Dissertations / Theses: 'Aortic tissue'

1

Nowell, Justin L. "Anticoagulation Following Tissue Aortic Valve Replacement." Thesis, St George's, University of London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517184.

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Liu, Janet. "Design of a Novel Tissue Culture System to Subject Aortic Tissue to Multidirectional Bicuspid Aortic Valve Wall Shear Stress." Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1527077368757049.

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3

Smuts, Adriaan Nicolaas. "Design of tissue leaflets for a percutaneous aortic valve." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/1625.

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MScEng
Thesis (MScEng (Mechanical and Mechatronic Engineering))--University of Stellenbosch, 2009.
In this project the shape and attachment method of tissue leaflets for a percutaneous aortic valve is designed and tested as a first prototype. Bovine and kangaroo pericardium was tested and compared with natural human valve tissue by using the Fung elastic constitutive model for skin. Biaxial tests were conducted to determine the material parameters for each material. The constitutive model was implemented using finite element analysis (FEA) by applying a user-specified subroutine. The FEA implementation was validated by simulating the biaxial tests and comparing it with the experimental data. Concepts for different valve geometries were developed by incorporating valve design and performance parameters, along with stent constraints. Attachment techniques and tools were developed for valve manufacturing. FEA was used to evaluate two concepts. The influence of effects such as different leaflet material, material orientation and abnormal valve dilation on the valve function was investigated. The stress distribution across the valve leaflet was examined to determine the appropriate fibre direction for the leaflet. The simulated attachment forces were compared with suture tearing tests performed on the pericardium to evaluate suture density. In vitro tests were conducted to evaluate the valve function. Satisfactory testing results for the prototype valves were found which indicates the possibility for further development and refinement.

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4

Kermani, Golriz. "Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/412554.

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Mechanical Engineering
Ph.D.
Traumatic aortic rupture (TAR) is one of the leading causes of morbidity and mortality in motor-vehicle accidents with the majority of injuries occurring in the peri-isthmus region. To date, the mechanisms of aorta injury are poorly understood as this injury cannot be replicated reliably in cadaver crash tests. Due to inconclusiveness of the experimental tests, finite element (FE) modeling is often used to gain a better insight into the mechanisms of TAR. However, the FE models are also hindered by many unknowns particularly the soft tissues biomechanical responses. A crucial step to improve the FE models of blunt chest trauma is to advance our understanding of the local mechanical properties of aortic tissue subject to high loading rates associated with TAR. The objective of this dissertation was to investigate the effects of tissue rate dependency and inhomogeneity in the modeling of loading conditions that lead to TAR. The material properties of human aorta in large deformations and high loading rates were characterized based on oscillatory biaxial tests. It was shown that a quasilinear viscoelastic (QLV) model with the instantaneous elastic response of the second order and the reduced relaxation function with one exponentially decaying term could describe the experimental results between 20 Hz and 130 Hz. The obtained decay rates (in the range of 70 to 550 s-1) were 10 to 100 folds higher than previously reported values and showed significant rate dependence within 10 ms after the loading. It was shown that the rate dependent properties, similar to the elastic properties, were anisotropic with generally higher decay rate and stiffness observed in the circumferential direction compared to the longitudinal direction. The inhomogeneity of porcine descending thoracic aorta was characterized in three dimensions using a nano-indentation technique and QLV modeling approach. The tests were conducted in the axial, circumferential, and radial orientations with about 100 micrometer spatial resolution. Aortic tissue was divided into 10 regions across the thickness, 4 quadrants in the circumferential direction, and 3 sections in the longitudinal direction. While across the thickness, the results in different orientations were significantly different, four distinct layers were identified that were matched with the anatomical features. In the axial direction, the medial quadrant, and in all directions, the proximal DTA had the lowest stiffness. The results predict that under equal stresses, the inner layers of the medial quadrant in upper DTA would undergo more strains and will be therefore more prone to failure. This prediction is in agreement with clinical observations. The inhomogeneity and rate dependency of aorta were implemented in the Global Human Body Models Consortium full-body FE model. It was demonstrated that in a simulation of blunt chest impact, both features significantly affected the tissue strain levels particularly in the isthmus, arch, and ascending aorta. Accurate quantifications of these features are essential to assess the risk of aortic injury based on FE models.
Temple University--Theses

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Korossis, Sotirios Anastasios. "Biomechanics and hydrodynamics of decellularised aortic valves for tissue engineering." Thesis, University of Leeds, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270873.

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6

Rastgar, Agah Mobin. "Material Characterization of Aortic Tissue for Traumatic Injury and Buckling." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/324268.

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Mechanical Engineering
Ph.D.
While traumatic aortic injury (TAI) and rupture (TAR) continue to be a major cause of morbidity and mortality in motor vehicle accidents, its underlying mechanisms are still not well understood. Different mechanisms such as increase in intraluminal pressure, relative movement of aorta with respect to mediastinal structures, direct impact to bony structures have been proposed as contributing factors to TAI/TAR. At the tissue level, TAI is assumed to be the result of a complex state of supra-physiological, high rate, and multi-axial loading. A major step to gain insight into the mechanisms of TAI is a characterization of the aortic tissue mechanical and failure properties under loading conditions that resemble traumatic events. While the mechanical behavior of arteries in physiological conditions have been investigated by many researchers, this dissertation was motivated by the scarcity of reported data on supra-physiological and high rate loading conditions of aorta. Material properties of the porcine aortic tissue were characterized and a Fung-type constitutive model was developed based on ex-vivo inflation-extension of aortic segments with intraluminal pressures covering a range from physiological to supra-physiological (70 kPa). The convexity of the material constitutive model was preserved to ensure numerical stability. The increase in ë_è from physiological pressure (13 kPa) to 70 kPa was 13% at the outer wall and 22% at the inner wall while in this pressure range, the longitudinal stretch ratio ë_z increased 20%. A significant nonlinearity in the material behavior was observed as in the same pressure range, the circumferential and longitudinal Cauchy stresses at the inner wall were increased 16 and 18 times respectively. The effect of strain-rate on the mechanical behavior and failure properties of the tissue was characterized using uniaxial extension experiments in circumferential and longitudinal directions at nominal strain rates of 0.3, 3, 30 and 400 s-1. Two distinct states of failure initiation (FI) and ultimate tensile strength (UTS) were identified at both directions. Explicit direct relationships were derived between FI and UTS stresses and strain rate. On the other hand, FI and UTS strains were rate independent and therefore strain was proposed as the main mechanism of failure. On average, engineering strain at FI was 0.85±0.03 for circumferential direction and 0.58±0.02 for longitudinal direction. The engineering strain at UTS was not different between the two directions and reached 0.89±0.03 on average. Tissue pre-failure linear moduli showed an average of 60% increase over the range of strain rates. Using the developed material model, mechanical stability of aorta was studied by varying the loading parameters for two boundary conditions, namely pinned-pinned boundary condition (PPBC) and clamped-clamped boundary condition (CCBC). The critical pressure for CCBC was three times higher than PPBC. It was shown that the relatively free segment of aorta at the isthmus region may become unstable before reaching the peak intraluminal pressures that occur during a trauma. The mechanical instability mechanism was proposed as a contributing factor to TAI, where elevations in tissue stresses and strains due to buckling may increase the risk of injury.
Temple University--Theses

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Treibel, Thomas Alexander. "Aortic stenosis : a myocardial disease : insights from myocardial tissue characterisation." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1574742/.

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Aortic stenosis (AS) is a disease of not just the valve, but also of the myocardium. Patient symptoms and outcome are determined by the myocardial response; a crucial but poorly understood process. Diffuse and focal myocardial fibrosis play a key role. Until recently, both could only be assessed using invasive histology, but now cardiovascular magnetic resonance (CMR) offers late gadolinium enhancement (LGE) and extracellular volume fraction (ECV) techniques. In this thesis, I developed new methods to quantify ECV by synthetic ECV and cardiac CT. I then explored myocardial remodelling and fibrosis in patients with severe AS undergoing aortic valve replacement (AVR) using myocardial biopsy, CMR, biomarkers and a wide range of clinical parameters. Prior to AVR, CMR in patients with severe AS revealed important differences in myocardial remodelling between sexes, otherwise missed on echocardiography alone. Given apparently equal valve severity, the myocardial response to AS appeared unexpectedly maladaptive in men compared to women. Intra-operative myocardial biopsy revealed three pattern of fibrosis: endocardial fibrosis, microscars (mainly in the subendomyocardium), and diffuse interstitial fibrosis. Biopsy best captured the transmural gradient of fibrosis and microscars, while on CMR, LGE captured mainly microscars and ECV captured mid-myocardial related functional changes beyond LGE. Combining LGE and ECV allowed better stratification of AS patients. Incidentally, I found that 6% of AS patients older then 65 years had wild-type transthyretin amyloid deposits on cardiac biopsy, which was associated with poor outcome. This is now the basis of a BHF research fellowship. Following AVR, I demonstrated for the first time non-invasively that diffuse fibrosis regresses (focal fibrosis did not), which is accompanied by structural and functional improvements suggesting that human diffuse fibrosis is plastic, measurable by CMR and a potential therapeutic target.

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Luo, Yuanming. "Local properties and rupture characteristics of thoracic aortic aneurysm tissue." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6186.

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Ascending thoracic aortic aneurysms (ATAAs) are focal dilatations in the aorta that are prone to rupture or dissect. Currently, the clinically used indicator of the rupture risk is the diameter. However, it has been demonstrated that the diameter alone may not properly predict the risk. To evaluate the rupture risk, one must look into the local mechanical conditions at the rupture site and understand how rupture is triggered in the tissue which is a layered fibrous media. A challenge facing experimental studies of ATAA rupture is that the ATAA tissue is highly heterogeneous; experimental protocols that operate under the premise of tissue homogeneity will have difficulty delineating the heterogeneous properties. In general, rupture initiates at the location where the micro-structure starts to break down and consequently, it is more meaningful to investigate the local conditions at the rupture site. In this work, a combined experimental and computational method was developed and employed to characterize wall stress, strain, and property distributions in harvested ATAA samples to a sub-millimeter resolution. The results show that all tested samples exhibit a significant degree of heterogeneous in their mechanical properties. Large inter-subject variability is also observed. A heterogeneous anisotropic finite strain hyperelastic model was introduced to describe the tissue; the distributions of the material parameters were identified. The elastic energy stored in the tissue was computed. It was found that the tissue fractures preferentially in the direction of the highest stiffness, generating orifices that are locally transverse to the peak stiffness direction. The rupture appears to initiate at the position absorbed of the highest energy. Machine learning was used to classify the curves at rupture and non-rupture locations. Features including material properties and curve geometric characteristics were used. The work showed that the rupture and non-rupture states can indeed be classified using pre-rupture response features. Support vector machine(SVM) and random forest algorithm was employed to provide insight on the importance of the features. Inspired by the importance scores provided by random forest, the rupture groups were interrogated and some strong correlations between the strength and the response features were revealed. In particular, it was found that the strength correlates strongly with the tension at the point where the curvature of the total tension strain curve attains maximum, which occurs early in the response.

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Joda, Akram Abdelazim Osman. "Fluid-structure interaction of the aortic valve for tissue engineering applications." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.550815.

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Currently, tissue-engineered heart valves (TEHV) have shown a great prospective to replace the conventional prosthetics heart valves for their ability to grow and remodel. It is well established that in order for the seeded cells to behave in an appropriate manner and infiltrate, populate and remodel during in vitro culture, they need to be exposed to appropriate levels of mechanical stimulation that favour the regeneration of the valve-equivalent tissue with appropriate valvular-tissue- specific functionality. Mathematical modelling is an important tool that can be used alongside TEHV bioreactors with a view to optimising their function by relating the stress-strain distributions in the valve leaflets to the flow and pressure conditions generated by the bioreactor. For that, physiologically accurate 3D fluid structure interaction (FSI) models of fresh and decellularised aortic valves were developed. At first two FSI methods were used to study FSI of a 20 aortic valve, the Arbitrary Lagrangian Eulerian (ALE) method and the Multi-Material Arbitrary Lagrangian Eulerian (MM- ALE) method. The ALE method uses a dynamic mesh in the fluid domain to account for the valve deformations, while in the MM-ALE method, the fluid mesh remains fixed during the computation. Good agreement was found between the results of the two FSI methods. Furthermore, the MM-ALE method was employed to perform FSI of a bileaflet mechanical valve and the results were validated by comparison with pulsatile flow experim~nts. 3D FSI models of the natural aortic valve were developed using three material models for the leaflet (nonlinear isotropic, fiber-reinforced and Fung-type nonlinear orthotropic) and comparisons were conducted to in vivo and in vitro data. Finally, FSI models of decellularised aortic valve scaffolds cultured in vitro under different operation conditions were performed using the nonlinear orthotropic model for optimising a TEHV bioreactor.

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Fraser, Katharine H. "Computational estimation of haemodynamics and tissue stresses in abdominal aortic aneurysms." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/24588.

