Academic literature on the topic 'Pulmonary Biomechanics'
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Journal articles on the topic "Pulmonary Biomechanics"
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Karzilov, A. I. "The respiratory system biomechanical homeostasis and its maintenance mechanisms in normal conditions and at obstructive pulmonary diseases." Bulletin of Siberian Medicine 6, no. 1 (March 30, 2007): 13–38. http://dx.doi.org/10.20538/1682-0363-2007-1-13-38.
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Parameters of breathing biomechanics in healthy persons (n = 20), patients with bronchial asthma (n = 30) and chronic obstruc-tive pulmonary disease (n = 30) are analyzed during electrical stimulation of the diaphragm. Methodology of homeostatic parame-ters searching and their classification is offered. Descriptive and comparative analyses are performed. Homeostatic parameters of biomechanics describing the condition of elastic and non -elastic properties of respiratory system, of respiratory muscles, of general pulmonary hysteresis, breathing regulation are differentiated. Basic homeostatic parameter is the ratio of inspiratory capacity to the lungs elastic recoil. The model of lungs with the biomechanical buffer and retractive-elastic- surfactant complex of lungs is offered. Biomechanical homeostasis idea of respiratory system as ability of an organism to support in dynamics balance normal and patho-logical conditions essentially important for preservation of respiratory system biomechanical parameters in admissible limits is for-mulated.
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Nappi, Francesco, and Sanjeet Singh Avtaar Singh. "Biomechanics of Pulmonary Autograft as Living Tissue: A Systematic Review." Bioengineering 9, no. 9 (September 8, 2022): 456. http://dx.doi.org/10.3390/bioengineering9090456.
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Introduction: The choice of valve substitute for aortic valve surgery is tailored to the patient with specific indications and contraindications to consider. The use of an autologous pulmonary artery (PA) with a simultaneous homograft in the pulmonary position is called a Ross procedure. It permits somatic growth and the avoidance of lifelong anticoagulation. Concerns remain on the functionality of a pulmonary autograft in the aortic position when exposed to systemic pressure. Methods: A literature review was performed incorporating the following databases: Pub Med (1996 to present), Ovid Medline (1958 to present), and Ovid Embase (1982 to present), which was run on 1 January 2022 with the following targeted words: biomechanics of pulmonary autograft, biomechanics of Ross operation, aortic valve replacement and pulmonary autograph, aortic valve replacement and Ross procedure. To address the issues with heterogeneity, studies involving the pediatric cohort were also analyzed separately. The outcomes measured were early- and late-graft failure alongside mortality. Results: a total of 8468 patients were included based on 40 studies (7796 in pediatric cohort and young adult series and 672 in pediatric series). There was considerable experience accumulated by various institutions around the world. Late rates of biomechanical failure and mortality were low and comparable to the general population. The biomechanical properties of the PA were superior to other valve substitutes. Mathematical and finite element analysis studies have shown the potential stress-shielding effects of the PA root. Conclusion: The Ross procedure has excellent durability and longevity in clinical and biomechanical studies. The use of external reinforcements such as semi-resorbable scaffolds may further extend their longevity.
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Chesler, Naomi C., John Thompson-Figueroa and, and Ken Millburne. "Measurements of Mouse Pulmonary Artery Biomechanics." Journal of Biomechanical Engineering 126, no. 2 (April 1, 2004): 309–13. http://dx.doi.org/10.1115/1.1695578.
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Background: Robust techniques for characterizing the biomechanical properties of mouse pulmonary arteries will permit exciting gene-level hypotheses regarding pulmonary vascular disease to be tested in genetically engineered animals. In this paper, we present the first measurements of the biomechanical properties of mouse pulmonary arteries. Method of Approach: In an isolated vessel perfusion system, transmural pressure, internal diameter and wall thickness were measured during inflation and deflation of mouse pulmonary arteries over low (5–40 mmHg) and high (10–120 mmHg) pressure ranges representing physiological pressures in the pulmonary and systemic circulations, respectively. Results: During inflation, circumferential stress versus strain showed the nonlinear “J”-shape typical of arteries. Hudetz’s incremental elastic modulus ranged from 27±13kPan=7 during low-pressure inflation to 2,700±1,700kPan=9 during high-pressure inflation. The low and high-pressure testing protocols yielded quantitatively indistinguishable stress-strain and modulus-strain results. Histology performed to assess the state of the tissue after mechanical testing showed intact medial and adventitial architecture with some loss of endothelium, suggesting that smooth muscle cell contractile strength could also be measured with these techniques. Conclusions: The measurement techniques described demonstrate the feasibility of quantifying mouse pulmonary artery biomechanical properties. Stress-strain behavior and incremental modulus values are presented for normal, healthy arteries over a wide pressure range. These techniques will be useful for investigations into biomechanical abnormalities in pulmonary vascular disease.
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Mookhoek, Aart, Kapil Krishnan, Sam Chitsaz, Heide Kuang, Liang Ge, Paul H. Schoof, Ad J. J. C. Bogers, Johanna J. M. Takkenberg, and Elaine E. Tseng. "Biomechanics of Failed Pulmonary Autografts Compared With Normal Pulmonary Roots." Annals of Thoracic Surgery 102, no. 6 (December 2016): 1996–2002. http://dx.doi.org/10.1016/j.athoracsur.2016.05.010.
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Haak, Andrew J., Qi Tan, and Daniel J. Tschumperlin. "Matrix biomechanics and dynamics in pulmonary fibrosis." Matrix Biology 73 (November 2018): 64–76. http://dx.doi.org/10.1016/j.matbio.2017.12.004.
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Ghadiali, Samir N., and Donald P. Gaver. "Biomechanics of liquid–epithelium interactions in pulmonary airways." Respiratory Physiology & Neurobiology 163, no. 1-3 (November 2008): 232–43. http://dx.doi.org/10.1016/j.resp.2008.04.008.
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Pyrgar, D. P. "Biomechanics of breathing in young smokers." Kazan medical journal 68, no. 2 (April 15, 1987): 134–35. http://dx.doi.org/10.17816/kazmj96052.
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It is known that one of the main causes contributing to the development of chronic bronchitis, as well as pulmonary emphysema, is smoking. We followed up 66 healthy men from 17 to 34 years old who had no contact with occupational hazards. The examined subjects were subdivided into 2 groups - smokers (31 persons) and nonsmokers (35), which differed little from each other by age and occupation. Smokers consumed at least 6 cigarettes (cigarettes) per day for 6.5 years.
