the airway wall as a nonlinear fibre-reinforced elastic cylinder. Local contractile agonist drives ASM cell contraction, generating mechanical stresses in the tissue that drive further release of mitogenic mediators and contractile agonists via underlying mechanotransductive signalling pathways. Our model predictions are consistent with previously described inflammation-induced remodelling within an axisymmetric airway geometry. Additionally, our simulations reveal novel mechanotransductive feedback by which hyper-responsive airways exhibit increased remodelling, for example, via stress-induced release of pro-mitogenic and procontractile cytokines. Simulation results also reveal emergence of a persistent contractile tone observed in asthmatics, via either a pathological mechanotransductive feedback loop, a failure to clear agonists from the tissue, or a combination of both. Furthermore, we identify various parameter combinations that may contribute to the existence of different asthma phenotypes, and we illustrate a combination of factors which may predispose severe asthmatics to fatal bronchospasms

Abdominal aortic aneurysm inception and evolution - A computational model

Abdominal aortic aneurysm (AAA) is characterized by a bulge in the abdominal aorta. AAA development is mostly asymptomatic, but such a bulge may suddenly rupture, which is associated with a high mortality rate. Unfortunately, there is no medication that can prevent AAA from expanding or rupturing. Therefore, patients with detected AAA are monitored until treatment indication, such as maximum AAA diameter of 55 mm or expansion rate of 1 cm/year. Models of AAA development may help to understand the disease progression and to inform decision-making on a patient-specific basis. AAA growth and remodeling (G&amp;R) models are rather complex, and before the challenge is undertaken, sound clinical validation is required. In Paper A, an existing thick-walled model of growth and remodeling of one layer of an AAA slice has been extended to a two-layered model, which better reflects the layered structure of the vessel wall. A parameter study was performed to investigate the influence of mechanical properties and G&amp;R parameters of such a model on the aneurysm growth. In Paper B, the model from Paper A was extended to an organ level model of AAA growth. Furthermore, the model was incorporated into a Fluid-Solid-Growth (FSG) framework. A patient-specific geometry of the abdominal aorta is used to illustrate the model capabilities. In Paper C, the evolution of the patient-specific biomechanical characteristics of the AAA was investigated. Four patients with five to eight Computed Tomography-Angiography (CT-A) scans at different time points were analyzed. Several non-trivial statistical correlations were found between the analyzed parameters. In Paper D, the effect of different growth kinematics on AAA growth was investigated. The transverse isotropic in-thickness growth was the most suitable AAA growth assumption, while fully isotropic growth and transverse isotropic in-plane growth produced unrealistic results. In addition, modeling of the tissue volume change improved the wall thickness prediction, but still overestimated thinning of the wall during aneurysm expansion.Bukaortaaneurysm (AAA) kännetecknas av en utbuktning hos aortaväggen i buken. Tillväxt av en AAA är oftast asymtomatisk, men en sådan utbuktning kan plö̈tsligt brista, vilket har hög dödlighet. Tyvärr finns det inga mediciner som kan förhindra AAA från att expandera eller brista. Patienter med upptä̈ckt AAA hålls därför under uppsikt tills operationskrav är uppnådda, såsom maximal AAA-diameter på 55 mm eller expansionstakt på 1 cm/år. Modeller för AAA-tillväxt kan bidra till att öka förståelsen för sjukdomsförloppet och till att förbättra beslutsunderlaget på en patientspecifik basis. AAA modeller för tillväxt och strukturförändring (G&amp;R) är ganska komplicerade och innan man tar sig an denna utmaning krävs de god klinisk validering. I Artikel A har en befintlig tjockväggig modell för tillväxt av ett skikt av en AAA-skiva utö̈kats till en två-skiktsmodell. Denna modell återspeglar bättre den skiktade strukturen hos kärlväggen. Genom en parameterstudie undersö̈ktes påverkan av mekaniska egenskaper och G&amp;R-parametrar hos en sådan modell för AAA-tillväxt. I Artikel B utvidgades modellen från Artikel A till en organnivå-modell för AAA-tillväxt. Vidare inkorporerades modellen i ett “Fluid–Solid–Growth” (FSG) ramverk. En patientspecifik geometri hos bukaortan användes för att illustrera möjligheterna med modellen. I Artikel C undersöktes utvecklingen av patientspecifika biomekaniska egenskaper hos AAA. Fyra patienter som skannats fem till åtta gånger med “Computed Tomography-Angiography” (CT-A) vid olika tillfällen analyserades. Flera icke triviala statistiska samband konstaterades mellan de analyserade parametrarna. I Artikel D undersöktes effekten av olika tillväxt-kinematik för AAA tillväxt. En modell med transversellt-isotrop-i-tjockleken-tillväxt var den bäst lämpade för AAA tillväxt, medans antagandet om fullt-isotrop-tillväxt och transversellt-isotrop-i-planet-tillväxt producerade orimliga resultat. Dessutom gav modellering av vävnadsvolymsförändring ett förbättrat väggtjockleks resultat men en fortsatt överskattning av väggförtunningen under AAA-expansionen.QC 20161201</p