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Abdominal aortic aneurysm is a vascular disease involving a focal dilation of the aorta. The exact cause is unknown but possibilities include infection and weakening of the connective tissue. Risk factors include a history of atherosclerosis, current smoking and a close relative with the disease. Although abdominal aortic aneurysm can affect anyone, it is most often seen in older men, and may be present in up to 5.9% of the population aged 80 years. Biomechanical factors such as tissue stresses and shear stresses have been shown to play a part in aneurysm progression, although the specific mechanisms are still to be determined. The growth rate of the abdominal aortic aneurysm has been found to correlate with the peak stress in the aneurysm wall and the blood flow is thought to influence disease development. In order to resolve the connections between biology and biomechanics, accurate estimations of the forces involved are required. The first part of this thesis assesses the use of computational fluid dynamics for modelling haemodynamics in abdominal aortic aneurysms. Boundary conditions from the literature on healthy patients are used, along with patient specific aneurysm geometries, to obtain a first estimate of blood flow patterns and haemodynamic wall parameters within the aneurysms. The use of healthy patient boundary conditions is difficult to justify as the presence of the aneurysm is likely to alter the flow rate in the aorta. This is investigated with a Doppler ultrasound study of blood velocities in the normal and aneurysmal aorta. Archetypal waveforms reveal a significant difference in the diastolic maximum of young healthy volunteers and AAA patients. The archetypal aortic velocity wave for patients with abdominal aortic aneurysm is used to calculate the haemodynamics in a group of patients and these calculations are compared with those obtained using patient specific boundary conditions, and with phase-contrast magnetic resonance imaging measurements of blood velocity. With the correct z-velocity profile at the entrance to a short inlet section proximal to the aneurysm, the calculated velocities agreed qualitatively with the measured velocities. However, the velocities calculated using the correct inlet flow rate, but a simple velocity profile, are quite different from the measurements. These results show that the correct velocity profile at the aneurysm entrance is required to predict velocities within the aneurysm cavity. In reality the blood and the artery wall interact: the blood flow domain continually dilates and contracts, altering the flow patterns; the flow controls the pressure on the wall and therefore the stresses within it. The influence of this fluid-structure interaction on the blood flow and tissue stresses is investigated in axially symmetric models of abdominal aortic aneurysm. Modelling of the complete fluid-structure interaction reveals how the pressure and flow waves are distorted by the aneurysm geometry. This distortion, which is absent from both static pressure and one way coupled models, accounts for the small errors in tissue and wall shear stresses obtained when using these models with lower computational complexity. These errors vary with the type of modelling as well as the aneurysm diameter and elasticity. A one dimensional, lumped parameter model of the aneurysm is developed to elucidate the effect of aneurysm geometry on the propagation of pressure and flow waves. It reveals interesting consequences of the diameter of the aneurysm on its inductance and resistance, and its use in improving the outlet pressure boundary condition is investigated.

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Chu, Boby. "Characterization of aortic tissue fracture toughness and stiffness under cyclical fatigue loading." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86772.

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An ascending aortic aneurysm is an asymptomatic disease that, if left untreated, could lead to death through its eventual rupture. Current clinical management practices are based primarily on the monitoring of an aneurysm's growth, followed by surgical resection of the affected aortic segment when its diameter reaches 5 to 5.5 centimetres. Unfortunately, this method is based solely on clinical observations and is frequently inaccurate in predicting the risk of an imminent rupture. More sophisticated tools have been developed and do not depend on aneurysm size alone, but these have focused mostly on the distribution of stresses within an aneurismal aortic wall and do not give clinicians an estimate of the time to failure.
This present work incorporates the temporal aspect by examining the effects of fatigue on aortic wall properties, and adopts an energetics approach to evaluating the aorta's resistance to rupture. Tissue samples from porcine aortas were fatigued and were subjected to both biaxial and guillotine tests to assess stiffness and fracture toughness. The experiments indicate that both properties decreased according to a power function. After 1 000 000 loading cycles, the final/initial stiffness ratio dropped to 0.85, while its toughness counterpart fell to 0.80.
This work constitutes the first tentative steps towards the development of a clinical tool that can evaluate the fracture toughness of aneurismal aortic tissues and predict the temporal likelihood of aneurismal rupture.
L'anévrisme de l'aorte ascendante est une maladie asymptomatique. Sans traitement, un anévrisme peut se rompre, ce qui est fatal. Les pratiques cliniques actuelles reposent d'abord sur l'observation de la croissance de la taille de l'anévrisme qui est suivie de la résection chirurgicale de l'aorte lorsque son diamètre atteint 5 à 5,5 cm. Malheureusement, cette méthode est peu précise comme indicateur de risque de rupture et ne s'appuie que sur les observations cliniques pour justifier son application. Plusieurs outils de prédiction plus sophistiqués sont en voie de développement, mais les efforts récents se concentrent surtout sur la distribution des tensions au sein des parois anévrysmales, mais les résultats ne donnent aucune prédiction sur le délai avant que la résection soit nécessaire.
Ce travail incorpore l'aspect temporel en examinant l'effet de la fatigue sur les propriétés mécaniques des parois aortiques, tout en adoptant l'approche énergétique pour évaluer la résistance à la rupture du vaisseau. À cette fin, des échantillons de tissus d'aortes porcines sont étirés cycliquement. Leur rigidité et leur résistance à la rupture sont ensuite mesurées grâce aux tests biaxiaux et aux tests à la guillotine. Les résultats expérimentaux montrent une décroissance selon une loi de puissance. Après un million de cycles de tension, le rapport rigidité finale/rigidité initiale a baissé à 0,85, et celui de la résistance à la rupture a chuté jusqu'à 0,80.
Ce travail est une première étape dans le développement d'un outil clinique pour mesurer la résistance à la rupture des tissus aortiques anévrysmaux afin de prédire la probabilité d'une rupture sur une échelle de temps.

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12

Bevis, Paul Michael. "Abdominal aortic aneurysms and the association with a systemic connective tissue disorder." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544428.

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13

Han, Richard I.-Ming. "Early calcification patterns of bioprosthetic aortic tissue : a comparison of amino versus carboxyl group and combination cross-linked tissue." Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/2780.

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14

Weston, Matthew W. "Characterization of the shear stress on the aortic valve leaflet surface and its effects on cellular biosynthetic activity." Diss., Georgia Institute of Technology, 2000. http://hdl.handle.net/1853/9369.

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Xing, Yun. "Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/6828.

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Cardiac valves are dynamic, sophisticated structures which interact closely with the surrounding hemodynamic environment. Altered mechanical stresses, including pressure, shear and bending stresses, are believed to cause changes in valve biology, but the cellular and molecular events involved in these processes are not well characterized. Therefore, the overall goal of this project is to determine the effects of pressure and shear stress on porcine aortic valve leaflets biology. Results from the pressure study showed that elevated constant pressure (140 and 170 mmHg) causes significant increases in collagen synthesis. The increases were 37.5% and 90% for 140 and 170 mmHg, respectively. No significant differences in DNA and sGAG synthesis were observed under constant pressure. In the cyclic pressure study, the effects of both pressure magnitude and pulse frequency were studied. With the frequency fixed at 1.167 Hz, collagen and sGAG synthesis increased proportionally with mean pressure level. At a fixed pressure level (80-120 mmHg), collagen and sGAG synthesis were slightly increased by 25% and 14% at 0.5 Hz, respectively. DNA synthesis was significantly increased by 72% at 2 Hz. An experiment combining high magnitude (150-190 mmHg) and high frequency (2 Hz) demonstrated significant increases in collagen and sGAG synthesis (collagen: 74%, sGAG: 56%), but no significant changes in cell proliferation. Shear levels ranging from 1 to 80 dyne/cm2 were studied. Scanning electron microscopy results indicated that 48 hrs exposure to shear stress did not alter the circumferential alignment of endothelial cells. Collagen synthesis was significantly enhanced at 9 and 25 dyne/cm2, but not different from static controls under other shear conditions. Leaflets denuded of the endothelium were exposed to identical shear stress and showed very different responses. Collagen synthesis was not affected at any shear levels, but sGAG content was increased at shear of 9, 25 and 40 dyne/cm2. Further studies showed that the increases in collagen synthesis under pressure or shear stress was concurrent with a decline in the expression and activities of cathepsins L and S. This converse relationship between collagen synthesis and cathepsin activity indicated that cathepsins might be involved in valvular ECM remodeling.

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Dahal, Shataakshi. "Stem Cells Based Elastic Matrix Regeneration for Small Abdominal Aortic Aneurysms (AAAs) Repair." Cleveland State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=csu1599137475237285.

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Dahal, Shataakshi. "Stem Cells Based Elastic Matrix Regeneration for Small Abdominal Aortic Aneurysms (AAAs) Repair." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1599137475237285.

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Zemánek, Miroslav. "Influence of Geometrical Parameters on Rupture Risk of Abdominal Aortic Aneurysm." Doctoral thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2010. http://www.nusl.cz/ntk/nusl-233934.

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Tato práce je zaměřena na problematiku výpočtového a experimentálního modelování deformačně napjatostních stavů měkkých tkání se zaměřením na riziko ruptury u výdutě břišní aorty (AAA). V první části (kap. 1) je stručně nastíněn současný stav dané problematiky. Tato část shrnuje důležité poznatky publikované v dostupné literatuře. Pozornost je věnována zejména klíčovým faktorům pro stanovení rizika ruptury AAA. V další kapitole (kap. 2) je stručně popsána histologie cévní stěny a její výsledné mechanické chování, jakož i její patologie, především AAA. Druhá část práce (kap.3) je věnována experimentálnímu vyhodnocování deformačně napjatostního chování měkkých tkání, které je nutným předpokladem k věrohodnému výpočtovému modelování tohoto chování. V této kapitole je stručně popsáno experimentální zařízení speciálně vyvinuté pro testování měkkých tkání a typy zkoušek, které lze na tomto zařízení provádět. Dále jsou shrnuty klíčové faktory ovlivňující deformačně napjatostní chování měkkých tkání a experimentální ověření těchto faktorů na vzorcích z prasečích hrudních aort. V závěru této kapitoly jsou shrnuty nové poznatky vyplývající z experimentálního testování. Třetí část disertační práce (kap.4) je zaměřena na matematický popis deformačně napjatostního chování měkkých tkání, stručný popis používaných konstitutivních vztahu a postup při identifikaci parametrů pro tyto konstitutivní modely určované na základě provedených experimentálních zkoušek. Poslední část disertační práce (kap.5) je věnována výpočtovému modelování deformačně napjatostního chování AAA. V této kapitole jsou nejdříve shrnuty klíčové faktory a předpoklady pro vytváření modelů a pro vyhodnocování výsledku a dále jsou uvedeny materiálové parametry pro konstitutivní modely implementované do programu ANSYS. Byly provedeny testovací výpočty při použití hypotetické zjednodušené geometrie AAA, na kterých byly vyhodnoceny vlivy změny geometrie a vliv změny konsitutivního modelu na extrémní napětí ve stěně AAA. U reálné geometrie AAA byla navržena a otestována metoda výpočtu nezatížené geometrie z reálných CT snímků. Dále byl testován vliv zvýšení vnitřního tlaku jako rizika ruptury AAA. V závěru práce jsou shrnuty poznatky a možnosti výpočtového modelování a návrhy na další práce.

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Garst, Christopher, Makenie Fulmer, Doug Thewke, and Stacy D. Brown. "Optimized Extraction of 2-Arachidonyl Glycerol and Anandamide from Aortic Tissue and Plasma for Quantification by LC-MS/MS." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/5304.

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Atherosclerosis is a disease characterized by plaque formation due to an accumulation of fat, cholesterol, and immune cells in the walls of arteries. If a plaque ruptures, an occlusive thrombosis may form that causes either a heart attack or stroke. Macrophages express CB-2 receptors, and are one type of immune cell that plays a role in plaque destabilization and rupture. Endocannabinoids anandamide (AEA) and 2-arachidonyl glycerol (2-AG) have been found to have activity on CB-1 and CB-2 receptors throughout the body and immune system. In this study, we investigated several sample preparation options for the LC-MS quantification of AEA and 2-AG from plasma and aortic tissue. The extractions considered included liquid–liquid (LLE), solid-phase (SPE), and supported liquid (SLE). Some extraction protocols yielded high analyte recovery and prevention of 1-AG/2-AG isomerization. Our results indicate that a liquid-liquid extraction using toluene yields the highest recovery for both analytes, coupled with low ionization suppression in the mass spectrometer. This extraction and corresponding LC-MS/MS assay provides a simple, high throughput mechanism for the quantification of 2-AG and AEA in matrices relevant to the study of endocannabinoids’ role in atherosclerosis.

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Nejjar, Ibtissam. "Etude morphologique et biochimique du tissu elastique de l'aorte thoracique humaine lors du vieillissement et de l'atherosclerose." Toulouse 3, 1988. http://www.theses.fr/1988TOU30154.

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Kumar, Vivek Ashok. "Design and evaluation of scaffolds for arterial grafts using extracellular matrix based materials." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/45869.