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Tabima, Diana M., and Naomi C. Chesler. "The effects of vasoactivity and hypoxic pulmonary hypertension on extralobar pulmonary artery biomechanics." Journal of Biomechanics 43, no. 10 (July 2010): 1864–69. http://dx.doi.org/10.1016/j.jbiomech.2010.03.033.
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Mookhoek, Aart, Kapil Krishnan, Sam Chitsaz, Heide Kuang, Liang Ge, Paul H. Schoof, Ad J. J. C. Bogers, Johanna J. M. Takkenberg, and Elaine E. Tseng. "Biomechanics of Failed Pulmonary Autografts Compared to Native Aortic Roots." Annals of Thoracic Surgery 103, no. 5 (May 2017): 1482–88. http://dx.doi.org/10.1016/j.athoracsur.2016.08.061.
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Garanin, Andrei A. "Early signs of disorders of cardiovascular biomechanics." Science and Innovations in Medicine 7, no. 1 (January 15, 2021): 39–44. http://dx.doi.org/10.35693/2500-1388-2022-7-1-39-44.
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Aim a comprehensive study of disorders of the biomechanics of blood circulation for early diagnostics of atherosclerosis.
Material and methods. The study included 120 people having one of the following risk factors for cardiovascular diseases: smoking, hypertension, Type 1 or Type 2 diabetes. All subjects underwent computer-assisted rheopulmonography, rheovasography, apexcardiography, and direct sphygmography of the major arteries. The functioning of the heart, the arterial wall, the vascular bed of the pulmonary and systemic circulation was evaluated.
Results. Smoking patients mainly had violations of the pulmonary circulation hemodynamics and the biomechanics of the arterial wall of the peripheral arteries due, obviously, to direct damage by nicotine. In patients with arterial hypertension, there was an increase in the work of the myocardium, obviously as a result of the formation of a hyperkinetic type of blood circulation in this disease. Patients with type 1 and type 2 diabetes mellitus were characterized primarily by the development of systolic-diastolic vascular dysfunction, which may be a predictor of the development of angiopathies in the future. In addition, the study of the kinetics of the major arteries revealed violations of the biomechanics of the wall of all vessels under study with risk factors for atherosclerosis. At the same time, it should be noted that more pronounced changes were found in the distal arteries of the muscular type than in the arteries of the muscular-elastic type, which is obviously associated with hemodynamic overloads experienced by peripheral vessels, both as a result of the hydraulic shock that occurs with hyperkinetic type of blood circulation, and the effect of hydrodynamic forces on the vessel wall under the influence of gravity.
Conclusion. Each factor contributes to the development of disorders of cardiovascular biomechanics and hemodynamics. It is necessary to consider changes in the biomechanics of the heart and vascular bed as early manifestations of the circulatory system malfunction with present risk factors for cardiovascular diseases.
Dissertations / Theses on the topic "Pulmonary Biomechanics"
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Jang, Sae, Rebecca R. Vanderpool, Reza Avazmohammadi, Eugene Lapshin, Timothy N. Bachman, Michael Sacks, and Marc A. Simon. "Biomechanical and Hemodynamic Measures of Right Ventricular Diastolic Function: Translating Tissue Biomechanics to Clinical Relevance." WILEY, 2017. http://hdl.handle.net/10150/626001.
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Background Right ventricular (RV) diastolic function has been associated with outcomes for patients with pulmonary hypertension; however, the relationship between biomechanics and hemodynamics in the right ventricle has not been studied. Methods and Results Rat models of RV pressure overload were obtained via pulmonary artery banding (PAB; control, n=7; PAB, n=5). At 3 weeks after banding, RV hemodynamics were measured using a conductance catheter. Biaxial mechanical properties of the RV free wall myocardium were obtained to extrapolate longitudinal and circumferential elastic modulus in low and high strain regions (E-1 and E-2, respectively). Hemodynamic analysis revealed significantly increased end-diastolic elastance (E-ed) in PAB (control: 55.1 mm Hg/mL [interquartile range: 44.785.4 mm Hg/mL]; PAB: 146.6 mm Hg/mL [interquartile range: 105.8155.0 mm Hg/mL]; P=0.010). Longitudinal E1 was increased in PAB (control: 7.2 kPa [interquartile range: 6.718.1 kPa]; PAB: 34.2 kPa [interquartile range: 18.144.6 kPa]; P=0.018), whereas there were no significant changes in longitudinal E-2 or circumferential E-1 and E-2. Last, wall stress was calculated from hemodynamic data by modeling the right ventricle as a sphere: (stress = Pressure x radius/2 x thickness Conclusions RV pressure overload in PAB rats resulted in an increase in diastolic myocardial stiffness reflected both hemodynamically, by an increase in E-ed, and biomechanically, by an increase in longitudinal E-1. Modest increases in tissue biomechanical stiffness are associated with large increases in E-ed. Hemodynamic measurements of RV diastolic function can be used to predict biomechanical changes in the myocardium.
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Schickel, Maureen Erin. "Biomechanics of Idiopathic Pulmonary Fibrosis and Inferior Vena Cava Filter Perforation." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1406048985.
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Liu, Yifei. "A Correlative Workflow for Imaging Murine Extracellular Matrix to Determine Pulmonary Valve Biomechanics." The Ohio State University, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1619095019644309.
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Patte, Cécile. "Personalized pulmonary mechanics : modeling, estimation and application to pulmonary fibrosis." Thesis, Institut polytechnique de Paris, 2020. http://www.theses.fr/2020IPPAX076.
