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endothelial cells</title> <meta name="description" content="Search results for: aortic endothelial cells"> <meta name="keywords" content="aortic endothelial cells"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button 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action="https://publications.waset.org/abstracts/search"> <div id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="aortic endothelial cells"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 3325</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: aortic endothelial cells</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3325</span> Effects of Stiffness on Endothelial Cells Behavior</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Forough%20Ataollahi">Forough Ataollahi</a>, <a href="https://publications.waset.org/abstracts/search?q=Sumit%20Pramanik"> Sumit Pramanik</a>, <a href="https://publications.waset.org/abstracts/search?q=Belinda%20Pingguan-Murphy"> Belinda Pingguan-Murphy</a>, <a href="https://publications.waset.org/abstracts/search?q=Wan%20Abu%20Bakar%20Bin%20Wan%20Abas"> Wan Abu Bakar Bin Wan Abas</a>, <a href="https://publications.waset.org/abstracts/search?q=Noor%20Azuan%20Bin%20Abu%20Osman"> Noor Azuan Bin Abu Osman</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Endothelium proliferation is an important process in cardiovascular homeostasis and can be regulated by extracellular environment, as cells can actively sense mechanical environment. In this study, we evaluated endothelial cell proliferation on PDMS/alumina (Al2O3) composites and pure PDMS. The substrates were prepared from pure PDMS and its composites with 5% and 10% Al2O3 at curing temperature 50˚C for 4 h and then characterized by mechanical, structural and morphological analyses. Higher stiffness was found in the composites compared to the pure PDMS substrate. Cell proliferation of the cultured bovine aortic endothelial cells on substrate materials were evaluated via Resazurin assay and 1, 1’-Dioctadecyl-1, 3, 3, 3’, 3’-Tetramethylindocarbocyanine Perchlorate-Acetylated LDL (Dil-Ac-LDL) cell staining, respectively. The results revealed that stiffer substrates promote more endothelial cells proliferation to the less stiff substrates. Therefore, this study firmly hypothesizes that the stiffness elevates endothelial cells proliferation. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=stiffness" title="stiffness">stiffness</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=bovine%20aortic%20endothelial%20cells" title=" bovine aortic endothelial cells"> bovine aortic endothelial cells</a>, <a href="https://publications.waset.org/abstracts/search?q=extra%20cellular%20matrix" title=" extra cellular matrix"> extra cellular matrix</a>, <a href="https://publications.waset.org/abstracts/search?q=vascular" title=" vascular"> vascular</a> </p> <a href="https://publications.waset.org/abstracts/4843/effects-of-stiffness-on-endothelial-cells-behavior" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/4843.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">343</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3324</span> An Increase in Glucose Uptake per se is Insufficient to Induce Oxidative Stress and Vascular Endothelial Cell Dysfunction</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Heba%20Khader">Heba Khader</a>, <a href="https://publications.waset.org/abstracts/search?q=Victor%20Solodushko"> Victor Solodushko</a>, <a href="https://publications.waset.org/abstracts/search?q=Brian%20Fouty"> Brian Fouty</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Hyperglycemia is a hallmark of uncontrolled diabetes and causes vascular endothelial dysfunction. An increase in glucose uptake and metabolism by vascular endothelial cells is the presumed trigger for this hyperglycemia-induced dysfunction. Glucose uptake into vascular endothelial cells is mediated largely by Glut-1. Glut-1 is an equilibrative glucose transporter with a Km value of 2 mM. At physiologic glucose concentrations, Glut-1 is almost saturated and, therefore, increasing glucose concentration does not increase glucose uptake unless Glut-1 is upregulated. However, hyperglycemia downregulates Glut-1 and decreases rather than increases glucose uptake in vascular endothelial cells. This apparent discrepancy necessitates further study on the effect of increasing glucose uptake on the oxidative state and function of vascular endothelial cells. To test this, a Tet-on system was generated to conditionally regulate Glut-1 expression in endothelial cells by the addition and removal of doxycycline. Glut-1 overexpression was confirmed by Western blot and radiolabeled glucose uptake measurements. Upregulation of Glut-1 resulted in a 4-fold increase in glucose uptake into endothelial cells as determined by 3H deoxy-D-glucose uptake. Increased glucose uptake through Glut-1 did not induce an oxidative stress nor did it cause endothelial dysfunction in rat pulmonary microvascular endothelial cells determined by monolayer resistance, cell proliferation or advanced glycation end product formation. Increased glucose uptake through Glut-1did not lead to an increase in glucose metabolism, due in part to inhibition of hexokinase in Glut-1 overexpressing cells. In summary, this study demonstrates that increasing glucose uptake and intracellular glucose by overexpression of Glut-1 does not alter the oxidative state of rat pulmonary microvascular endothelial cells or cause endothelial cell dysfunction. These results conflict with the current paradigm that hyperglycemia leads to oxidative stress and endothelial dysfunction in vascular endothelial cells through an increase in glucose uptake. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=endothelial%20cells" title="endothelial cells">endothelial cells</a>, <a href="https://publications.waset.org/abstracts/search?q=glucose%20uptake" title=" glucose uptake"> glucose uptake</a>, <a href="https://publications.waset.org/abstracts/search?q=Glut1" title=" Glut1"> Glut1</a>, <a href="https://publications.waset.org/abstracts/search?q=hyperglycemia" title=" hyperglycemia"> hyperglycemia</a> </p> <a href="https://publications.waset.org/abstracts/40571/an-increase-in-glucose-uptake-per-se-is-insufficient-to-induce-oxidative-stress-and-vascular-endothelial-cell-dysfunction" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/40571.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">340</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3323</span> Chronic Hypertension, Aquaporin and Hydraulic Conductivity: A Perspective on Pathological Connections</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chirag%20Raval">Chirag Raval</a>, <a href="https://publications.waset.org/abstracts/search?q=Jimmy%20Toussaint"> Jimmy Toussaint</a>, <a href="https://publications.waset.org/abstracts/search?q=Tieuvi%20Nguyen"> Tieuvi Nguyen</a>, <a href="https://publications.waset.org/abstracts/search?q=Hadi%20Fadaifard"> Hadi Fadaifard</a>, <a href="https://publications.waset.org/abstracts/search?q=George%20Wolberg"> George Wolberg</a>, <a href="https://publications.waset.org/abstracts/search?q=Steven%20Quarfordt"> Steven Quarfordt</a>, <a href="https://publications.waset.org/abstracts/search?q=Kung-ming%20Jan"> Kung-ming Jan</a>, <a href="https://publications.waset.org/abstracts/search?q=David%20S.%20Rumschitzki"> David S. Rumschitzki</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Numerous studies examine aquaporins’ role in osmotic water transport in various systems but virtually none focus on aquaporins’ role in hydrostatically-driven water transport involving mammalian cells save for our laboratory’s recent study of aortic endothelial cells. Here we investigate aquaporin-1 expression and function in the aortic endothelium in two high-renin rat models of hypertension, the spontaneously hypertensive genomically altered Wystar-Kyoto rat variant and Sprague-Dawley rats made hypertensive by two kidney, one clip Goldblatt surgery. We measured aquaporin-1 expression in aortic endothelial cells from whole rat aortas by quantitative immunohistochemistry, and function by measuring the pressure driven hydraulic conductivities of excised rat aortas with both intact and denuded endothelia on the same vessel. We use them to calculate the effective intimal hydraulic conductivity, which is a combination of endothelial and subendothelial components. We observed well-correlated enhancements in aquaporin-1 expression and function in both hypertensive rat models as well as in aortas from normotensive rats whose expression was upregulated by 2h forskolin treatment. Upregulated aquaporin-1 expression and function may be a response to hypertension that critically determines conduit artery vessel wall viability and long-term susceptibility to atherosclerosis. Numerous studies examine aquaporins’ role in osmotic water transport in various systems but virtually none focus on aquaporins’ role in hydrostatically-driven water transport involving mammalian cells save for our laboratory’s recent study of aortic endothelial cells. Here we investigate aquaporin-1 expression and function in the aortic endothelium in two high-renin rat models of hypertension, the spontaneously hypertensive genomically altered Wystar-Kyoto rat variant and Sprague-Dawley rats made hypertensive by two kidney, one clip Goldblatt surgery. We measured aquaporin-1 expression in aortic endothelial cells from whole rat aortas by quantitative immunohistochemistry, and function by measuring the pressure driven hydraulic conductivities of excised rat aortas with both intact and denuded endothelia on the same vessel. We use them to calculate the effective intimal hydraulic conductivity, which is a combination of endothelial and subendothelial components. We observed well-correlated enhancements in aquaporin-1 expression and function in both hypertensive rat models as well as in aortas from normotensive rats whose expression was upregulated by 2h forskolin treatment. Upregulated aquaporin-1 expression and function