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For small diameter (<6 mm) blood vessel replacements, lack of collaterals and vascular disease preclude homografts; while synthetic analogs, ePTFE, expanded polytetrafluoroethylene, and PET, polyethyleneterephathalate, are prone to acute thrombosis and restenosis. It is postulated that the hierarchical assembly of cell populated matrices fabricated from protein analogs provides a new design strategy for generating a structurally viable tissue engineered vascular graft. To this end, synthetic elastin and collagen fiber analogs offer a novel strategy for creating tissue engineered vascular grafts with mechanical and biological properties that match or exceed those of native vessels. This work details techniques developed for the fabrication of prosthetic vascular grafts from a series of extracellular matrix analogs composed of nanofibrous collagen matrices and elastin-mimetic proteins, with and without cells, and subsequent evaluation of their biocompatibility and mechanical properties. The work details the fabrication and mechanical analysis of vascular grafts made from aforementioned protein analogs. Subesequent studies detail seeding and proliferation of rodent mesenchymal stem cells on protein-based composites to recapitulate the media of native vasculature. Finally detailing in vivo biocompatibility and stability of tissue engineered vascular grafts.

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Sadeghi, Malvajerdi Neda. "Preliminary Analysis of an Internal Annuloplasty Ring for the Aortic Valve." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36142.

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Among the four valves of the heart, the aortic valve (AV) is frequently affected by disease. When progressive dilatation of the valve produces a leak when the valve should close (regurgitation), repair may be possible. AV repair is a desirable option because, contrary to AV replace-ment using a prosthesis, it does not require life-long anticoagulation treatment, and retains the original tissues that naturally combat structural degradation. All the AV repair procedures developed by cardiac surgeons require a good stabilization of the ventriculo-aortic junction (VAJ) diameter, through annuloplasty or reimplantation, for long-term success. In the present work, a preliminary design for a new type of annuloplasty ring is proposed that surgeons could tailor to the each valve’s shape and suture inside the VAJ. The design consists in wrapping a commonly available surgical biomaterial into a ring of controlled radial flexibility. For sizing and material selection, several models of increasing complexity were created to account for the anisotropic, hyperelastic nature of all the materials involved. First, an analytical model was programmed in MATLAB to assess the radial flexibility of annuloplasty rings formed with different biomaterials and select those that could match the physiological VAJ radial flexibility between systolic and diastolic pressures. The same program was also used to reproduce the experimental radial and longitudinal stretches of the human VAJ from 0 to 140 mmHg pressures. The analytical models were used to calibrate the parameters of independent finite element (FE) models of the VAJ and ring. Finally, the FE approach was extended to simulate the ring after suturing inside the VAJ, to determine the radial flexibility of the assembly under pulsatile pressure. Supple Peri-Guard® bo-vine pericardium patches used in transverse orientation emerged as the best currently available material option for the proposed ring, although a material providing more physiological radial flexibility would be desirable.

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Pekar, Tonya M. "Phosphoproteomic studies of smooth muscle contraction investigation of differential phosphorylation in relaxed/contracted rat aortic smooth muscle tissue using MALDI-TOF MS /." Huntington, WV : [Marshall University Libraries], 2003. http://www.marshall.edu/etd/descript.asp?ref=370.

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Thesis (M.S.)--Marshall University, 2003.
Title from document title page. Document formatted into pages; contains xv, 148 p. including illustrations. Includes bibliographical references (p. 131-148).

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24

Konduri, Suchitra. "The Influence of normal physiological forces on porcine aortic heart valves in a sterile ex-vivo pulsatile organ culture system." Thesis, Available online, Georgia Institute of Technology, 2005, 2005. http://etd.gatech.edu/theses/available/etd-03042005-135623/unrestricted/konduri%5Fsuchitra%5F200505%5Fmast.pdf.

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Thesis (M. S.)--Chemical and Biomolecular Engineering, Georgia Institute of Technology, 2005.
Dr. Athanassios Sambanis, Committee Member ; Dr. Timothy M. Wick, Committee Member ; Dr. Ajit P.Yoganathan, Committee Chair. Includes bibliographical references.

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Williams, Alex. "The Oscillatory Shear Index: Quantifications for Valve Tissue Engineering and a Novel Interpretation for Calcification." FIU Digital Commons, 2018. https://digitalcommons.fiu.edu/etd/3784.

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Heart valve tissue engineering (HVTE) stands as a potential intervention that could reduce the prevalence of congenital heart valve disease in juvenile patients. Prior studies in our laboratory have utilized mechanobiological testing to quantify the forces involved in the development of heart valve tissue, utilizing a Flow-Stretch-Flexure (FSF) bioreactor to condition bone marrow stem cells (BMSCs)-derived valve tissue. Simulations have demonstrated that certain sets of flow conditions can introduce specific levels of oscillatory shear stress (OSS)-induced stimuli, augmenting the growth of engineered valves as well as influencing collagen formation, extracellular matrix (ECM) composition and gene expression. The computational findings discussed in this thesis outline the methods in which flow conditions, when physiologically relevant, induce specific oscillatory shear stresses which could not only lead to an optimized valve tissue phenotype (at 0.18≤ OSI≤ 0.23), but could identify native valve tissue remodeling indicative of aortic valve disease.

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Arbesu, Y. Miar Anais. "Cellule interstitielle de valve et sténose aortique : impact de la voie du facteur tissulaire." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S062/document.

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Définie comme étant le rétrécissement de la valve, la sténose aortique (SA) est la 3ème pathologie cardiovasculaire dans les pays industrialisés. Touchant essentiellement les personnes âgées de plus de 65 ans, cette pathologie représente un véritable problème de santé publique compte tenu du vieillissement de la population. Considérée initialement comme issue d’un processus passif de dégénérescence, il est désormais établi que la sténose aortique est une pathologie dite « atherosclerosis-like » caractérisée par les processus d’inflammation, de fibrose, de néo-angiogenèse et de calcification. Certaines protéines de la voie de coagulation tel que le facteur tissulaire (FT) sont connues pour avoir un rôle pro-fibrotique et participent activement au développement des lésions athéroscléreuses. Leurs rôles dans la SA semblent donc probables et restent à être identifiés.Composante cellulaire majeure de la valve aortique, les VICs présentent 5 sous-populations distinctes : les cellules progénitrices embryonnaires (EPCs), les cellules progénitrices (pVICs), quiescentes (qVICs), activées (aVICs) et ostéoblastiques (obVICs). Au cours de la valvulogenèse, les EPCs permettent la cellularisation de la valve en se différenciant en qVIC. Celles-ci maintiennent l’homéostasie valvulaire et, en cas de lésion, s’activent (aVICs) pour réparer efficacement le tissu valvulaire. L’inflammation valvulaire et l’activation des VICs initient la sécrétion de protéines pro-calcifiantes induisant la différenciation des aVICs en obVICs. Enfin, les pVICs, naturellement présentes au sein de la valve (appelées résidantes) ou issues de la circulation sanguine (appelées hématopoïétiques), semblent favoriser le renouvellement cellulaire et peuvent être impliquées dans les processus angiogénique et ostéoblastique.Bien que décrites, la validation de la culture primaire des VICs par le suivi de ces sous-populations n’avait pas été réalisé et à constituer notre premier objectif. Nous avons ensuite étudié l’implication des voies de signalisation du FT dans le développement de la SA.Dans le cadre du suivi longitudinal des VICs depuis les valves aortiques humaines contrôles et pathologiques jusqu’à la culture in vitro réalisée sur plastique et sur collagène, nous avons tout d’abord montré que les différentes sous-populations étaient présentes au sein de ces valves avec des localisations et des proportions différentes selon l’état physiopathologique du tissu. Après digestion enzymatique de la valve, elles sont toutes retrouvées mais lors de la mise en culture, les pVICs hématopoïétiques ont disparu, quel que soit le support. Nous avons ainsi validé le modèle de culture primaire des VICs tout en mettant en lumière ses limites : absence des pVICs hématopoïétique, activation et différenciation ostéoblastique spontanée des VICs au cours de la culture.Dans le cadre de l’’étude de l’implication du FT dans le développement de la SA, nous avons montré sa colocalisation avec la thrombine et les calcifications de valves pathologiques. A partir de la culture primaire de VICs issues de valves humaines contrôles et pathologiques, nous avons montré que l’expression et l’activité du FT étaient constitutivement plus importantes pour les VICs pathologiques et que son expression pouvait être induite par l’IL1β. De plus, l’activation du FT, en présence de son ligand le facteur VII, induit, directement et via le récepteur PAR2, différentes voies de signalisation impliquées dans la prolifération cellulaire et les processus de fibrose et de calcification. Cette étude suggère ainsi que le FT produit par les VICs est un médiateur clef dans le développement de la sténose aortique
Defined as the narrowing of the aortic valve, aortic stenosis (AS) is the third cardiovascular pathology in industrialized countries. Affecting mainly people aged over 65 years, AS represents a major public health problem because of the aging of the population. After initially been considered as a passive degenerative process, it is now established that AS is an "atherosclerosis-like " disease characterized by the processes of inflammation, fibrosis, neo-angiogenesis and calcification. Some proteins of the coagulation pathway such as tissue factor (TF) are known to have a pro-fibrotic role and actively participate in the development of atherosclerotic lesions. Their implication in AS seems, therefore, probable and remain to be identified.Prevalent cellular component of the aortic valve, VICs have five distinct subpopulations: embryonic progenitor cells (EPCs), progenitor cells (pVICs) quiescent (qVICs), activated (aVICs) and osteoblastic (obVICs). During the valvulogenesis, EPCs allow the cellularization of the valve, differentiating into qVICs. These cells maintain the valvular homeostasis and, in case of damage, are activated (aVICs) to effectively repair the valve tissue. The valvular inflammation and VICs activation initiate the secretion of pro-calcifying proteins inducing the differentiation of aVICs into obVICs. Finally, pVICs, naturally present within the valve (called resident) or from the blood circulation (called hematopoietic), seem to promote cell renewal and may be involved in the angiogenic and osteoblastic processes.Although described, these subpopulations have never been studied longitudinally, in respect to their behavior in vitro. Our first objective was to perform this investigation. Our second objective was to study the potential role of TF pathway in the deleterious mechanisms of AS.As part of the longitudinal follow-up of VICs from control and pathological human aortic valves to the in vitro culture performed on plastic and collagen, we first showed that different subpopulations were present in these valves with different locations and proportions according to the pathophysiological state of the tissue. After enzymatic digestion, all subpopulations are found but, in culture, hematopoietic pVICs disappeared, whichever the support. Thus, we validated the primary culture model of VICs while highlighting its limitations: lack of hematopoietic pVICs, spontaneous osteoblastic differentiation and activation of VICs in culture.As part of the study the involvement of FT in the AS development, we showed its colocalization with thrombin and calcifications of pathological valves. We showed that the expression and activity of TF were constitutively more important in VICs from fibrocalcified valves than control ones and that IL-1β for pathological VICs and that its expression could be induced by IL1 beta. In addition, TF activation in the by its ligand FVII, induced, directly and via the PAR-2 receptor, different signaling pathways involved in cell proliferation and the processes of fibrosis and calcification. Thus, our findings suggest that the FT expressed by VICs mediates fibrocalcific processes of aortic stenosis

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Junior, Antonio Aurelio de Paiva Fagundes. "Estudo do fluxo sanguíneo regional e dos marcadores de perfusão tecidual em pacientes com insuficiência cardíaca em uso de balão intra-aórtico." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-10122013-102948/.