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Les poumons réalisent leur fonction vitale d'échanges gazeux grâce notamment à leur élasticité et leur porosité. La fibrose pulmonaire idiopathique (FPI), une maladie pulmonaire interstitielle, impacte fortement la mécanique pulmonaire, soulevant des problématiques cliniques. L'objectif de ce travail est d'améliorer la compréhension et le diagnostic de la FPI en s'appuyant sur une modélisation poromécanique du poumon, personnalisée grâce à des données d'imagerie médicale. Dans une première partie, une analyse bibliographique fait l'état de l'art de la physiologie pulmonaire en relation avec les modélisations mécaniques existantes, en insistant sur les caractères multiéchelle, multiphasique et multiphysique de l'organe. Nous proposons ensuite un modèle poromécanique du poumon à l'échelle spatiale de l'organe et à l'échelle temporelle de la respiration, dérivé d'une théorie générale de poromécanique récemment formulée dans l'équipe MΞDISIM. La loi de comportement proposée reproduit notamment le comportement pression-volume du poumon ainsi que la quasi-incompressiblité de la phase solide. Les conditions aux limites prennent en compte l'environnement du poumon (cage thoracique, diaphragme, plèvre) et distinguent les cas de la respiration libre vs ventilée. La configuration déchargée, non observée au cours d'un cycle respiratoire, est estimée, avec une attention particulière apportée pour contraindre la positivité de la porosité. Plusieurs éléments du modèle sont ensuite personnalisés à partir de données cliniques standards, i.e., deux images 3DCT prises en début et en fin d'inspiration. Un problème inverse est notamment formulé pour estimer la compliance pulmonaire en zones saines et fibrosées, la formulation poromécanique permettant de distinguer l’effet de la porosité de celui de la compliance du tissu interstitiel. Appliqué sur trois patients atteints de FPI, le modèle personnalisé permet de retrouver les propriétés pressenties de la FPI, i.e., la rigidification des zones malades. Des surcontraintes sont aussi observées en bordure de la région malade, corroborant ainsi l'hypothèse d'un cercle vicieux mécanique régissant l'évolution de la FPI, où la fibrose entraînerait des contraintes importantes, qui à leur tour favoriseraient la fibrose. Cet outil numérique pourrait servir par la suite au diagnostic objectif et quantitatif de la FPI et, avec des données longitudinales, à l'étude de son remodelage induit par la mécaniqueIdiopathic pulmonary fibrosis (IPF), an interstitial lung disease, strongly impacts lung mechanics, which raises clinical issues. The objective of this work is to improve the understanding and diagnosis of IPF based on poromechanical modeling of the lung, personalized with clinical imaging data. In a first part, a literature review analyzes the state of the art of pulmonary physiology in relation to the existing mechanical models, insisting on the multi-scale, multi-phase and multi-physics characteristics of the organ. We then propose a poromechanical model of the lung at the organ spatial scale and breathing time scale, derived from a general poromechanical theory formulated recently in the MΞDISIM team. The constitutive law proposed reproduces mainly the pressure-volume behaviour of the lung as well as the quasi-incompressiblity of the solid phase. The boundary conditions take into account the lung environment (thoracic cage, diaphragm, pleura) and distinguish between free and ventilated breathing. The unloaded configuration, non observed during a breathing cycle, is estimated, with a special attention given to maintain a positive porosity. Various elements of the model are then personalized with standard clinical data, i.e., two 3DCT images acquired at end-exhalation and end-inhalation. In particular, an inverse problem is formulated to estimate the pulmonary compliance of the healthy and fibrotic regions, since the poromechanical formulation allows to distinguish the effect of the porosity from that of the absolute compliance of the interstitial tissue. Applied to three patients suffering from IPF, the personalized model allows to find the foreseen properties of IPF, i.e., the stiffening of the diseased region. Stress concentrations are also observed at the diseased region interface, supporting the hypothesis of a mechanical vicious circle governing the IPF progress, where fibrosis induces large stresses, which in turn favors fibrosis. This numerical tool could later be used for objective and quantitative diagnosis of IPF and, with longitudinal data, to study the mechanics-induced remodeling
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Gayzik, Francis S. "Development of a Finite Element Based Injury Metric for Pulmonary Contusion." Diss., Virginia Tech, 2003. http://hdl.handle.net/10919/28532.
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Motor vehicle crash (MVC) and its associated injuries remain a major public health problem world wide. In 2005 alone there were 6 million police-reported crashes in the United States resulting in 2.5 million injuries and 46,000 fatalities. The thorax is second only to the head in terms of frequency of injury following MVC, and pulmonary contusion (PC) is the most common intra-thoracic soft tissue injury sustained as a result of blunt chest trauma. The goal of this dissertation research is to mitigate this commonly-sustained and potentially life threatening injury. We have taken a computational approach to solving this problem by developing a predictive injury metric for PC using finite element analysis (FEA).
The dissertation begins with an epidemiological examination of the crash modes, vehicles, and patient demographics most commonly associated with PC. This study was conducted using real world crash data from the Crash Injury Research and Engineering Network (CIREN) database and data from government-sponsored vehicle crash tests. The CIREN data showed that a substantial portion of the crashes resulting in PC were lateral impacts (48%). Analysis of the thoracic loading of dummy occupants in lateral crash tests resulted in mean values of medial-lateral chest compression and deflection velocity of 25.3 ± 2.6 % and 4.6 ± 0.42 m⠢s-1 respectively. These data provided quantified loading conditions associated with crash-induced PC and a framework for the remaining research studies, which were focused on blunt impact experiments examining the relationship between insult and outcome in a living model of this injury.
A combined experimental and computational approach was used to develop injury metrics for PC. The animal model selected for this research was the Sprague-Dawley male rat. In the remaining studies that comprise this dissertation, an outcome measure of the inflammatory response in the lung parenchyma was correlated with a mechanical analog calculated via a finite element model of the lung.
For all studies, a precise and instrumented electronic piston was used to apply prescribed insults directly to the lungs of the subjects. In the first set of experiments, contusion volume was calculated from MicroPET (Micro Positron Emission Tomography) scans and normalized on the basis of liver uptake of 18F-FDG. The subjects were scanned at 24 hours, 7 days, and 28 days (15 scans), and the contused volume was measured. A tentative criteria based on first principal strain in the parenchyma between 9 and 36% was established. In subsequent experiments Computed Tomography was used to acquire volumetric contusion data. The second set of experiments introduced two important aspects of this dissertation; a semi-automated algorithm for CT segmentation and a technique to match the spatial distribution of contusion within the lung to finite element analysis results. The results of this study indicated that the product of first principal strain and strain rate is the most appropriate output variable upon which to base an injury metric for PC. Digital analysis of histology from study subjects that underwent CT scanning prior to sacrifice was conducted and showed good agreement between CT and histology.
A final set of experiments was conducted to synthesize the techniques developed in previous studies to determine an injury metric for PC. A concurrent optimization technique was applied to the FEA model to match force vs. deflection traces from four distinct impact cohorts. The resulting predictive injury metrics for PC were exceeding 94.5 sec-1, first principal strain exceeding 0.284 (true strain, dimensionless), and first principal strain rate exceeding 470 sec-1.