Computational model of abdominal aortic aneurysm inception and evolution

Incidence of abdominal aortic aneurysm (AAA) is increasing in the aging society of the western world. Development of AAA is mostly asymptomatic and is characterized by a bulge in the abdominal aorta. However, AAA may suddenly rupture, which results in an internal bleeding associated with a high mortality rate. Patients with AAA undergo regular screening until treatment indication. To date, statistical criteria are used to decide whether the risk of rupture exceeds the risk of intervention. Models of AAA development help to understand the disease progression and to yield patient-specific criterion for AAA rupture. Up to date, sophisticated models of AAA development exist. These models assume the abdominal aorta as a thin-walled structure, which saves the computational effort. This thesis aims at investigating the importance of employing a thick-walled model of the aorta. The effects on AAA development that cannot be captured with a thin-walled model are of interest. In Paper A, the thick-walled model of growth and remodeling of one layer of a AAA slice has been extended to a two-layered model. The parameter study has been performed to investigate the influence of mechanical properties and growth and remodeling (G&amp;R) parameters of two individual layers on the gross mechanical response and G&amp;R of the artery. It was concluded that the adventitia acts to protect the arterial wall against rupture even in pathological state. In Paper B, the model was extended to an organ level model of AAA development. Furthermore, the model was incorporated into a so-called Fluid-Solid-Growth (FSG) framework, where the AAA development is loosely coupled to the blood flow conditions such as wall shear stress. One patient-specific geometry of the abdominal aorta is used to illustrate the model capabilities. A transmurally non-uniform distribution of the strains of individual arterial constituents was observed. In addition, an increased aneurysm tortuosity was observed in comparison to a thin-walled approach. These findings signify the importance of a thick-walled approach to model the aneurysm development. Finally, the proposed methodology provides a realistic basis to further explore the growth and remodeling of AAA on a patient-specific basis.QC 20140311</p

A thick-walled fluid–solid-growth model of abdominal aortic aneurysm evolution: application to a patient-specific geometry

We propose a novel thick-walled fluid–solid-growth (FSG) computational framework for modeling vascular disease evolution. The arterial wall is modeled as a thick-walled nonlinearly elastic cylindrical tube consisting of two layers corresponding to the media-intima and adventitia, where each layer is treated as a fiber-reinforced material with the fibers corresponding to the collagenous component. Blood is modeled as a Newtonian fluid with constant density and viscosity; no slip and no-flux conditions are applied at the arterial wall. Disease progression is simulated by growth and remodeling (G&amp;R) of the load bearing constituents of the wall. Adaptions of the natural reference configurations and mass densities of constituents are driven by deviations of mechanical stimuli from homeostatic levels. We apply the novel framework to model abdominal aortic aneurysm (AAA) evolution. Elastin degradation is initially prescribed to create a perturbation to the geometry which results in a local decrease in wall shear stress (WSS). Subsequent degradation of elastin is driven by low WSS and an aneurysm evolves as the elastin degrades and the collagen adapts. The influence of transmural G&amp;R of constituents on the aneurysm development is analyzed. We observe that elastin and collagen strains evolve to be transmurally heterogeneous and this may facilitate the development of tortuosity. This multiphysics framework provides the basis for exploring the influence of transmural metabolic activity on the progression of vascular disease

Growth description for vessel wall adaptation : a thick-walled mixture model of abdominal aortic aneurysm evolution

Modeling the soft tissue volumetric growth has received considerable attention in the literature.However, due to the lack of experimental observations, the growth kinematics, that are reported in the literature, are based on a number of assumptions.The present study tested the plausibility of different growth descriptions when applied to the abdominal aortic aneurysm (AAA) evolution. A structurally motivated material model and the multi-constituent tissue growth descriptions were utilized. The mass increment of the individual constituents preserved either the density or the volume.Four different growth descriptions were tested, namely isotropic (IVG), in-plane (PVG), in-thickness (TVG) growth and no volume growth (NVG) models. Based on the model sensitivity to the increased collagen deposition, TVG and NVG models were found to be plausible scenarios, while IVG and PVG were found to be implausible. In addition, TVG and NVG models were less sensitive to the initial constituent volume fractions, than IVG and PVG models.In conclusion, the choice of the growth kinematics is of crucial importance when modeling the AAA growth and remodeling, and,probably, also for other soft biological tissues.QC 20161201</p

Biomechanical changes during abdominal aortic aneurysm growth

<div><p>The biomechanics-based Abdominal Aortic Aneurysm (AAA) rupture risk assessment has gained considerable scientific and clinical momentum. However, such studies have mainly focused on information at a single time point, and little is known about how AAA properties change over time. Consequently, the present study explored how geometry, wall stress-related and blood flow-related biomechanical properties change during AAA expansion. Four patients with a total of 23 Computed Tomography-Angiography (CT-A) scans at different time points were analyzed. At each time point, patient-specific properties were extracted from (i) the reconstructed geometry, (ii) the computed wall stress at Mean Arterial Pressure (MAP), and (iii) the computed blood flow velocity at standardized inflow and outflow conditions. Testing correlations between these parameters identified several nonintuitive dependencies. Most interestingly, the Peak Wall Rupture Index (PWRI) and the maximum Wall Shear Stress (WSS) independently predicted AAA volume growth. Similarly, Intra-luminal Thrombus (ILT) volume growth depended on both the maximum WSS and the ILT volume itself. In addition, ILT volume, ILT volume growth, and maximum ILT layer thickness correlated with PWRI as well as AAA volume growth. Consequently, a large ILT volume as well as fast increase of ILT volume over time may be a risk factor for AAA rupture. However, tailored clinical studies would be required to test this hypothesis and to clarify whether monitoring ILT development has any clinical benefit.</p></div

La Charente

15 octobre 18801880/10/15 (A9,N4174)-1880/10/15.Appartient à l’ensemble documentaire : PoitouCh