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INTRODUÇÃO: O balão intra-aórtico (BIA) representa o mecanismo de assistência ventricular mais frequentemente utilizado em pacientes com insuficiência cardíaca (IC), no Brasil. OBJETIVO: Neste trabalho, avaliamos a ação do BIA sobre o fluxo sanguíneo carotídeo e braquial, além do seu efeito sobre os marcadores de perfusão tecidual e sobre o peptídeo natriurético cerebral (BNP). MÉTODOS: Entre julho de 2006 e maio de 2009, 33 pacientes foram avaliados, sendo 10 excluídos. Os pacientes foram inicialmente mantidos com o BIA em modo 1:1, com insuflação máxima, para a fase inicial do estudo (condição 1). Realizou-se coleta de gasometria arterial, venosa central e BNP (condição EXA1). Foi realizada ultrassonografia vascular de alta definição, para captação de imagens das curvas de velocidade de fluxo sanguíneo, e medida dos diâmetros arteriais sistólico e diastólico (condição MD1). Em seguida, foi avaliada a resposta vascular frente à hiperemia reativa (condição HR1). Realizado o estudo na condição 1, o BIA foi modificado para 1:3 com insuflação mínima (condição 2) e todos os exames laboratoriais (condição EXA 2) e ultrassonográficos (condição MD2 e condição HR2) foram repetidos. Após a condição 2, passou-se à condição 3, na qual o BIA foi novamente modificado para a assistência 1:1, com insuflação máxima. Da mesma forma que nas condições anteriores, foram realizados exames laboratoriais (condição EXA 3) e a ultrassonografia (condição MD3 e HR3). A avaliação estatística foi realizada através da análise de variância para medidas repetidas e o uso do teste não paramétrico de Friedman. RESULTADOS: A idade média dos pacientes selecionados foi de 49,7 ± 13 anos, sendo 17 (74%) do sexo masculino e 6 (26%) do sexo feminimo. Quanto à etiologia, 9 (39%) pacientes eram portadores de miocardiopatia isquêmica, 8 (34%) miocardiopatia dilatada idiopática, 4 (17%) tinham etiologia chagásica e 2 (8%) por valvopatias. A fração de ejeção, estimada pelo ecocardiograma variou de 14 a 40%, com Resumo média de 22 +-8%. Nove pacientes (39%) encontravam-se em fila para transplante cardíaco, no momento da inclusão no protocolo, e a mortalidade durante a internação foi de 60,8%. Analisados os dados laboratoriais, não houve, entre as três medidas realizadas, diferença com significância estatística nos valores de bicarbonato arterial (BIC), assim como, nos valores de excesso de base (BE). Também não detectamos mudanças na saturação venosa central de oxigênio (SVcO2), no nível sérico de BNP e no gradiente venoarterial de CO2(DeltaPCO2). Os resultados das análises da velocidade de fluxo, índice de fluxo carotídeo e integral velocidade-tempo na condição MD1, MD2 e MD3 não revelaram diferenças estatisticamente significantes. Analisado o território braquial, considerando a velocidade de fluxo braquial não houve diferença entre a condição MD1 e a condição MD2 e entre a condição MD1 e a condição MD3. Entretanto, identificamos diferença entre as condições MD2 e MD3 (p=0,01). Não encontramos diferença com significância entre as três condições considerando o índice de fluxo e a integral velocidade-tempo. Na prova de hiperemia reativa não encontramos alteração entre as condições HR1, HR2 e HR3, quando avaliamos a velocidade de fluxo, o índice de fluxo e a integral velocidade-tempo. A dilatação fluxo mediada da artéria braquial (DILA) encontrava-se alterada desde o momento inicial, porém o protocolo não revelou alterações entre HR1, HR2 e HR3. CONCLUSÃO: Em pacientes com insuficiência cardíaca, a assistência com o BIA não modificou o fluxo sanguíneo regional em território cerebral e muscular esquelético avaliados pelo fluxo da carótida e artéria braquial, respectivamente. Da mesma forma, não houve alteração da perfusão tecidual e função cardíaca avaliados pelos marcadores do metabolismo oxidativo e sobrecarga hídrica utilizados. A função endotelial avaliada na condição de duplo pulso de fluxo da artéria braquial propiciada pela assistência circulatória do BIA evidenciou-se alterada com dimunuição da reatividade vascular
BACKGROUND: The intra-aortic balloon (IAB) represents the mechanism of ventricular assist more often used in patients with heart failure (HF) in our midst. OBJECTIVE: In this study, we evaluated the action of the IAB on the carotid and brachial blood flow, in addition to its effect on markers of tissue perfusion and the brain natriuretic peptide (BNP). METHODS: Between July 2006 and May 2009, 33 patients were evaluated, 10 were excluded. Patients were initially maintained with the IAB in 1:1 mode with maximum insufflation, for the initial phase of the study (condition 1). Held collection of arterial and central venous blood gases, and BNP (condition EXA1). Vascular ultrasonography was performed in high definition, to capture images of the curves of blood flow velocity, and measurement of systolic and diastolic arterial diameters (condition MD1). Then we evaluated the vascular responses to reactive hyperemia (condition HR1). Conducted the study in condition 1, the IAB was changed to 1:3 with minimal insufflation (condition 2) and all laboratory tests (condition EXA 2) and ultrasound (condition MD2 and HR2) were repeated. After the second condition, the IAB was again modified to 1:1, with maximum insufflation (condition 3). Similarly to the previous conditions, laboratory tests (condition EXA 3) and ultrasound (condition MD3 and HR3) were performed. Statistical evaluation was performed by analysis of variance for repeated measures and the use of Friedman nonparametric test. RESULTS: The mean age of the selected patients was 49.7 +- 13 years, 17 (74%) males and 6 (26%) were females. Concerning etiology, 9 (39%) patients had ischemic cardiomyopathy, 8 (34%), idiopathic dilated cardiomyopathy, 4 (17%) had Chagas disease and 2 were (8%) related to valvulopathy. Ejection fraction estimated by echocardiography ranged from 14 to 40%, with a mean of 22 +- 8%. Nine patients (39%) were in line for a heart transplant at the time of inclusion in the protocol and mortality during hospitalization was 60.8%. Analyzed laboratory data, among the three measurements, there was not statistically significant difference in the values of arterial bicarbonate (BIC) and base excess (BE). We also did not detect changes in central venous oxygen saturation (SCVO2) or in serum BNP level and venoarterial carbon dioxide gradient (DeltaPCO2). The results of the analysis of carotid flow velocity, index of carotid flow and velocity time integral in condition MD1, MD2 and MD3 revealed no statistically significant difference. Examined the brachial territory, there was no difference between the condition MD1 and MD2 and between MD1 and MD3 considering the flow velocity. However, there was difference between conditions MD2 and MD3 (p = 0.01). We found no significant difference between the three conditions considering the brachial flow index and velocity time integral. The flow-mediated dilation of the brachial artery (FMD) found itself changed from the initial moment, but the protocol does not reveal changes between HR1, HR2 and HR3. CONCLUSION: In heart failure patients, assistance with the BIA did not alter regional blood flow in brain and skeletal muscle territory assessed by flow carotid and brachial artery, respectively. Likewise, there was no change in tissue perfusion and cardiac function assessed by markers of oxidative metabolism and fluid overload used. Endothelial function evaluated on condition of dual pulse brachial artery flow provided by BIA circulatory support showed up changed with decreased vascular reactivity

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28

Cheheltani, Rabee. "Development of infrared spectroscopic methods for assessment of extracellular matrix changes in cardiovascular diseases." Thesis, Temple University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3623127.

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Extracellular matrix (ECM) is a key component and regulator of many biological tissues. Several cardiovascular pathologies are associated with significant changes in the composition of the matrix. Better understanding of these pathologies and the physiological phenomenon behind their development depends on reliable methods that can measure and characterize ECM content and structure. In this dissertation, infrared spectroscopic methodologies are developed to study the changes in extracellular matrix of cardiovascular tissue in two cardiovascular pathologies; myocardial infarction and abdominal aortic aneurysm.

The specific aims of this dissertation were: 1. To develop a Fourier transform infrared imaging spectroscopy (FT-IRIS) methodology for creating distribution maps of collagen in remodeled cardiac tissue sections after myocardial infarction, and to quantitatively compare maps created by FT-IRIS with conventional staining techniques. 2. To develop an FT-IRIS method to assess elastin and collagen composition in the aortic wall. This will be accomplished using ex vivo animal aorta samples, where the primary ECM components of the wall will be systematically enzymatically degraded. 3. To apply the newly developed FTIR imaging methodology to evaluate changes in the primary ECM components (collagen and elastin) in the wall of human AAA tissues. The infrared absorbance band centered at 1338 ^cm-1, was used to map collagen deposition across heart tissue sections of a rat model of myocardial infarction, and was correlated strongly in the size of the scar (R=0.93) and local intensity of collagen deposition (R=0.86).

In enzymatically degraded pig aorta samples, as a model of ECM degradation in abdominal aortic aneurysm (AAA), partial least squares (PLS) models were created to predict collagen and elastin content in aorta based on collected FTIR spectra and biochemically measured values. PLS models based on FT-IRIS spectra were able to predict elastin and collagen content of the samples with strong correlations (^R2=0.90 and 0.70 respectively). Elastin content prediction from IFOP spectra was successful through a PLS regression model with high correlation (^R2=0.81).

The PLS regression coefficient from the FT-IRIS models were used to map collagen and elastin human AAA biopsy tissue sections, creating a similar map of each component compared to histologically stained images. The mean value of collagen deposition in each tissue was calculated for 13 pairs of AAA samples where stress had been calculated using finite element modeling. In most pairs with stress values higher than 5 N/m², collagen content was lower in the sample with higher stress value. Collagen maturity had a weak negative correlation (R=-0.35) with collagen content in these samples.

These results confirm that infrared spectroscopy is a powerful tool that can be applied to replace or complement conventional methods such as histology and biochemical analysis to characterize ECM components in cardiovascular tissues. Furthermore, infrared spectroscopy has the potential for translation to a clinical environment to examine ECM changes in aorta in a minimally invasive fashion using fiber optic technology.

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Simmers, Phillip Charles. "Benefits of Nitric Oxide Cues to Matrix Synthesis by Healthy and Aneurysmal Human Smooth Muscle Cells within 3D Cocultures." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1399977973.

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Tremblay, Dominique. "Mechanical and structural characterization of ascending aortic tissues and graft materials used in the aortic arch reconstruction." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86901.

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The exact mechanisms involved in the pathogenesis of aortic aneurysms of the human ascending aorta (AA) are unknown. It is believed that the remodeling capabilities of the endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) combined with abnormal and non-uniform shear and tissue stresses, generated by a perturbed hemodynamics produced by a diseased aortic valve, are the precursors in the disease progression. In this work, we hypothesize that local remodeling of the dilated AA exists and is valve type dependent. However, very little data exists on the local mechanical and structural properties of healthy and dilated AA. A detailed description of these tissues will provide valuable clues about the progression of the disease and help identify the mechanisms involved. The regional analysis has revealed a significant location dependency in stiffness, thickness and collagen content in healthy and dilated BAV-T1 AA tissues. However, these natural regional variations were not evident in dilated TAV tissues, which suggests a loss of the natural heterogeneity with dilation. On average, collagen content and thickness have shown differences between dilated TAV and BAV-T1 tissues, which suggests two distinct remodeling processes. Regional variations in the density and orientation of the VSMCs have also been found in pig AA. The outer curvature has a higher cell density with cells tilting towards the axial direction in response to higher tissue stresses in this quadrant. Although, VSMCs activation with phenylephrine had a significant effect on the stiffness of the pig AA, which was independent of location or direction. Local remodeling often occurs after an aortic arch reconstruction surgery because of compliance mismatch between the native AA and the replacement material. Since no study has carefully quantified this degree of mismatch in the repaired AA, such an investigation was needed. We have found significant differences in stiffness and anisotropy between re
Les mécanismes impliqués dans le développement des maladies aortiques telles que les anévrismes de l'aorte ascendante (AA) humaine sont inconnus. On pense que la capacité de remodelage des cellules endothéliales (CE) et musculaires lisses (CML) combinées avec une distribution non uniforme des contraintes à la surface et dans le tissu aortique dû à une hémodynamie perturbée produit par une valve aortique malade jouent un rôle important dans la progression de la maladie. Dans cette thèse, on fait l'hypothèse qu'il existe un remodelage aortique local dans les tissus aortiques dilatés et que ce remodelage dépendent du type valve. Cependant, très peu de données sont disponibles sur les propriétés mécaniques et structurelles de l'AA saine et dilatée. Une description détaillée de ce tissu fournira des indices essentiels pour mieux comprendre la progression de la maladie et aidera à identifier les mécanismes impliqués. L'analyse régionale a révélé une variation circonférentielle de la rigidité, de l'épaisseur et du contenu en collagène dans les tissus sain et BAV-T1 dilatés mais non présents dans les tissus TAV dilatés. En moyenne, on a montré des différences d'épaisseur et du contenu en collagène entre les tissus dilatés TAV et BAV-T1. On a également trouvé des variations régionales de la densité et de l'orientation des CML dans l'AA porcine. La grande courbure montre une densité plus élevée de CML orientées dans la direction axiale. Bien que l'activation des CML à la phenylephrine ait eu un effet significatif sur la rigidité de l'AA, aucunes variations circonférentielles ou directionelles de cet effet ont été trouvées. On observe la présence de remodelage local, suite à une reconstruction de l'arche aortique, causé par la différence de compliance entre l'aorte native et le greffon de remplacement. Aucune étude n'avait essayé de quantifier cette différence dans l'aorte reconstruite. Nous avons trouvé des$

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31

Bode, M. (Michaela). "Characterization of type I and type III collagens in human tissues." Doctoral thesis, Oulun yliopisto, 2000. http://urn.fi/urn:isbn:9514255534.

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Abstract Fibrillar type I and III collagens are the major constituents of the extracellular matrix, providing the tissue with tensile strength and influencing cell attachment and migration. The amount of type III collagen and the extent of its processing and cross-link maturation were studied in human atherosclerotic plaques, abdominal aortic aneurysms, colon and ovarian cancer, and finally, colon diverticulosis, using a novel radioimmunoassay for the cross-linked aminoterminal telopeptide of type III collagen. In addition, immunoassays for different structural domains of type I and type III collagens, together with immunohistochemical methods, were applied. In atherosclerotic plaques, the fully cross-linked type III collagen was the major collagen type. Type III collagen was completely processed, since the amount of type III pN-collagen was negligible. The amounts of free type I and III procollagen propeptides in the soluble fraction were small, indicating a low rate of collagen turnover. The proportion of type III collagen was lower in abdominal aortic aneurysms than in atherosclerotic aortic control samples. Furthermore, the amount of type III pN-collagen was significantly increased in aneurysms. Type I and III collagens were also maturely cross-linked in colon diverticulosis, the only difference from normal colon tissue being the increased amount of the aminoterminal propeptide of type III procollagen in the soluble tissue extract, indicating a slightly increased metabolic activity of type III collagen. In malignant ovarian tumors, the cross-linking of type I and III collagens was defective. A similar trend was also seen for type I collagen in colon cancer. Even though procollagen synthesis was increased in these malignancies, the total collagen content and the amounts of cross-linked collagens were decreased. The amount of type III pN-collagen was increased in malignant ovarian tumors, whereas no such tendency was seen in colon cancer. These findings suggest a wide variety of changes in the metabolism of type I and III collagens in diseases. Defective processing and cross-link maturation of these collagen types might result in impaired fibril formation or increased susceptibility of collagens to proteolytic attack - both of them processes with a potential role in the pathogenesis of diseases.