The method used in this dissertation and the resulting injury metrics for PC are based on quantified inflammatory response observed in a living model, specifically in the organ of interest. This injury metric improves upon current thoracic injury criteria that rely on gross measures of chest loading such as acceleration, or deflection, and are not specific to a particular injury. We anticipate that the findings of this work will lead to more data-driven improvements to vehicular safety systems and ultimately diminish the instance of PC and mitigate its severity.Ph. D.
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Gayzik, F. Scott. "Development of a Finite Element Based Injury Metric for Pulmonary Contusion." Diss., Virginia Tech, 2008. http://hdl.handle.net/10919/28532.
Full textAbstract:
Motor vehicle crash (MVC) and its associated injuries remain a major public health problem world wide. In 2005 alone there were 6 million police-reported crashes in the United States resulting in 2.5 million injuries and 46,000 fatalities. The thorax is second only to the head in terms of frequency of injury following MVC, and pulmonary contusion (PC) is the most common intra-thoracic soft tissue injury sustained as a result of blunt chest trauma. The goal of this dissertation research is to mitigate this commonly-sustained and potentially life threatening injury. We have taken a computational approach to solving this problem by developing a predictive injury metric for PC using finite element analysis (FEA).
The dissertation begins with an epidemiological examination of the crash modes, vehicles, and patient demographics most commonly associated with PC. This study was conducted using real world crash data from the Crash Injury Research and Engineering Network (CIREN) database and data from government-sponsored vehicle crash tests. The CIREN data showed that a substantial portion of the crashes resulting in PC were lateral impacts (48%). Analysis of the thoracic loading of dummy occupants in lateral crash tests resulted in mean values of medial-lateral chest compression and deflection velocity of 25.3 ± 2.6 % and 4.6 ± 0.42 m⠢s-1 respectively. These data provided quantified loading conditions associated with crash-induced PC and a framework for the remaining research studies, which were focused on blunt impact experiments examining the relationship between insult and outcome in a living model of this injury.
A combined experimental and computational approach was used to develop injury metrics for PC. The animal model selected for this research was the Sprague-Dawley male rat. In the remaining studies that comprise this dissertation, an outcome measure of the inflammatory response in the lung parenchyma was correlated with a mechanical analog calculated via a finite element model of the lung.
For all studies, a precise and instrumented electronic piston was used to apply prescribed insults directly to the lungs of the subjects. In the first set of experiments, contusion volume was calculated from MicroPET (Micro Positron Emission Tomography) scans and normalized on the basis of liver uptake of 18F-FDG. The subjects were scanned at 24 hours, 7 days, and 28 days (15 scans), and the contused volume was measured. A tentative criteria based on first principal strain in the parenchyma between 9 and 36% was established. In subsequent experiments Computed Tomography was used to acquire volumetric contusion data. The second set of experiments introduced two important aspects of this dissertation; a semi-automated algorithm for CT segmentation and a technique to match the spatial distribution of contusion within the lung to finite element analysis results. The results of this study indicated that the product of first principal strain and strain rate is the most appropriate output variable upon which to base an injury metric for PC. Digital analysis of histology from study subjects that underwent CT scanning prior to sacrifice was conducted and showed good agreement between CT and histology.
A final set of experiments was conducted to synthesize the techniques developed in previous studies to determine an injury metric for PC. A concurrent optimization technique was applied to the FEA model to match force vs. deflection traces from four distinct impact cohorts. The resulting predictive injury metrics for PC were exceeding 94.5 sec-1, first principal strain exceeding 0.284 (true strain, dimensionless), and first principal strain rate exceeding 470 sec-1.
The method used in this dissertation and the resulting injury metrics for PC are based on quantified inflammatory response observed in a living model, specifically in the organ of interest. This injury metric improves upon current thoracic injury criteria that rely on gross measures of chest loading such as acceleration, or deflection, and are not specific to a particular injury. We anticipate that the findings of this work will lead to more data-driven improvements to vehicular safety systems and ultimately diminish the instance of PC and mitigate its severity.Ph. D.
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THOMAS, VINEET SUNNY. "A Multiscale Framework to Analyze Tricuspid Valve Biomechanics." University of Akron / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=akron1542255754172363.
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Munteanu, Bogdan. "Actions de particules d’usure aéroportées sur les propriétés mécaniques et physicochimiques des «films» de surfactant pulmonaire : Conséquences sur la conception de particules tribo-bio-compatibles." Thesis, Lyon, INSA, 2015. http://www.theses.fr/2015ISAL0034/document.
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Paradoxalement, la sécurité routière est assurée entre autre par la production de particules d’usure ! Ainsi, près de 20 000 tonnes de garnitures de frein sont usées par an en France, dont 9 000 tonnes sous forme de particules d’usure aéroportées. Ces particules posent des problèmes de santé car leur composition chimique et leur morphologie font qu’elles interagissent avec la paroi alvéolaire entrainant des pathologies. Au cours de ces pathologies la phase la plus étudiée est la phase inflammatoire qui s’installe une fois que la particule a passé la première barrière de protection qui est le film de surfactant pulmonaire. En revanche, très peu d’études portent sur l’interaction directe des particules aéroportées avec le film de surfactant pulmonaire à cause de difficultés liées aux résolutions des moyens d’investigations cliniques. Alors-que ces études sont d’un intérêt fondamental puisque, de par ses propriétés physicochimiques de surfactant, ce film contrôle la mécanique respiratoire donc la capacité pulmonaire. Dans ce contexte, cette thèse analyse les mécanismes d’action de particules d’usure aéroportées modèles sur les propriétés physicochimiques et mécaniques des parois alvéolaires et plus particulièrement du film de surfactant pulmonaire. Pour cela, un modèle ex vivo de paroi alvéolaire reproduisant la composition, la microstructure du surfactant ainsi que les sollicitations mécaniques pendant les cycles respiratoires, a été mis au point. L’utilisation de ce modèle et les mesures associées ont permis d’élaborer une démarche d’identification des paramètres significatifs des particules qui déterminent leurs interactions avec le film de surfactant pulmonaire. Cela a permis de montrer que l’électronégativité des particules aéroportées est l’un des paramètres significatifs qui induit des changements couplés à différentes échelles, qui vont de la conformation moléculaire (nano), à la microstructure (micro) et aux propriétés mécaniques (macro) de la paroi alvéolaire, conduisant à la diminution de la capacité respiratoire. Ce modèle et les premiers résultats permettront à court terme, d’identifier les autres paramètres significatifs qui caractérisent les actions de particules d’usure aéroportées sur les propriétés mécaniques et physicochimiques des parois alvéolaires. Ceci permettra de connaitre leurs effets sur la capacité pulmonaire. Par conséquent, à plus long terme, cette connaissance permettra de modifier les matériaux en contact et leurs conditions de frottement pour générer des particules satisfaisant les exigences tribologiques et biologiques, donc tribo-bio-compatiblesParadoxically, road safety is assured among others by the production of wear particles! Thus, almost 20 000 tons of brake linings are worn each year in France. 