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Mohand, Kaci Faïza. "Bioingénierie des cellules souches mésenchymateuses médullaires cultivées en 3D : application au traitement de l’anévrysme de l’aorte abdominale." Thesis, Paris Est, 2012. http://www.theses.fr/2012PEST0079.

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L'anévrisme de l'aorte abdominale (AAA) est une maladie dégénérative de la paroi vasculaire, actuellement traitée par chirurgie ou par endoprothèse. La diminution de la morbimortalité liée aux traitements et la réparation de ces vaisseaux pathologiques constituent un enjeu majeur de santé publique. L'objectif de ce travail de thèse est d'évaluer l'impact de la culture 3D sur les cellules souches mésenchymateuses (CSM), en particulier sur leur phénotype, leur multipotence, leur capacité à réparer les anévrysmes in vivo et à acquérir un phénotype adapté à la contrainte mécanique qu'elles subissent in vitro. Des conditions optimales de culture 3D dans un hydrogel d'acide hyaluronique préservant la multipotence des CSM in vitro ont ainsi été établies. Sous l'effet de contraintes mécaniques reproduisant celles subies par la paroi aortique in vivo, les CSM 2D et CSM 3D semblent garder une multipotence. Toutefois, dans ces conditions dynamiques, la viabilité des CSM 3D augmente contrairement à celle des CSM 2D. Les résultats montrent également que l'injection des CSM 2D ou 3D, en utilisant un modèle de xénogreffe chez le rat, stabilisent les AAA et améliorent la résistance mécanique de la paroi vasculaire anévrismale. L'étude réalisée chez le rat a été complétée par une approche thérapeutique cellulaire à base de CSM 3D dans le cas de faux anévrysmes chroniques de l'isthme chez le porc. Cette étape conduit à la caractérisation des CSM 3D et la mise au point du modèle expérimental chez le porc, ce qui permet d'envisager une thérapie cellulaire dans ce modèle. Plus généralement, ce travail contribue à la compréhension de la biologie des CSM et à l'amélioration des approches utilisées en thérapie cellulaire et en médecine régénérative
Abdominal aortic aneurysm (AAA) is a degenarative disease of the arterial wall, which is usually treated with a conventional surgery or an andovascular stent. Due to its high morbidity and mortality, the AAA constitutes a major public health concern. The aim of this thesis is to evaluate the imapct of OD culture of mesenchymal stem cells (MSC), in particular on their phenotype, their multipotency, their ability to repair aneurysms in vivo and to acquire a phenotype suitable to the nechanical stress they support in vitro. Optmal culture conditions in a 3D hydrogel of hyaluronic acid preserving the multipotency of MSC in vitro have been established. Under mechanical effects, reproducing those supported by the aortic wall in vivo, 2D and 3D CSM seem to preserve their multipotency. However, under such dynamic conditions, the viability of 3D CSM increases unlike that of 2D CSM. By using a rat xenograft model, the results also show that injection of 2D or 3D CSM, stabilizes the AAA and improves the mechanical strenght of the aneurysmal vessel wall. The study in rat was supplemented by an evaluation of a therapeutic cell-based approach using 3D CSM in the case of chronic false aneurysms of the isthlus in pigs. This step allowed the characterization of 3D CSM and the development of an experimental model in pigs, which allows to consider cell therapy in this model. More genrally, this work contributes to a better understanding of CSM biology and to an improvement of the approaches used in cell therapy and regenerative medicine

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Choudhury, Nusrat Zabeen. "Characterization of healthy and diseased human ascending aorta tissue." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=83857.

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Little information is available on the structure or mechanical properties of the human ascending aorta (AA). Most studies to date have assumed homogeneous tissue mechanical properties. The objective of this study was to investigate the local variation in AA tissue structure and mechanics. Healthy and pathologic tissue samples of human AA were obtained at autopsy and surgical pathology. Each aortic ring was sectioned into quadrants; anterior, posterior, medial (inner curvature) and lateral (outer curvature). Samples from each quadrant were processed for histological analysis and biaxial tensile testing. The results from this study indicate that regional differences are present in both healthy and diseased human AA tissue. Overall, the medial quadrant contained significantly more elastin and mechanically, it was the thickest, least stiff and most likely to fail in comparison to the other quadrants. The assumption of homogeneity in AA tissue properties may not be a valid one.

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Eriksen, H. (Heidi). "Carboxyterminal telopeptide structures of type I collagen in various human tissues." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514262449.

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Abstract Type I collagen is the main connective tissue protein in vertebrates. The cross-linking and correct organisation of the molecules is crucial for the proper function of the tissue. Traditionally collagen cross-linking has been studied using chemical cross-link analyses. However, this does not distinguish between the collagen types or the location of the cross-link within the molecule. The focus in this work was to study the carboxyterminal telopeptide domain of type I collagen for the differently cross-linked forms. An immunochemical approach was used and a new immunoassay, SP4, was developed for the detection of immaturely cross-linked peptide forms. The differently cross-linked structures were purified and characterised from human bone by using SP4 together with the earlier developed ICTP assay for trivalently cross-linked C-terminal telopeptide form. It was found that the majority of the trivalent cross-links in the C-terminal telopeptide were presently unknown structures, other than pyridinoline. A non-cross-linked form of C-terminal telopeptide of α1-chain of type I collagen was also discovered in bone. The epitope of the ICTP assay was characterised and found to reside in the phenylalanine rich region of the ICTP peptide. MMP-9, but not cathepsin K, mediated breakdown of the collagenous matrix was found to produce a peptide detectable by the ICTP assay. Healthy human Achilles tendon comprises mainly of type I collagen. In ruptured Achilles tendons, an increased type III collagen content was found. Since the synthesis of type III collagen was not increased, it is postulated that the type III collagen must have accumulated over a long period of time indicative of a long-lasting microtraumatic process in the tendon before the total rupture occurred. The ICTP content was increased and the ratio of SP4 to ICTP decreased in calcified stenotic aortic valves suggesting a change in the molecular organisation and cross-linking towards the type found in human bone. The total collagen content was dramatically decreased in the calcified valves. Both in the Achilles tendons and in the aortic valves, the ICTP content was found to decrease with age with a concomitant increase in the variants of the C-terminal telopeptide structures detectable with the SP4 assay, pointing to a change in the molecular organisation of the collagenous matrix in these tissues.

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Sabia, Paulo Henrique Brossi. "Projeto e construção de um equipamento biaxial para a caracterização mecânica de tecidos biológicos tubulares." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/3/3152/tde-16112015-154649/.

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Com a evolução da medicina e o consequente envelhecimento da população, o aneurisma de aorta abdominal (AAA) se tornou uma doença cada vez mais presente, sobretudo em homens. A falta de conhecimento detalhado do comportamento mecânico do tecido aórtico abdominal é o principal gargalo no refinamento do critério para a recomendação de cirurgia corretiva, resultando, ainda hoje, no óbito decorrente da ruptura desses aneurismas. O entendimento do comportamento mecânico desse tecido permitirá o refinamento do critério atual, salvando mais vidas. Esse entendimento pode ser obtido através da Mecânica do Contínuo, utilizando dados experimentais de ensaios mecânicos para avaliar e descrever o comportamento do material. Para que isso ocorra, é necessário que o teste seja feito em dois eixos independentes. No presente trabalho, foram escolhidos os eixos longitudinal e circunferencial para a realização de testes mecânicos, levando em consideração aspectos de metodologias já utilizadas, seus pontos fortes e deficiências. São apresentados o projeto, a construção e e a calibração de um equipamento para ensaios biaxiais de tecidos biológicos tubulares, extraídos de cadáveres, e testados até a ruptura, com a possibilidade de realização de ensaios de pré-condicionamento. Tubos de látex foram utilizados na calibração do equipamento, de cuja utilização é esperada grande contribuição na ampliação do conhecimento da probabilidade de ruptura de AAAs e em uma melhor compreensão do comportamento do tecido da uretra peniana.
The evolution of Medicine has enabled humans to live longer. With that, the incidence of abdominal aortic aneurysms (AAAs) has grown, especially among males. The lack of detailed knowledge on the mechanical behavior of the abdominal aortic tissue is the main bottleneck in the improvement of the criterion for recommending corrective surgery. Therefore, many patients still die from the rupture of those aneurysms. Better understanding of the tissues mechanical behavior will allow the refinement of todays criterion, thus saving more lives. This understanding can be obtained from Continuum Mechanics, using mechanical test experimental data to evaluate and describe the behavior of the material. The data has to come from tests performed in two independet axes. This Masters thesis presents the project, manufacturing and calibration of an apparatus for the test of cylindrical biological tissues in two directions, longitudinal and circumferential. Aspects of pre-existent tests and methods and their positive and negative sides were taken into account. The specimens will come from cadavers, and it will be possible to pre-condition them, as well as to test them to the rupture. Latex tubes were used in the calibration of the apparatus, whose utilization is expected to improve the knowledge on AAA rupture probability, as well as to improve the comprehension of the penile urethral tissues behavior.

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Syvannarath, Varouna. "Rôle du CD31 dans l'issu des lésions tissulaires cardiovasculaire aigues." Thesis, Sorbonne Paris Cité, 2019. https://theses.md.univ-paris-diderot.fr/SYVANNARATH_Varouna_va2.pdf.

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Le CD31, aussi appelé PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1) est une glycoprotéine transmembranaire de 130 kDa comprenant 6 domaines de type « immunoglobuline » dans sa portion extracellulaire et deux motifs « ITIM » (Immunoreceptor Tyrosine based Inhibition Motif, qui recrutent des phosphatases) dans sa queue cytoplasmique. De par sa nature trans-homophile et son expression exclusive et constitutive par les cellules endothéliales, les plaquettes et les leucocytes, le CD31 joue un rôle central dans les mécanismes de régulation des cellules interagissant au niveau de l’interface sang-vaisseaux. L’engagement de ses motifs ITIMs favorise les voies de signalisation phosphatase-dépendantes alors que la signalisation tyrosine/inositol-dépendante se retrouve découplée. Ainsi, l’effet inhibiteur ou activateur du CD31 dépend de la nature de la cellule et du rôle des phosphatases recrutées par le CD31 dans chaque type cellulaire : l’engagement éphémère du CD31 par les cellules circulantes exerce un effet plutôt « inhibiteur » en provoquant le détachement cellulaire et l’élévation de seuil d’activation des plaquettes et des leucocytes alors qu’à l’inverse, son engagement pérenne aux niveau des jonctions des cellules endothéliales, stablement ancrées sur leur membrane basale et enchaînées entre elles, est essentiel pour assurer la survie et les fonctions physiologiques de l’endothélium. La régulation des interactions entre endothélium, plaquettes, et leucocytes par le CD31 pourrait être particulièrement importante au cours des réponses biologiques qui se mettent en place suite à une lésion du système cardiovasculaire. Pour évaluer cette hypothèse, j’ai étudié au cours de ma thèse le rôle du CD31 dans l’issue des lésions dues à la dissection de l’aorte et à l’ischémie reperfusion myocardique, deux conditions cliniques aiguës comportant un risque vital élevé non seulement dans l’immédiat mais aussi à distance, si le remodelage tissulaire n’est pas approprié. Mes travaux ont montré que la fonction du CD31 est importante dans l’issue des lésions cardiovasculaires aiguës : non seulement elle favorise le retour à l’homéostasie dans la microcirculation pour garantir la perfusion du tissu lésé mais elle contribue activement à la réparation tissulaire, en favorisant l’acquisition d’un phénotype réparateur par les leucocytes infiltrés aux sites de lésion. En effet, dans le cas de la dissection aortique, nos résultats montrent que la fonction du CD31 est cruciale pour permettre la résorption rapide de l’hématome et la formation d’une cicatrice riche en collagène au niveau de la lésion artérielle permettant ainsi de prévenir l’évolution anévrismale et le risque de rupture de l’aorte. Dans le cas de l’infarctus du myocarde faisant suite à une séquence d’ischémie reperfusion, l’efficacité des procédures de recanalisation, aussi promptes soient-elles, dépend du rétablissement de la circulation microvasculaire. En effet, la survie de chaque fibre musculaire cardiaque va dépendre de son propre capillaire. Chez des souris déficientes en CD31, nous avons constaté que la réponse des plaquettes, des leucocytes, et de l’endothélium au sein même de la microcirculation de l’infarctus est inappropriée. Ainsi, en l’absence de CD31, la dysfonction des éléments sanguins interagissant avec l’endothélium dans la microcirculation prévient la reperfusion à l’échelle tissulaire. Ce phénomène, connu comme le « no-reflow », correspond à une absence de reperfusion microvasculaire malgré la réouverture de l’artère occluse et se traduit par un élargissement de la nécrose myocardique. L’ensemble des résultats de mon travail de thèse indique que les fonctions régulatrices du CD31 jouent un rôle particulièrement déterminant dans l’issue des lésions aiguës du système cardiovasculaire, où les contraintes hémodynamiques rendent d’autant plus difficile et urgente la réparation tissulaire
CD31 also called PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1) is a 130-kDa single pass transmembrane glycoprotein composed of 6 extracellular Ig-like domains and a cytoplasmic tail with two ITIMs motifs (Immunoreceptor Tyrosine based Inhibitory Motifs). The CD31 trans-homophilic receptor is exclusively and constitutively expressed by endothelial cells, platelets and all leukocytes and play a crucial role in cells regulation at blood-vessel interface.Upon sequential phosphorylation, the two ITIMs of CD31 promote phosphatase-dependent pathway while tyrosine/inositol-dependent pathway is uncoupled. Thus, activator or inhibitor CD31 effect depends on cell type. CD31 engagement drives mutual cell-cell detachment signals and raises the activation threshold of CD31+ cells, globally acting as a negative co-signaling receptor on platelet and leukocytes. The case is different for the endothelial cells, which adhere on their basal membrane and establish permanent CD31-CD31 interactions at their lateral borders. Indeed, the permanent trans-homophilic interaction of CD31 molecules engaged at the cell-cell junctions of the adherent endothelial cells and their basal serine phosphorylation may account for the prevalent positive effect on endothelial cell survival and physiologic functions. Regulation of endothelial, platelet and leukocyte interactions by CD31 may be particularly important during biological responses that develop following cardiovascular injury.To evaluate this hypothesis, I studied during my thesis the role of CD31 in the outcome of aortic dissection and myocardial ischemia reperfusion, two clinical conditions related to acute and high life-threatening lesions not only immediately but also in the long term, if tissue remodeling is not appropriate. My work has shown that the function of CD31 is important in the outcome of acute cardiovascular lesions: it promotes the return to homeostasis in the microcirculation to ensure perfusion of the injured tissue but it also actively contributes to the tissue repair, in particular favoring the acquisition of a repair phenotype by the leucocytes infiltrated at the lesion sites. In the case of aortic dissection, our results show that the function of CD31 is crucial to allow rapid resorption of the hematoma and the formation of a collagen-rich scar in the arterial lesion thus preventing aneurysmal evolution and the risk of rupture of the aorta. In the case of myocardial infarction, the effectiveness of recanalization procedures depends on the restoration of microvascular circulation. Indeed, the survival of each heart muscle fiber will depend on its own capillary. In CD31 KO mice, we found that the response of platelets, leukocytes, and endothelium within the microcirculation in the infarct area is inappropriate. Thus, in the absence of CD31, dysfunction of the blood cells interacting with the endothelium in microcirculation prevents tissus reperfusion. This phenomenon, also known as "no-reflow", corresponds to an absence of microvascular reperfusion despite the re-opening of the occluded artery and results in an enlargement of necrosis zone.Thus, the regulatory functions of CD31 seem to play a particularly determining role in the outcome of acute lesions of the cardiovascular system, where hemodynamic stresses make the tissue repair even more difficult and urgent