9000 tons are airborne wear particles. Due to their size, chemical composition and morphology these particles will interact with the alveolar wall causing pathologies. In these pathologies the most studied is the inflammatory phase that appear after the particle has passed the first protective barrier which is the pulmonary surfactant film. However, very few studies have examined the direct interaction of airborne wear particles with pulmonary surfactant film. These studies are of fundamental interest because, by its physicochemical properties, the pulmonary surfactant film control the respiratory mechanics, hence the pulmonary capacity. In this context, this thesis analyzes the interaction mechanism of model airborne wear particles on the physicochemical and mechanical properties of the alveolar wall and more particularly of pulmonary surfactant film. For this, an ex vivo model of alveolar wall reproducing the composition of the surfactant, its microstructure and the mechanical stresses during the breathing cycles has been developed. This model and the associated measures allowed to develop a method for identifying significant parameters of the particles that determine their interaction with the pulmonary surfactant film. The results showed that the electronegativity of airborne particles is one of the significant parameters which induces changes at different scales ranging from molecular conformation (nano), microstructure (micro) and mechanical properties (macro) of the alveolar wall, leading to the diminution of the pulmonary capacity. This model and the first results will allow, at short term, to identify other significant parameters which characterize the actions of airborne wear particles on mechanical and physicochemical properties of alveolar walls, allowing to know their effects on lung capacity. Therefore, at longer term, this knowledge will permit to change the materials in contact and their friction conditions to generate wear particles satisfying tribological and biological requirements, so tribo-bio-compatibles
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Peyraut, Alice. "Modeling and Estimation of Pulmonary Poromechanics : towards a Robust High-Fidelity Digital Twin Approach for Idiopathic Pulmonary Fibrosis." Electronic Thesis or Diss., Institut polytechnique de Paris, 2024. http://www.theses.fr/2024IPPAX136.
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La Fibrose Pulmonaire Idiopathique (FPI) est une maladie au pronostic extrêmement sévère, qui affecte directement le parenchyme pulmonaire, et dont les mécanismes d’apparition et d’évolution restent encore mal compris. L’objectif de ce travail de thèse est d’approfondir la compréhension de la FPI en couplant modélisation biomécanique et traitement d’images biomédicales.Tout d'abord, une revue de la littérature relative à la FPI ainsi qu’aux modèles pulmonaires actuels a été effectuée. Un accent particulier est mis sur l’analyse des mécanismes qui pourraient expliquer l’évolution de cette pathologie. En particulier, l’hypothèse d’un lien étroit entre la mécanique, et notamment les concentrations de contraintes, et la progression de la fibrose a été formulée dans la littérature.Le premier axe de ce travail se concentre sur l’amélioration du modèle poromécanique pulmonaire développé dans l’équipe M3DISIM, en y intégrant la gravité et en supprimant le contact avec la cage thoracique. Inclure la gravité dans le modèle permet en effet de reproduire des hétérogénéités physiologiques de contraintes et de déformations lors de la respiration, absentes dans le modèle sans gravité, et permet également la prise en compte de l'orientation (e.g., pronation ou supination) du patient. Le contact avec la cage thoracique, instable et coûteux numériquement, a été remplacé par un champs de pression pleural contraint à vérifier l’équilibre global, modélisant l’ensemble des forces appliquées sur l’extérieur du poumon.De plus, l’identification des paramètres d’un modèle est une étape cruciale pour sa personnalisation. Néanmoins, de nombreuses méthodes existent, chacune présentant ses propres avantages et inconvénients en termes de robustesse et de coût. Cette étude propose donc une méthode de quantification de la robustesse face au bruit et aux erreurs de modèle pour diverses méthodes d’identification. En particulier, une nouvelle formulation de la Méthode d’Écart à l’Équilibre (EGM) en grandes transformations est proposée. Il est démontré que l’EGM, qui est une méthode directe et donc naturellement assez instable, quand couplée à une régularisation par écart à l’équilibre du problème de suivi de mouvement, permet une estimation robuste des paramètres.Le troisième axe de cette étude porte sur la quantification des incertitudes sur l’identification des paramètres du modèle poromécanique pulmonaire à partir d’images cliniques. L’identifiabilité des paramètres, ainsi que leur robustesse aux erreurs de modèle et de mesure, sont analysées afin de déterminer la meilleure paramétrisation du problème d’identification. L’influence du jeu de données utilisé en entrée sur la qualité de l’estimation est également évaluée.Enfin, le dernier axe se concentre sur l’application de l’approche de jumeaux numériques à des jeux de données longitudinales de dix patients atteints de FPI. Pour chaque patient, deux images, l’une en fin d’expiration et l’autre en fin d’inspiration, sont fournies à trois instants d’évolution de la maladie. L’identification de biomarqueurs susceptibles de contribuer à l’explication de l’évolution de la maladie est explorée, notamment en étudiant la corrélation entre certaines quantités d'intérêt et la progression de la fibrose.Ce travail constitue une avancée, en termes de modélisation et personnalisation, du jumeau numérique de poumon développé par l’équipe M3DISIM. Il améliore la physiologie du modèle, sa fiabilité numérique, et quantifie les incertitudes liées aux bruits de mesure et aux erreurs de modèle sur les biomarqueurs calculés. Ces avancées ouvrent la voie à des applications cliniques prometteuses et fournissent des premiers résultats permettant de mieux comprendre l’évolution de la Fibrose PulmonaireIdiopathic Pulmonary Fibrosis (IPF) is a disease with an extremely severe prognosis, which directly affects the lung parenchyma, and whose mechanisms of appearance and progression remain poorly understood. The objective of this thesis work is to improve the understanding of IPF by coupling biomechanical modeling and biomedical image processing.Firstly, a review of the literature relating to IPF as well as current pulmonary models was conducted. Particular emphasis is placed on the analysis of the mechanisms that could explain the evolution of this pathology. Notably, the hypothesis of a close link between mechanics, and in particular stress concentrations, and the progression of fibrosis has been formulated in the literature.The first axis of this work focuses on improving the pulmonary poromechanical model developed in the M3DISIM team, by integrating gravity and removing contact with the rib cage. Including gravity in the model indeed allows to reproduce physiological heterogeneities of constraints and deformations during breathing, absent in the model without gravity, and also allows to take into account the orientation (e.g., pronation or supination) of the patient. The contact with the rib cage, unstable and numerically expensive, has been replaced by a pleural pressure field constrained to verify the global equilibrium, modeling all the forces applied on the outside of the lung. In addition, the identification of the parameters of a model is a crucial step for its personalization. Nevertheless, many methods exist, each with its own advantages and drawbacks in terms of robustness and cost. This study therefore proposes a method for quantifying the robustness to noise and model errors for various identification methods. In particular, a new formulation of the Equilibrium Gap Method (EGM) in large transformations is proposed. It is shown that the EGM, which is a direct method and therefore naturally quite unstable, when coupled with a regularization by equilibrium gap of the motion tracking problem, allows a robust estimation of the parameters.The third axis of this study focuses on the quantification of uncertainties on the identification of the parameters of the pulmonary poromechanical model from clinical images. The identifiability of the parameters, as well as their robustness to model and measurement errors, are analyzed in order to determine the best parameterization of the identification problem. The influence of the dataset used as input on the quality of the estimation is also evaluated.Finally, the last axis focuses on the application of the digital twin approach to longitudinal datasets of ten patients with IPF. For each patient, two images, one at the end-exhalation and the other at the end-inhalation, are provided at three different moments of the evolution of the disease. The identification of biomarkers likely to contribute to the explanation of the evolution of the disease is explored, in particular by studying the correlation between certain quantities of interest and the progression of fibrosis.This work constitutes an advance, in terms of modeling and personalization, of the digital twin of the lung developed by the M3DISIM team. It improves the physiology of the model, its numerical reliability, and quantifies the uncertainties related to measurement noise and model errors on the calculated biomarkers. These advances pave the way for promising clinical applications and provide initial results to better understand the evolution of Pulmonary Fibrosis
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Giménez, Hidalgo Alicia. "Cribratge biomecànic per a la identificació de potencials dianes en la fibrosi pulmonar." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/300298.
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Nombroses malalties resulten d’una alteració de las propietats mecàniques dels teixits i/o d’una alteració en la resposta cel·lular a les forces (mecanotransducció). La fibrosi es el paradigma de la mecànica tissular alterada, caracterizant-se per una excessiva acumulació de matriu extracel·lular (MEC) que destrueix l’arquitectura de l’òrgan. La fibrosi pulmonar idiopàtica (FPI) és una forma de malaltia pulmonar intersticial (MPI) de causa desconeguda i molt mal pronòstic, amb una supervivència del 30-50% als 5 anys.
En aquest treball s’ha desenvolupat una estratègia de cribratge biomecànic que s’ha aplicat l’estudi de la FPI per identificar gens mecanosensibles potencialment rellevants com a dianes terapèutiques. Es van cultivar fibroblasts pulmonars primaris, la cèl·lula responsable del remodelat i enduriment de la MEC, en substrats coberts de col·lagen I de 5 rigideses distintes al llarg del rang fisiopatològic del pulmó, des de la normal (<1 kPa) fins la pròpia de la fibrosi (~30-40 kPa) i en presència de TGF-β. Es van incloure 3 classes de fibroblasts: FPI, control i MPI distintes de la FPI i es va realitzar un perfilat transcripcional mitjançant microarrays d’expressió.
S’ha definit el mecanotranscriptoma dels fibroblasts pulmonars, format per 63 gens mecanosensibles, la transcripció dels quals està controlada pels canvis en les propietats mecàniques de la MEC. Un 57% dels gens van ser sobreexpressats amb l’enduriment i 21 gens van discriminar entre la FPI i las altres dos classes de fibroblasts.
Para entendre las xarxes reguladores associades al mecanotranscriptoma, es va construir l’interactoma dels seus components, el qual va revelar tres xarxes emergents, les quals poden ser rellevants per entendre l’adaptació de les cèl·lules a l’enduriment del substrat en la FPI i en la mecanobiologia en general: 1) elements del citoesquelet i les fibres d'estrés, 2) quinases MAPK i les seves fosfatases i 3) proteïnes relacionades amb el factor de creixement similar a la insulina (IGF) i proteases del sistema de fibrinòlisi.
Després de validar l’expressió a nivell de mRNA i de proteïna de diversos candidats del mecanotranscriptoma, es van caracteritzar diversos aspectes de la proteïna d’unió al factor de creixement similar a la insulina 3 (IGFBP-3).
La concentració d’IGFP-3 secretada pels fibroblasts va ser distintivament superior en els fibroblasts de FPI. Per altra banda, amb l’enduriment del substrat es va detectar un factor de mecanosensibilitat de l’odre 3X en totes les classes de fibroblasts, mentre que el TGF-β la va induir 150 vegades. L’efecte dels dos factors va ser independent, mentre que la seva combinació va potenciar sinèrgicament els nivells d’IGFBP-3. L’efecte de la duresa del substrat en l’acumulació d’IGFBP-3 va ser independent de la senyalització a través del receptor de TGF-β. Per altra banda, els efectes van ser dependents del receptor de col·lagen integrina β1.
Aquests resultats mostren que la IGFBP-3 es una proteïna important en la fibrogènesi pulmonar mediada por l’enduriment, que portaria a una acumulació de MEC i a la destrucció de l’arquitectura del teixit.A new strategy based on a biomechanical screening has been developed and it was applied to the study of idiopathic pulmonary fibrosis (IPF) to identify mechanosensitive genes that might be potential therapeutic targets for the disease. The transcriptional profile of lung fibroblasts (control and fibrotic of different types) cultured on substrates of different stiffness spanning the normal to fibrotic (stiffened) range was obtained. The mechanotranscriptome of the cells was established, which consisted of 63 mechanosensitive genes, 57% of which were upregulated by tissue stiffening. It was built an interactome, showing the regulatory networks associated with the mechanotranscriptome, revealing three different subnetworks: 1) elements of the cytoskeleton and stress fibers; 2) MAPK quinases and their phosphatases; 3) proteins associated with insulin-like growth factor and the fibrinolysis pathway. After validating expression at the mRNA and protein levels for different selected candidates from the mechanotranscriptome, different biological aspects of insulin-like growth factor binding protein 3 (IGFBP-3) were analyzed. Concentration of IGFBP-3 secreted by fibroblasts was distinctively higher in IPF fibroblasts. With substrate stiffening, a mechanosensitivity factor of 3X was detected in all classes of lung fibroblasts, while transforming growth factor- β (TGF- β) induced protein levels by 150X. The effect of tissue stiffening on IGFBP-3 accumulation was independent of signaling through the TGF-β receptor and dependent of the collagen receptor integrin β1. These results show that IGFBP-3 is an important protein for lung fibrogenesis mediated through stiffness and that it could lead to an accumulation of extracellular matrix and contribute to the destruction of the lung architecture.