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Scott-Emuakpor, D. "Human aorta tissue matrix constituents : Changes with age and in disease." Thesis, Lancaster University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355489.

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38

Spear, Rafaëlle. "Analyse transcriptomique des cellules vasculaires isolées du tissu anévrysmal de l'aorte abdominale sous-rénale chez l'homme." Thesis, Lille 2, 2014. http://www.theses.fr/2014LIL2S050/document.

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L'anévrysme de l'aorte abdominale (AAA) est un problème de Santé Publique qui touche principalement les hommes de plus de 65 ans. L'AAA souvent asymptomatique évolue vers la rupture associée à un taux de mortalité élevé. Parmi les acides ribonucléiques (ARNs) non codants, les microARNs (miARNs), stables dans le tissu et les biofluides, sont des candidats intéressant dans la recherche de biomarqueurs. L'inflammation, la dégradation de la matrice extra-cellulaire (MEC) et la raréfaction de la média participent à l'AAA. De nombreuses cellules inflammatoires sont impliquées dans l'AAA. La raréfaction des cellules musculaires lisses (CML) est secondaire à l'anoïkis, apoptose par détachement cellulaire de la MEC. Une analyse protéomique différentielle de CML en culture, issues de patients porteurs d'AAA, réalisée au laboratoire a montré que la désintégrine et metalloprotéinase avec un motif de thrombospondine 5 (ADAMTS 5) est surexprimée dans les CML de patients présentant un AAA. L'isolement des cellules par la microdissection laser permet de conserver le phénotype des cellules isolées et de mettre en évidence des marqueurs potentiels de l'AAA masqués par l'analyse du tissu global. Mon travail de thèse a consisté à partir des cellules isolées de la paroi anévrysmale de l'aorte abdominale sous-rénale chez l'Homme: à effectuer une analyse globale des miARNS et une analyse ciblée de l'ADAMTS 5, métalloprotéase qui a une action enzymatique sur les protéines de la MEC. Les objectifs de ce travail sont une meilleure compréhension de l'AAA et l'identification de nouveaux biomarqueurs.La distribution des cellules dans la paroi anévrysmale est étudiée par immunohistochimie sur des biopsies anévrysmales et d'aortes saine obtenues chez l'Homme. Les cellules localisées sont isolées par microdissection laser. L'analyse par criblage de l'expression des miARNs des cellules isolées de l'AAA et des CML issues d'aorte saine est réalisée sur puce. L'expression différentielle de miARNs sélectionnés est analysée par PCR quantitative dans des cellules isolées de l'AAA et dans du tissu global. L'expression des miARNs sélectionnés est ensuite comparée dans le plasma des patients présentant un AAA et de patients athérosclérotiques sans AAA par PCR pour identifier de potentiels biomarqueurs. Dans l'AAA, les macrophages M1 proinflammatoires sont retrouvés dans l'adventice et les macrophages M2 anti inflammatoires dans le thrombus intraluminal, les lymphocytes de type B sont retrouvés organisé en organe lymphoïde tertiaire adventitielle ou ATLOs dans 11 échantillons sur 20 analysés. Les CML sont rares et strictement localises au niveau de la média. Sur 850 miARNs testés dans la puce, 205 miARNs sont exprimés dans les cellules isolées. Les miR-29b et let-7f sont augmentés dans le plasma de patients porteurs d'AAA et représentent de potentiel biomarqueurs.L'expression d'ADAMTS 5 dans les CML de la paroi anévrysmale est évaluée par immunohistochimie dans la paroi aortique saine et anévrysmale et quantifiée par Western-blot dans les CML isolées de la paroi aortique saine et anévrysmale.Deux morphotypes de CML anévrysmales ont été identifiés: un morphotype arrondi positif au marqueur de l'apoptose, caspase 3 et un morphotype allongé, similaire aux CML de l'aorte saine. Le profil d'expression des sous-unités d'ADAMTS 5 est diffèrent dans les CML arrondies et les CML allongées anévrysmales et saines. La mise en apoptose des CML a été mise au point in vitro pour étudier les mécanismes impliqués dans les modifications d’ expression d'ADAMTS 5 dans l'AAA et les conséquences sur son action enzymatique.L'approche systématique de l'expression transcriptomique des cellules anévrysmales isolées a identifié des marqueurs potentiels de l'AAA, les miR-29b et let-7f et l'analyse ciblée suggère l'implication d'ADAMTS 5 dans le profil évolutif des CML vers l'anoïkis dans l'AAA. Des études complémentaires permettront une meilleure compréhension de l'AAA
Abdominal aortic aneurysm (AAA) is a public health problem, which mainly affects men older than 65 year. AAA are usually asymptomatic with a natural evolution towards rupture associated with a high mortality rate. Among non coding ribonucleic acids (RNAs), microRNAs are stable in tissue and biofluids and are interesting candidates for the search of biomarkers. Inflammation, extracellular matrix (ECM) degradation and media rarefaction are involved in AAA. Many inflammatory cells are involved in AAA. Anoikis is an apoptosis secondary to a cell detachment from ECM and is responsible for rarefaction of smooth muscle cells (SMC). Differential proteomic analysis of cultured SMC from AAA patients was performed in the laboratory and highlighted the overexpression of a disintegrin and metalloproteinase with thrombospondin motif of type 5 (ADAMTS 5) in SMC of AAA patients. Isolation of cells with laser microdissection allows to keep their phenotype and to find potential markers that may be masked by global tissue analysis.The aim of my PhD work was to perform a global miRNA screening of cells isolated from human aneurysmal wall and an analysis targeted on ADAMTS 5, a metalloprotease with an enzymatic activity on ECM proteins. The main objectives were a better understanding of AAA and the identification of new biomarkers.The distribution of cells in the aneurysmal wall was studied by immunohistochemistry in human aneurysmal and healthy aortic samples. Once located, the cells were isolated by laser microdissection and screened for miRNAs by microarrays. Differential expression of selected miRNAs was quantified by PCR in the cells isolated by laser microdissection and in whole aortas. They were then compared in plasma of AAA patients and atherosclerotic patients without AAA by quantitative PCR to identify potential biomarkers.In AAA, the M1 proinflammatory macrophages were located in the adventitia and the M2 antiinflammatory macrophages in the intraluminal thrombus; the type B lymphocytes were organized in tertiary lymphoid organs (ATLOs) in 11/20 of analysed samples. SMC were rare and restricted to the media. Among the 850 miRNAs tested on microarray, 205 miRNAs were detected in isolated cells. MiR-29b and let-7f were upregulated in plasma of AAA patients, and thus are potential biomarkers.The expression of ADAMTS 5 in aneurysmal SMC was evaluated by immunohistochemistry of healthy and aneurysmal aortic wall and quantified by Western blot in isolated SMC from healthy and aneurysmal wall.Two aneurysmal SMC morphotypes were identified: a rounded morphotype positive for caspase 3, an apoptotic marker, and a spindle-shaped morphotype similar to the healthy aortic SMC. The expression profile of ADAMTS 5 subunits was different in rounded SMC compared to aneurysmal and healthy spindle-shaped SMC. In vitro induction of apoptosis of SMC was established in order to study the mechanisms involved in ADAMTS 5 expression in AAA and their consequences on enzymatic actions.The global transcriptomic screening of aneurysmal cells isolated by laser microdissection has identified potential markers of AAA, miR-29b and let-7f. The targeted analysis suggested that ADAMTS 5 is involved in the evolution profile of SMC towards anoikis in AAA. Further investigations will allow a better understanding of AAA pathophysiology

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Chung, Timothy Kwang-Joon. "Study of multi-axial failure properties of planar biological soft tissues." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5732.

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Rupture of abdominal aortic aneurysm (AAA) is a catastrophic event that leads to high mortality and morbidity in patients. The primary causes associated with aneurysm rupture remain poorly understood despite rigorous investigations. Reports have shown that AAA that went on to rupture or present ruptured had higher peak wall tension (stress resultant) than those that did not go on to rupture or present ruptured. Studies investigating the material strength of ruptured AAA and unruptured AAA revealed that the uniaxial failure strength in ruptured AAA is no different on average than unruptured AAA. However, it is poorly understood whether uniaxial failure properties are reliable as they are not indicative of the manner in which failure occurs in biological soft tissues. Multi-axial failure properties using a bubble inflation test (BIT) have been implemented by various groups but have not been directly compared against uniaxial failure properties. The current study seeks to develop a BIT apparatus, to compare multi-axial and uniaxial failure properties of fibrous anisotropic biological soft tissues (bovine aorta) and non-fibrous isotropic molded silicon, and to perform a survey of computational indices at the rupture sites of four ruptured AAA. Two versions of the BIT apparatus were developed: a manual that was developed allows for a large amount of failure properties to be extracted that can identify localized weaknesses. It was found that circumferentially oriented multi-axial failure was correlated with longitudinally oriented uniaxial failure properties, however, for oblique oriented multi-axial failure the correlation decreased. Utilizing the insights gained from the multi-axial experiments it was determined that the failure properties used in the computational study with the data from Raghavan et al. were appropriate for use in retrospective assessment of the rupture site in four ruptured AAA computational models. Although the study was inconclusive in finding causation, the rupture line of each aneurysm had indices ranging between the third quartile and peak values for tension to failure tension ratio, nodal displacement magnitude, strain energy per unit volume and strain energy per unit surface area. This study provides a framework for interrogating failure properties at a higher density of measurement and a heterogeneous computational model that has the potential to predict AAA rupture in the future.

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Thomas, Vineet Sunny. "A Comparative Study for the Effect of Tissure Anisotropy on the Behavior of a Single Cardiac Pressure Cycle for a Symmetric Tri-Leaflet Valve." University of Akron / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=akron1284703306.

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Laville, Colin. "Caractérisation mécanique et modélisation numérique des tissus de valve aortique." Thesis, Paris Sciences et Lettres (ComUE), 2017. http://www.theses.fr/2017PSLEM069/document.