Books on the topic "Pulmonary Biomechanics"
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Leondes, Cornelius T. Biomechanical Systems: Techniques and Applications, Volume IV: Biofluid Methods in Vascular and Pulmonary Systems. CRC, 2000.
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Leondes, Cornelius T. Biomechanical Systems : Techniques and Applications, Volume IV: Biofluid Methods in Vascular and Pulmonary Systems. Taylor & Francis Group, 2000.
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Arena, Ross, Dejana Popovic, Marco Guazzi, Amy McNeil, and Michael Sagner. Cardiovascular response to exercise. Edited by Guido Grassi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0026.
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The body’s response to an exertional stimulus, if performed adequately to meet the imposed demand, is an orchestrated response predominantly among the cardiovascular, pulmonary, and skeletal systems. These physiological systems work together to ensure that up-titrated energy and force production demands are met. The magnitude of the exertional stimulus these systems are able to respond to, when an individual is in a true state of physiological health, is influenced by multiple factors including age, sex, biomechanics, genomics, and exercise training history. When one or more of these systems suffers from dysfunction, as is the case when an individual is at risk for (i.e. unhealthy lifestyle history) or diagnosed with a chronic disease, the response to a physical stimulus ultimately fails and exertional capacity is limited. There is a clear and well-established clinical relevance to the cardiovascular response to an exertional stimulus, commonly assessed through a graded aerobic exercise test on a treadmill or cycle ergometer. In fact, aerobic capacity has been referred to a key vital sign. We are also gaining an appreciation of how communication and presentation of information between health professionals and individuals receiving care significantly impacts comprehension and adherence to a plan of care. This chapter addresses these areas, beginning with a brief granular description of exertional cardiovascular physiology, transitioning to practical clinical implications of this information for health professionals, and ending with how the individuals seeking healthcare receive, process, and comprehend this information with the ultimate goal being real-world application and improved health outcomes.
Book chapters on the topic "Pulmonary Biomechanics"
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Wagner, Wiltz W. "Recruitment of Pulmonary Capillaries." In Respiratory Biomechanics, 123–29. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_15.
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Lee, J. S., and L. P. Lee. "Distensibility of the Pulmonary Capillaries." In Respiratory Biomechanics, 117–22. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_14.
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Yen, R. T., D. Tai, Z. Rong, and B. Zhang. "Elasticity of Pulmonary Blood Vessels in Human Lungs." In Respiratory Biomechanics, 109–16. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_13.
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Linehan, John H., and Christopher A. Dawson. "Sites of Pulmonary Vasoconstriction: Indirect and Direct Measurements." In Respiratory Biomechanics, 137–44. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_17.
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Maarek, Jean-Michel, and H. K. Chang. "Pulsatile pulmonary capillary pressure measured with the arterial occlusion technique." In Respiratory Biomechanics, 130–36. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_16.
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Robertson, H. Thomas, and Robb W. Glenny. "Quantitation of the Regional Distribution of Pulmonary Blood Flow by Fractal Analysis." In Respiratory Biomechanics, 196–200. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_26.
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Schuster, D. P., J. Markham, J. Kaplan, T. Warfel, and M. Mintun. "An Error Analysis of Pulmonary Vascular Permeability Measurements Made with Positron Emission Tomography." In Respiratory Biomechanics, 147–54. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3452-4_18.
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Yen, R. T., and S. S. Sobin. "Pulmonary Blood Flow in the Cat: Correlation Between Theory and Experiment." In Frontiers in Biomechanics, 365–76. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4866-8_26.
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Alderink, Gordon J., and Blake M. Ashby. "Thoracic Spine and Rib Cage Pain with a Comorbidity of Chronic Obstructive Pulmonary Disease." In Clinical Kinesiology and Biomechanics, 179–204. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-25322-5_8.
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Liang, Jianming, Tim McInerney, and Demetri Terzopoulos. "Analyzing the Shape and Motion of the Lungs and Heart in Dynamic Pulmonary Imaging." In Lecture Notes in Computational Vision and Biomechanics, 291–314. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03813-1_9.
Full textConference papers on the topic "Pulmonary Biomechanics"
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Chesler, Naomi C., John A. Thompson-Figueroa, and Kenneth M. Millburne. "Ex Vivo Measurement of Mouse Pulmonary Artery Biomechanics." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32783.
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Primary pulmonary hypertension (PPH) is a rapidly progressing and often fatal disease that induces substantial pulmonary vascular remodeling [1]. Although a genetic factor has been identified in familial and sporadic cases of pulmonary hypertension [2], the etiology of the disease for most victims remains unknown.
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Wang, Zhijie, Roderic S. Lakes, and Naomi C. Chesler. "Changes in Conduit Pulmonary Arterial Static and Dynamic Mechanical Properties During Severe Hypoxic Pulmonary Hypertension." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80382.
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Pulmonary hypertension (PH) is a complex disorder that manifests as abnormally high blood pressure in the vasculature of the lungs. The chronic structural and mechanical changes in the proximal pulmonary artery (PA) associated with PH include smooth muscle cell hypertrophy and proliferation, accumulation of extracellular matrix (ECM) protein and increased stiffness1–4. Recent evidence has shown that conduit PA stiffness is a strong predictor of mortality in pulmonary arterial hypertension5,6. This suggests a potential association between large PA biomechanics and right ventricle failure.
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Kobs, Ryan W., Nidal E. Muvarak, and Naomi C. Chesler. "Hypoxia-Induced Changes in the Mechanical Properties of the Mouse Pulmonary Artery." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43086.