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L’objectif de cette thèse de doctorat est de développer des outils expérimentaux et numériques pour la caractérisation mécanique et la modélisation des tissus, naturels ou artificiels, de valve aortique. Ces outils sont destinés à être utilisés pour l'élaboration de nouveaux implants biomimétiques en matériaux polymères. Chaque année, près de 300 000 prothèses de valves sont implantées à travers le monde. Ces implants peuvent être de deux types~: mécaniques ou biologiques. Les deux solutions souffrent cependant d'inconvénients majeurs. Dans ce contexte, les prothèses en matériaux polymères représentent une alternative prometteuse même si elles ne disposent pas encore de propriétés mécaniques suffisantes. Dans ce travail, un protocole expérimental combinant essais de traction biaxiale, mesure de champs et microscopie confocale est proposé. La mise au point de nouveaux implants peut aussi largement bénéficier de la modélisation numérique afin d'étudier leur comportement mécanique. Ainsi, un solveur structure et un solveur fluide ont été implémentés et couplés. À partir des résultats expérimentaux, les modèles de comportements ont été calibrés en utilisant une procédure d'analyse inverse
This PhD thesis aims to develop experimental and numerical tools for the mechanical characterization and the numerical modeling of natural or artificial aortic valve tissues. These tools are intended to be used for the development of new biomimetic polymeric implants. Nowadays, almost 300 000 prosthetic valves are implanted every year worldwide. Two families of prosthetic valves are currently available~: mechanical and biological prostheses. However, both solutions suffer from major drawbacks. In this context, polymeric prostheses represent a promising alternative but currently suffer from insufficient material properties to be suitable for a long--lasting implantation. In this work, an experimental protocol using biaxial tensile tests together with full--field surface measurement and confocal microscopy is proposed. Since numerical simulation is intended to assist the design phase of new implants by predicting their mechanical behavior, a structure and a fluid solver are developed and coupled. Using experimental results, implemented constitutive models are calibrated through an inverse analysis procedure

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BARISEEL, HERVE. "Devenir tardif des protheses polyesters tissees en position aortique : recul de 76,2 mois." Nice, 1994. http://www.theses.fr/1994NICE6558.

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Neves, Karla Bianca. "Efeito da adipocina chemerin sobre a reatividade vascular: análise em aortas de rato." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/60/60138/tde-27092012-094715/.

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Embora seja na obesidade onde se observa hipertrofia e hiperplasia dos adipócitos e aumento da síntese e liberação de adipocinas, condição associada com resistência à insulina e disfunção endotelial, é de suma importância entender os efeitos biológicos de adipocinas, mais especificamente da adipocina chemerin, em condições não patológicas. Os mecanismos pelos quais as citocinas liberadas pelo tecido adiposo podem interferir na função vascular ainda não estão totalmente esclarecidos. Além disso, praticamente não se conhecem os efeitos da citocina/adipocina chemerin sobre a função vascular. Levando-se em consideração que o receptor para chemerin está presente no músculo liso vascular e no endotélio, este trabalho avaliou a atividade biológica e celular desta adipocina sobre a vasculatura de animais não obesos. Investigou-se os efeitos produzidos por esta citocina na reatividade vascular, bem como os mecanismos pelos quais ela modifica a função vascular em animais não obesos. A hipótese deste trabalho é que chemerin aumenta a reatividade vascular a estímulos constritores de endotelina-1 (ET-1) e fenilefrina (PhE) e diminui a vasodilatação induzida pela acetilcolina (ACh) e nitroprussitao de sódio (NPS). Nossos objetivos específicos incluíram determinar: 1) se chemerin promove alterações na reatividade vascular; 2) se as alterações de reatividade vascular promovidas por chemerin são mediadas por modificações da função das células endoteliais ou células de músculo liso vascular; 3) quais vias de sinalização (foco na via das MAPKs) estão sendo modificadas por chemerin e como elas contribuem para as alterações de reatividade vascular produzidas por esta citocina. Nosso estudo demonstrou que a adipocina chemerin possui atividade biológica e celular em aortas de ratos não obesos. Chemerin aumentou respostas vasculares a estímulos contráteis (ET-1 e PhE), atuando tanto no endotélio quanto diretamente em células do músculo liso vascular. O aumento da resposta a estímulos contráteis à ET-1 e PhE foi mediado pela via MEK-ERK1/2, COX-1 e COX-2 e aumento da expressão dos receptores para ET-1, ETA e ETB. Além disso, esta adipocina diminuiu a vasodilatação induzida pela ACh, por meio do desacoplamento da eNOS e aparente envolvimento de estresse oxidativo, e pelo NPS, através de ação sobre a guanilato ciclase. Nossos estudos poderão contribuir para um melhor entendimento sobre o papel dos fatores liberados pelo tecido adiposo visceral sobre a função vascular e, consequentemente, sobre as alterações vasculares presentes na obesidade e patologias associadas.
Although hypertrophy and hyperplasia of adipocytes as well as increased synthesis and release of adipokines are commonly observed in obesity, a condition associated with insulin resistance and endothelial dysfunction, it is extremely important to understand the biological effects of adipokines, or more specifically of the adipokine chemerin, in non-pathological conditions,. The mechanisms by which cytokines released by the adipose tissue may interfere with vascular function are not yet fully understood. Furthermore, the effects of the cytokine/adipokine chemerin on vascular function are not known. Considering that the chemerin receptor is expressed by vascular smooth muscle and endothelial cells, this study investigated the effects produced by this cytokine in vascular reactivity, as well as the mechanisms by which it modifies vascular function in non-obese animals. Our working hypothesis is that chemerin enhances vascular reactivity to constrictor stimuli, such as endothelin-1(ET-1) and phenylephrine (Phe), and decreases the vasodilation induced by acetylcholine (ACh) and sodium nitroprussiate (SNP). Our specific aims were to determine: 1) whether chemerin induces changes in vascular reactivity, 2) if the alterations of vascular reactivity induced by chemerin are mediated by changes in the function of endothelial cells or vascular smooth muscle cells, 3) which signaling pathways (focus on the MAPKs pathway) are being modified by chemerin and how they contribute to changes in vascular reactivity produced by this cytokine. Our study showed that the adipokine chemerin has biological and cellular activity in aortas from non-obese rats. Chemerin increased vascular responses to contractile stimuli (ET-1 and PhE), producing effects both in the endothelial and vascular smooth muscle cells. The increased contractile responses to ET-1 and PhE were mediated via activation of MEK-ERK1/2, COX-1 and COX-2 and increased expression of the ETA and ETB receptors. Furthermore, this adipokine reduced the vasodilation induced by ACh via eNOS uncoupling and oxidative stress, and by SNP, via effects in the enzyme guanylate cyclase. Our studies may contribute to a better understanding of the role of factors released by the visceral adipose tissue on vascular function and, consequently, on the vascular lesions in obesity and obesity-associated diseases.

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Little, Marie-Térèse E. "The ontogeny of acyl coenzyme A: cholesterol acyltransferase in rat liver, intestine, adipose tissue, and aorta." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29416.

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Epidemiological studies have shown that cholesterol is a major risk factor for the development of atherosclerosis. Since the atherosclerotic plaque develops over a long period interventions early in life may be of some benefit. In addition, it has been shown that the enzymes involved in cholesterol metabolism can be manipulated in early life. Therefore, studies of the developmental patterns of the key enzymes in cholesterol metabolism are of great importance. Acyl coenzyme A: cholesterol acyltransferase (ACAT) is the primary enzyme which catalyzes the conversion of free cholesterol to cholesterol esters in cells. A better understanding of the role and control of ACAT during development is needed in order to trace the possible causes in early life that lead to atherosclerosis in the adult. This research focused on the developmental pattern of ACAT in the rat liver, intestine, brown and white adipose tissue (BAT and WAT, respectively) and aorta. Age specific changes were observed in the rat liver, intestine and BAT. The rat liver and intestine possess significant amounts of ACAT activity throughout development and there appears to be marked variations in activity during this time. The rat BAT and WAT appear to be devoid of ACAT activity throughout development with the exception of adult BAT. Due to the small amount of the aortic tissue samples and/or the insensitivity of the assay, no definite conclusions could be made from this aortic study. In searching for factors that might control the ACAT enzyme the immediate effects of short-term manipulation of diet on the activity of ACAT were studied. The rats were all weaned early on day 18 to one of the following diets: Purina Rat Chow, high carbohydrate (HG) , high fat (HF) , or 2% cholesterol. The HF was the only diet that consistently increased hepatic ACAT activity in all the age groups. The cholesterol diets significantly increased the activity of ACAT in the 22 and 25 day old rats. The HG diet increased the activity of ACAT in the 22, 25, and 30 day old rats. No significant differences were observed between the adult control and HG diet groups. Feeding rats a HF or HG diet precipitated a dramatic drop in intestinal ACAT activity in the 22 day old animals. These effects were not observed in the older animals. The high cholesterol diet had no significant effect on the intestinal enzyme's activity in 22 day old rats. There was no significant change in the BAT and WAT ACAT activity with the experimental diets with the exception that all the experimental diets decreased ACAT activity in the adult BAT.
Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate

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Radomychelski, I., Анатолій Миколайович Романюк, Анатолий Николаевич Романюк, Anatolii Mykolaiovych Romaniuk, Артем Михайлович Піддубний, Артем Михайлович Поддубный, Artem Mykhailovych Piddubnyi, et al. "Investigation of the presence of neutrophils and macrophages in the tissues of calcified aorta affected by atherosclerosis." Thesis, Springer, 2020. https://essuir.sumdu.edu.ua/handle/123456789/81352.

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The presence of aortic calcification causes severe tissue overstretching. Neutrophils and macrophages promote experimental abdominal aortic aneurysm formation. Aim: to compare the number of neutrophils andmacrophages in the tissue of the atherosclerotic aorta with calcification and without it.

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Walker, Rachel. "Perivascular adipose tissue and vascular function : the influence of nitric oxide, ageing and atherosclerosis." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/perivascular-adipose-tissue-and-vascular-function-the-influence-of-nitric-oxide-ageing-and-atherosclerosis(ea89f957-1a84-423a-b99b-5b180ea6874d).html.

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Background: The incidence of coronary heart diseases, including atherosclerosis, increases with ageing. The factors which influence arterial function, and which may be changed with ageing, are multiple but effects of perivascular adipose tissue (PVAT) on large arteries have not previously been considered. A key role for nitric oxide (NO) in mediating the anti-contractile capacity of PVAT has been suggested. Caveolin-1 (Cav-1) modulates the production of NO in vivo by tonic inhibition of eNOS. The influence of aortic PVAT and the contribution of NO to vascular reactivity in ageing C57BL/6 mice, atherosclerotic ApoE knockout mice (ApoE-/-), Cav-1 knockout mice (Cav-1-/-) and atheroprotected ApoECav-1 double knockout mice (ApoE-/-Cav-1-/-) is unknown. Hypothesis: The influence of PVAT on vascular function is modulated by ageing and the development of atherosclerosis via NO bioavailability. Methods: Male mice were used in this study. C57BL/6 mice were obtained at 4 weeks of age and maintained on a normal rodent diet (ND) for 8, 16 or 26 weeks. ApoE-/- and Cav-1-/- mice were bred from in-house colonies and ApoE-/-Cav-1-/- mice were generated by interbreeding ApoE-/- and Cav-1-/- mice. Upon weaning, ApoE-/-, Cav-1-/- and ApoE-/-Cav-1-/- mice were maintained on either a ND or Western-type diet (WD) for 8, 16 or 26 weeks. Vascular reactivity studies on isolated aortic ring preparations were performed in the presence or absence of PVAT. The contribution of NO to the vascular reactivity of aortic PVAT was determined using pharmacological inhibition of NO synthase. Aortic PVAT was assessed for evidence of morphological and/or compositional changes associated with ageing or a WD. Results: NO mediated an anti-contractile effect of aortic PVAT in C57BL/6 mice fed a ND up to 16 weeks. The anti-contractile capacity of aortic PVAT was lost after 26 weeks on a ND and preceded endothelial dysfunction. Loss of the PVAT anti-contractile effect was accompanied by alterations in PVAT morphology and composition. Aortic PVAT from ND-fed ApoE-/- mice was dysfunctional and did not exert an anti-contractile effect. Furthermore, a WD did not alter the influence of PVAT on vascular reactivity in ApoE-/- mice and PVAT morphology and composition was unchanged. NOS inhibition did not alter the contractile responses. The aortic PVAT of ND-fed Cav-1-/- mice did not exert an anti-contractile effect and PVAT composition was unchanged with increasing age. However, after 26 weeks on a WD, aortic PVAT from Cav-1-/- mice potentiated contractions to phenylephrine and white adipocyte hypertrophy was observed. NOS inhibition revealed a pro-contractile effect of aortic PVAT from Cav-1-/- mice. Loss of Cav-1-/- conferred significant protection against the development of atherosclerosis in WD-fed ApoE-/-Cav-1-/- mice despite a proatherogenic lipid profile. Aortic PVAT from ND-fed ApoE-/-Cav-1-/- mice did not exhibit an anti-contractile capacity and PVAT morphology was unchanged with ageing. Additionally, a WD did not influence the effect of PVAT on vascular reactivity in ApoE-/-Cav-1-/- mice although white adipocyte hypertrophy was observed after 26 weeks of high fat feeding. NOS inhibition revealed a pro-contractile effect of aortic PVAT in 8-week ND-fed ApoE-/-Cav-1-/- mice. Conclusions: This work has produced novel insights into the influence of aortic PVAT and NO on vascular reactivity and the morphology of aortic PVAT in ageing C57BL/6 mice, atherosclerotic ApoE-/- mice, Cav-1-/- mice and athero-protected ApoE-/-Cav-1-/- double knockout mice. Ageing to pre-middle age in C57BL/6 mice results in a loss of the anti-contractile effect of PVAT prior to endothelial dysfunction. This is associated with altered NO bioavailability and changes to the morphology and composition of PVAT. This may reveal potential therapeutic targets to restore the anti-contractile capacity of PVAT if comparable age-related PVAT dysfunction is observed in humans. Aortic PVAT of ApoE-/- mice does not exert an anti-contractile effect which may be attributed to decreased basal eNOS activity. A WD does not alter the vascular reactivity of PVAT. In addition, aortic PVAT from Cav-1-/- mice does not exhibit an anti-contractile capacity yet it exerts a pro-contractile effect after 26 weeks on a WD. The aortic PVAT of ApoE-/-Cav-1-/- mice does not modulate vascular reactivity and this is unaltered with feeding of a WD although white adipocyte hypertrophy was observed within the PVAT. The critical role of Cav-1 in the initiation and progression of atherosclerosis is reinforced by the atheroprotected phenotype of the ApoE-/-Cav-1-/- mice even though a severely proatherogenic lipid profile is observed in both the ND and WD-fed mice. Therapeutically targeting LDL transcytosis into the arterial wall could potentially prevent or halt the development of atherosclerosis. Aortic PVAT of ND-fed Cav-1-/- and ApoE-/-Cav-1-/- mice may not be dysfunctional but unable to modulate vascular reactivity due to attenuated vasoconstrictor responses of PVAT-denuded aortic rings as a result of excess NO, although this requires further investigation.

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La, Joie Elaine Naomi. "Tissue welding : studies of pulsed diode laser interaction with ICG stained porcine aorta and elastin-based biomaterial /." Full text open access at:, 1995. http://content.ohsu.edu/u?/etd,249.

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Vieira-Damiani, Gislaine 1976. "Análise computacional de fibras elásticas e colágenas da aorta humana." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310249.

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Orientadores: Konradin Metze, Carlos Lenz Cesar
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-21T10:46:07Z (GMT). No. of bitstreams: 1 Vieira-Damiani_Gislaine_D.pdf: 4044155 bytes, checksum: 7a862a3866981d1827845318ce37b121 (MD5) Previous issue date: 2012
Resumo: A hipertensão arterial sistêmica (HAS) bem como o envelhecimento provoca mudanças na estrutura dos grandes vasos sanguíneos - aorta e seus ramos - propiciando o desenvolvimento de processos degenerativos que são a causa de diversas doenças. O uso de ferramentas fotônicas na aquisição de imagens, associado a recursos matemáticos para a interpretação delas representa um avanço para as análises histopatológicas, pois permitem a visualização e compreensão de pequenas estruturas que antes eram impossíveis de serem observadas. O objetivo desse trabalho foi associar estas duas tecnologias (ferramentas fotônicas e recursos matemáticos) e com isso criar uma metodologia para a análise simultânea de fibras elásticas e colágenas na aorta. Para tanto utilizamos aorta ascendente de 72 pacientes, sendo 22 normotensos, 38 portadores de HAS e 12 aortas de dissecção. As lâminas coradas com hematoxilina eosina foram examinadas no microscópio multifoton, com dois fótons: laser de argônio para fluorescência da eosina, corante de fibras elásticas e Ti:safira para SHG, sinal gerado por moléculas de colágeno. A distribuição e organização das fibras elásticas e colágenas foram analisadas pelas seguintes variáveis: morfometria geométrica, derivadas da matriz de co-ocorrência de Haralick, Transformada de Fourier e fluorescência ótica integrada. Usando estes descritores da textura associados a fractais, observamos que a geração do SHG é dependente não só da presença do colágeno como também do arranjo destas fibras. Observamos ainda que em indivíduos normotensos, quando comparados aos portadores de HAS, ocorre uma diminuição na distribuição do sinal SHG ao longo da espessura da camada média partindo da íntima em sentido à adventícia. Dessa maneira concluímos que os maiores distúrbios das fibras elásticas, nos indivíduos normais ocorrem na transição do terço interno para o médio, enquanto que nos portadores de HAS eles estão distribuídos em toda a espessura da aorta. Além disso, estes estudos nos permitiram verificar que a dissecção da aorta ocorre entre dois reforços de colágeno, uma vez que este fenômeno foi constatado entre dois picos de SHG
Abstract: The arterial hypertension as well as aging induces changes in the structure of large blood vessels - aorta and its branches - leading to development of degenerative processes which are the cause of many diseases. The use of photonics tools for image acquisition, associated to mathematical resources for interpretation of them represents an advance in histopathological analysis, because it allows the visualization and understanding of small structures that were impossible to be observed before. The main objective of this study was to associate both technologies (photonics tool and mathematical resources) to create a new methodology to evaluate, simultaneously, elastic and collagen fibers in aorta. For this we've used autopsies of ascending aortas from 72 patients, being 22 samples from normotensives individuals, 38 from HAS patients and 12 aortas from dissection. HE-stained paraffin sections from ascending aortas were analyzed by multifoton microscopy, with 2 types of photons: Two-photon excited fluorescence (TPEF) for elastin and Ti:safira for SHG to analyze collagen fibers. The distribution and organization of elastic and collagen fibers were analyzed by the following variables: geometric morphometric, derived from the co-occurrence matrix of Haralick, Fourier Transform and Fluorescence optics integrated. Using these texture descriptors associated to analysis of fractals, we've observed that SHG generation is not only dependent on the presence of collagen but on the arrangement of these fibers as well. We also observed that in normotensives individuals, if compared to HAS patients, occurs a decrease in the SHG intensity along the medial thickness from intimate in direction to adventitia. Thus we conclude that the major disorders of elastic fibers in normal subjects occur in the transition from the third layer to the middle, while in HAS individuals these disorders are distributed throughout the thickness of the aorta. Furthermore, this study has allowed us to verify that the aortic dissection has occurred between two peaks of SHG, since this phenomenon was observed between two ribs collagen
Doutorado
Biologia Estrutural, Celular, Molecular e do Desenvolvimento
Doutora em Fisiopatologia Médica

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Loubser, Dirk Jacobus. "Nitric oxide and the endothelium : characterisation of in vitro nitric oxide detection techniques and an ex vivo method of measuring endothelial function." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86496.

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Thesis (MScMedSc)--Stellenbosch University, 2014.
ENGLISH ABSTRACT: Introduction: Nitric oxide (NO) is an important chemical messenger in the cardiovascular system. Despite considerable progress in this field, there remains an on-going need for affordable and user-friendly NO measurement techniques. Therefore, in this study we aimed to develop and characterise NO-detection techniques not previously used in our laboratory, and, in addition, characterise an ex vivo method to measure the functional effects of the endothelium and NO production in the vasculature. Methods: Three different NO-detection techniques were compared: (i) Amperometric NO sensors. Here, NO-increasing effects of known NO synthase (NOS) activators were investigated (insulin, acetylcholine and biosynthetic human insulin). Three different NO sensors were evaluated on cultured endothelial cells and aortic tissue. Putative NOincreasing effects of shear stress were also investigated; (ii) Nitrite (NO2 -) + nitrate (NO3 -) sensors. Here, I aimed to measure NO release from cultured endothelial cells; (iii) Colorimetric NO2 - measurement assay with the Griess reagent. Here, NO2 - production by endothelial cells was measured with a plate reader. In the second part of the study an organ bath - isometric tension technique was established to measure endothelium-dependent function of aortic rings. Functional differences in aortic rings isolated from diet-induced obese rats compared to lean rats were investigated. Ring contraction was induced with phenylephrine and relaxation with acetylcholine. These investigations were further supported by western blot analyses of selected critical proteins. Lastly, the effects of perivascular adipose tissue (PVAT) on contraction and relaxation were investigated in endothelium-containing or denuded aortic ring segments. Results: Although some success was achieved with the amperometric sensors regarding calibration, any experimental results obtained were difficult to repeat due to instability of the sensors. With the NO2 -/NO3 - sensor we were not able to carry out any planned experiments due to failure to properly calibrate and standardise the sensors. Success was achieved with the Griess method. All the drugs used as positive controls (DEA/NO, fenofibrate, oleanolic acid and IL-1ß) proved to be potent inducers of NO2 - release from endothelial cells. Interestingly, the isometric tension studies showed a higher % relaxation in high fat (HF) diet aortic rings compared to those from lean animals. Western blot data showed downregulation of eNOS activation and iNOS expression in obese groups, which was suggestive of endothelial dysfunction. Interestingly, proteins associated with oxidative stress (p22phox and nitrotyrosine) were downregulated in obese groups. The presence of PVAT exerted anti-contractile effects on the rings from HF rats, however in denuded aortic rings, PVAT showed a significant pro-contractile response in both lean and HF groups. PVAT also exerted anti-relaxation effects in aortic rings from both lean and HF rats. Conclusion: We managed to successfully establish two new techniques for our laboratory (Griess method and the organ bath – isometric tension method) which can complement the more established techniques in our laboratory in order to aid us in future vascular research. Finally, the isometric tension technique used in the obese rat studies generated interesting data, which further assisted in characterising the dietinduced obesity rat model in our laboratory.
AFRIKAANSE OPSOMMING: Inleiding: Stikstofoksied (NO) is ‘n belangrike chemiese boodskapper in die kardiovaskulêre sisteem. Ondanks vordering in die veld, bestaan daar ‘n aangaande behoefte aan bekostigbare en gebruikersvriendelike NO-metingstegnieke. Gevolglik het ons in hierdie studie daarna gemik om NO-metingstegnieke wat nie vantevore in ons laboratorium beskikbaar was nie, te ontwikkel en karakteriseer. Verder het ons ten doel gehad om ‘n ex vivo model te karakteriseer om die funksionele effekte van vaskulêre endoteel en NO produksie te meet. Metodes: Drie verskillende NO-metingstegnieke was ondersoek: (i) Amperometriese NO sensors. Hier het ons die verhogende effekte op NO van bekende aktiveerders van NO sintetase (NOS) ondersoek (Insulien, asetielcholien en biosintetiese menslike insulien). Drie verskillende NO-sensors was ge-evalueer in gekultuurde endoteelselle en aortaweefsel. Die vermeende NO verhogende effekte van die wrywingskragte opgewek deur laminere vloei (“shear stress”) is ook ondersoek. (ii) Nitriet (NO2 -) + nitraat (NO3 -) sensors. Hier het ons beplan om NO-vrystelling deur gekultuurde endoteelselle te meet. (iii) Kolorimetriese meting van NO2 - met die Griess reagens. Hier het ons m.b.v. ‘n mikroplaat leser die NO2 - - vrystelling deur endoteelselle gemeet. In die tweede deel van die studie het ons ‘n orgaan bad–isometriese spanningstegniek opgestel om endoteelafhanklike funksie van aortaringe te meet. Funksionele verskille in aortaringe van vetsugtige rotte is vergelyk met kontrole rotte. Ringkontraksie is met fenielefrien geïnduseer en verslapping met asetielcholien. Hierdie ondersoeke is verder ondersteun deur Western blot analises van sleutelproteïene in die aortaweefsel. Laastens het ons die effekte van perivaskulêre vetweefsel (PVAT) op kontraksie en verslapping in aortaringe met of sonder intakte endoteel ondersoek. Resultate: Alhoewel ‘n mate van sukses behaal was met die kalibrasie van die amperometriese sensors, was eksperimentele resultate moeilik om te herhaal a.g.v. sensor-onstabiliteit. Geen eksperimente kon met die NO2 -/NO3 - sensors uitgevoer word nie weens ‘n onvermoë om ordentlike kalibrasie en standardisering uit te voer. Ons het egter wel sukses behaal met die Griess-metode. Al die middels wat as positiewe kontroles gebruik was (DEA/NO, fenofibraat, oleanoliese suur and IL-1ß) het geblyk kragtige induseerders van NO2 - produksie vanaf endoteelselle te wees. Die isometriese spanningsstudies het ‘n hoer % verslapping getoon in die hoë vet (HF) dieet aortaringe in vergelyking met die kontroles. Western blot data het ‘n afregulering van eNOS en iNOS getoon in die HF diere, wat aanduidend is van endoteel disfunksie, terwyl proteïene geassosieer met oksidatiewe stress (p22phox en nitrotirosien) afgereguleer was in die HF groep. Die aanwesigheid van PVAT het ‘n anti-kontraktiele effek gehad op die ringe van die HF groep. Toe die endoteel egter verwyder was, het PVAT in beide kontrole en HF ringe ‘n beduidende pro-kontraktiele effek gehad. Verder het PVAT ook anti-verslappingseffekte op aortaringe beide kontrole en HF rotte uitgeoefen. Gevolgtrekking: Ons het daarin geslaag om twee nuwe tegnieke vir ons laboratorium suksesvol te vestig (Griess metode en die orgaanbad-isometriese spanningstegniek) wat in die toekoms die meer gevestigde tegnieke in ons laboratorium kan komplementeer. Laastens het die isometriese spanningstegniek wat in die dieetstudies gebruik is, data opgelewer wat ons verder sal help om die vetsug model in ons laboratorium te karakteriseer.

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Constantinidès-Mégret, Colette. "Etude de la structure physique de l'elastine par spectroscopies thermostimulees (aed, cts)." Toulouse 3, 1988. http://www.theses.fr/1988TOU30128.

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Dissertations / Theses on the topic 'Aortic tissue'

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