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Hypobaric hypoxia produces pulmonary hypertension in mice which causes pulmonary vascular remodeling. To study the biomechanics of this process, mice were exposed to hypoxia for 0-(control), 10-, and 15-days. Using a pressurized arteriograph system, mechanical properties of the main pulmonary artery were measured and compared to the biological changes in the vessel wall measured histologically. 10- and 15-day hypoxic vessels were significantly stiffer when compared to 0-day vessels. This stiffness correlated with greater elastin and collagen content in the vessel wall.
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Bayat, S., J. Cercos, L. Fardin, G. Perchiazzi, and A. Bravin. "Pulmonary acinar biomechanics imaged with synchrotron phase contrast microtomography in live rats." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1780.
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Bayat, S., J. Cercos, L. Fardin, G. Perchiazzi, and A. Bravin. "Pulmonary vascular biomechanics imaged with synchrotron phase contrast microtomography in live rats." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1741.
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Dadkhah, Arash, Sreyankar Nandy, Sarita R. Berigei, Ashok Muniappan, Amita Sharma, Melissa J. Suter, Martin Villiger, Corey Hardin, and Lida P. Hariri. "Lung parenchyma biomechanics in pulmonary fibrosis using endobronchial optical coherence tomography elastography imaging: a preliminary investigation." In Endoscopic Microscopy XVII, edited by Melissa J. Suter, Guillermo J. Tearney, and Thomas D. Wang. SPIE, 2022. http://dx.doi.org/10.1117/12.2610412.
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Huang, Hsiao-Ying Shadow, Brittany N. Balhouse, and Siyao Huang. "A Biomechanical and Biochemical Synergy Study of Heart Valve Tissue." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-87997.
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The function of heart valves is to allow blood to flow through the heart smoothly and to prevent retrograde flow of blood. Previous studies have shown that the mechanical properties of heart valve tissues, microstructures of extracellular matrix, and collagen concentrations are the keys to the healthy heart valves and, therefore, are crucial to the development of viable tissue-engineered heart valve replacements. Therefore, this study investigates the relationship between these factors in native porcine aortic and pulmonary valves and provides insights to the healthy heart valves. Heart valve leaflets are prepared for biaxial stretching to obtain mechanical properties. The average collagen concentrations of heart valve leaflets are determined via an assay kit. The results indicate that aortic valves are stiffer than pulmonary valves macroscopically and stiffness varies more in the circumferential direction for the aortic valve than it does for the pulmonary valve. Microscopically, it is due to collagen fibers in aortic valves are more in alignment than ones in pulmonary valves, which are more randomly in direction. Collagen assay results show that collagen concentrations are higher in the edges of pulmonary valves than in aortic valves. The results also suggest the duration of extraction may have significant affects on the concentration results. This work provides quantified stress and strain environment within heart valve tissues to help further studies on how to treat heart valve disease and create more viable heart valve replacements.
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Fata, Bahar, Christopher A. Carruthers, Gregory A. Gibson, Simon C. Watkins, Danielle Gottlieb, John E. Mayer, and Michael S. Sacks. "Regional Biomechanical and Microstructural Alterations of the Ovine Main Pulmonary Artery During Postnatal Growth." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80085.
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It has been estimated that worldwide 600,000 babies are born annually with significant congenital heart disease (1). Congenital heart and related vascular defects cause increased flow and pulmonary pressure leading to unfavorable vascular remodeling that results in pulmonary arterial hypertension (1). Developing tissue engineered replacements that mimic the growth and remodeling behavior of native tissue is the optimal approach in treatment of congenital arterial anomalies. The understanding of the underlying mechanisms leading to pulmonary arterial hypertension as well as replicating native pulmonary artery functionality in engineered replacements requires knowledge of native tissue mechanics and growth behavior. In the present study, we report novel information on the changes in the structure-mechanics behavior of the growing pulmonary artery.
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Fata, Bahar, Elena Galdi, and Michael S. Sacks. "A Comparative Study of the Main Pulmonary Artery and Ascending Aorta Biomechanical Behavior." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53932.
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During the prenatal period a state of physiologic pulmonary hypertension exists due to the equalization of pressures by the patent ductus arteriosus, resulting in similar wall thickness of the ascending aorta (AA) and main pulmonary artery (MPA). After birth, as the ductus arteriosus closes and pulmonary arterial pressure decreases, attenuation of medial smooth muscle occurs such that the ratio of medial thickness to external diameter decreases from about 25% in fetuses to less than 10% in infants 3 to 6 months of age. After the first year of life, thickness of the MPA is normally less than half that of the adjacent ascending aorta, although the diameters of the two great arteries remain the same relative to one another [1]. During homeostatic conditions, the total pulmonary and systemic blood flows are essentially identical. In spite of their comparable blood flow rate and common embryologic origin, the anatomic characteristics of these two segments of the cardiovascular system differ substantially [2]. Futhremore, both these arteries are affected by many congenital abnormalities and also are subject to hypertension. Knowledge of the normal biomechanical properties of these great arteries is important for surgical treamtment, angioplasty, and tissue engineering. It can also provide insight into the disease processes and is a prerequisite to the study of mechanical behavior during disease conditions. In this study we characterized the biaxial mechanical behavior of both arteries as a function of location, which has not been previously performed in the pulmonary trunk.
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Scott, Devon, Aaron Richman, Craig Lanning, Robin Shandas, and Wei Tan. "Devlopment of a Cell Coculture Microfluidic Shear Device for Mechano-Transmission Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176700.
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We have developed a microfluidic shear device that allows for the study of cell communication in a dynamically controlled biochemical and biomechanical environments simulating cells’ living environments in vivo. Such study may help to improve our understanding in the effects of hypertension-relevant and vascular development-relevant flow shear stress on cell behaviors. Endothelial cells may be a key factor for transmitting the blood flow conditions from the endothelial lining to interstitial layers and smooth muscle cells. The interstitial flow stress and the shear stress induced signaling factors may greatly alter vascular biology of these deep layers. Endothelial cells act as a mechano-transducer by converting shear stress into biochemical signaling factors. The biochemical factors diffuse to smooth muscle cells and further alter the biological structure of vascular tissues. Also, the flow shear stress will be transmitted to the interstitial tissue layer through the pores resulted from the pores in the fenestrated endothelial lining. Studies in both the mechano-transduction process and the mechano-transmission process will benefit from a biomimetic flow shear device with co-cultured cells. Our device will allow the co-culture of endothelial cells and smooth muscle cells to study these biomechanical processes. The pulmonary arterial cells are used as a model in the study. The microfluidic device developed here will be used to enhance the understanding of pulmonary vascular disease pathogenesis due to the variations in the flow shear stress.