may be a response to hypertension that critically determines conduit artery vessel wall viability and long-term susceptibility to atherosclerosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20hypertension" title="acute hypertension">acute hypertension</a>, <a href="https://publications.waset.org/abstracts/search?q=aquaporin-1" title=" aquaporin-1"> aquaporin-1</a>, <a href="https://publications.waset.org/abstracts/search?q=hydraulic%20conductivity" title=" hydraulic conductivity"> hydraulic conductivity</a>, <a href="https://publications.waset.org/abstracts/search?q=hydrostatic%20pressure" title=" hydrostatic pressure"> hydrostatic pressure</a>, <a href="https://publications.waset.org/abstracts/search?q=aortic%20endothelial%20cells" title=" aortic endothelial cells"> aortic endothelial cells</a>, <a href="https://publications.waset.org/abstracts/search?q=transcellular%20flow" title=" transcellular flow"> transcellular flow</a> </p> <a href="https://publications.waset.org/abstracts/39927/chronic-hypertension-aquaporin-and-hydraulic-conductivity-a-perspective-on-pathological-connections" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39927.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">232</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3322</span> Surface Adjustments for Endothelialization of Decellularized Porcine Pericardium</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=M.%20Markova">M. Markova</a>, <a href="https://publications.waset.org/abstracts/search?q=E.%20Filova"> E. Filova</a>, <a href="https://publications.waset.org/abstracts/search?q=O.%20Kaplan"> O. Kaplan</a>, <a href="https://publications.waset.org/abstracts/search?q=R.%20Matejka"> R. Matejka</a>, <a href="https://publications.waset.org/abstracts/search?q=L.%20Bacakova"> L. Bacakova</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The porcine pericardium is used as a material for cardiac and aortic valves substitutes. Current biological aortic heart valve prosthesis have a limited lifetime period because they undergo degeneration. In order to make them more biocompatible and prolong their lifetime it is necessary to reseed the decellularized prostheses with endothelial cells and with valve interstitial cells. The endothelialization of the prosthesis-surface may be supported by suitable chemical surface modification of the prosthesis. The aim of this study is to prepare bioactive fibrin layers which would both support endothelialization of porcine pericardium and enhance differentiation and maturation of the endothelial cells seeded. As a material for surface adjustments we used layers of fibrin with/without heparin and some of them with adsorbed or chemically bound FGF2, VEGF or their combination. Fibrin assemblies were prepared in 24-well cell culture plate and were seeded with HSVEC (Human Saphenous Vein Endothelial Cells) at a density of 20,000 cells per well in EGM-2 medium with 0.5% FS and without heparin, without FGF2 and without VEGF; medium was supplemented with aprotinin (200 U/mL). As a control, surface polystyrene (PS) was used. Fibrin was also used as homogeneous impregnation of the decellularized porcine pericardium throughout the scaffolds. Morphology, density, and viability of the seeded endothelial cells were observed from micrographs after staining the samples by LIVE/DEAD cytotoxicity/viability assay kit on the days 1, 3, and 7. Endothelial cells were immunocytochemically stained for proteins involved in cell adhesion, i.e. alphaV integrin, vinculin, and VE-cadherin, markers of endothelial cells differentiation and maturation, i.e. von Willebrand factor and CD31, and for extracellular matrix proteins typically produced by endothelial cells, i.e. type IV collagen and laminin. The staining intensities were subsequently quantified using a software. HSVEC cells grew on each of the prepared surfaces better than on control surface. They reached confluency. The highest cell densities were obtained on the surface of fibrin with heparin and both grow factors used together. Intensity of alphaV integrins staining was highest on samples with remained fibrin layer, i.e. on layers with lower cell densities, i.e. on fibrin without heparin. Vinculin staining was apparent, but was rather diffuse, on fibrin with both FGF2 and VEGF and on control PS. Endothelial cells on all samples were positively stained for von Willebrand factor and CD31. VE-cadherin receptors clusters were best developed on fibrin with heparin and growth factors. Significantly stronger staining of type IV collagen was observed on fibrin with heparin and both growth factors. Endothelial cells on all samples produced laminin-1. Decellularized pericardium was homogeneously filled with fibrin structures. These fibrin-modified pericardium samples will be further seeded with cells and cultured in a bioreactor. Fibrin layers with/without heparin and with adsorbed or chemically bound FGF2, VEGF or their combination are good surfaces for endothelialization of cardiovascular prostheses or porcine pericardium based heart valves. Supported by the Ministry of Health, grants No15-29153A and 15-32497A, and the Grant Agency of the Czech Republic, project No. P108/12/G108. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aortic%20valves%20prosthesis" title="aortic valves prosthesis">aortic valves prosthesis</a>, <a href="https://publications.waset.org/abstracts/search?q=FGF2" title=" FGF2"> FGF2</a>, <a href="https://publications.waset.org/abstracts/search?q=heparin" title=" heparin"> heparin</a>, <a href="https://publications.waset.org/abstracts/search?q=HSVEC%20cells" title=" HSVEC cells"> HSVEC cells</a>, <a href="https://publications.waset.org/abstracts/search?q=VEGF" title=" VEGF"> VEGF</a> </p> <a href="https://publications.waset.org/abstracts/49557/surface-adjustments-for-endothelialization-of-decellularized-porcine-pericardium" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/49557.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">264</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3321</span> Activation of TNF-α from Human Endothelial Cells by Exposure of the Mitochondrial Stress Protein (Hsp60) Secreted from THP-1 Monocytes to High Glucose</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ryan%20D.%20Martinus">Ryan D. Martinus</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Inflammation of the endothelium is an important process leading to diabetic atherosclerosis. However, the molecular mechanisms by which diabetes contributes to endothelial inflammation remain to be established. Using In-vitro cultured Human cells and Hsp60 specific ELISA assays, we show that Hsp60 is not only induced in Human monocyte cells under hyperglycaemic conditions but that the Hsp60 is also secreted from these cells. Furthermore, we also demonstrate that the Hsp60 secreted from these monocyte cells is also able to activate Toll-like receptor-4 (TLR4) from Human endothelial cells. This suggests that a potential link may exist between the hyperglycaemia-induced expression of Hsp60 in monocyte cells and vascular inflammation. Circulating levels of Hsp60 due to mitochondrial stress in diabetes patients could, therefore, be an important modulator of inflammation in endothelial cells and thus contribute to the increased incidences of atherosclerosis in diabetes mellitus. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=mitochondria" title="mitochondria">mitochondria</a>, <a href="https://publications.waset.org/abstracts/search?q=Hsp60" title=" Hsp60"> Hsp60</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=diabetes%20mellitus" title=" diabetes mellitus"> diabetes mellitus</a> </p> <a href="https://publications.waset.org/abstracts/107492/activation-of-tnf-a-from-human-endothelial-cells-by-exposure-of-the-mitochondrial-stress-protein-hsp60-secreted-from-thp-1-monocytes-to-high-glucose" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/107492.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">181</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3320</span> Endothelial Progenitor Cell Biology in Ankylosing Spondylitis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ashit%20Syngle">Ashit Syngle</a>, <a href="https://publications.waset.org/abstracts/search?q=Inderjit%20Verma"> Inderjit Verma</a>, <a href="https://publications.waset.org/abstracts/search?q=Pawan%20Krishan"> Pawan Krishan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aim: Endothelial progenitor cells (EPCs) are unique populations which have reparative potential in overcoming the endothelial damage and reducing cardiovascular risk. Patients with ankylosing spondylitis (AS) have increased risk of cardiovascular morbidity and mortality. The aim of this study was to investigate the endothelial progenitor cell population in AS patients and its potential relationships with disease variables. Methods: Endothelial progenitor cells were measured in peripheral blood samples from 20 AS and 20 healthy controls by flow cytometry on the basis of CD34 and CD133 expression. Disease activity was evaluated by using Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Functional ability was monitored by using Bath Ankylosing Spondylitis Functional Index (BASFI). Results: EPCs were depleted in AS patients as compared to the healthy controls (CD34+/CD133+: 0.027 ± 0.010 % vs. 0.044 ± 0.011 %, p<0.001). EPCs depletion were significantly associated with disease duration (r=-0.52, p=0.01) and BASDAI (r=-0.45, p=0.04). Conclusion: This is the first study to demonstrate endothelial progenitor cells depletion in AS patients. EPCs depletion inversely correlates with disease duration and disease activity, suggesting the pivotal role of inflammation in depletion of EPCs. EPC would possibly also serve as a therapeutic target for preventing cardiovascular disease in AS. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ankylosing%20spondylitis" title="ankylosing spondylitis">ankylosing spondylitis</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20progenitor%20cells" title=" endothelial progenitor cells"> endothelial progenitor cells</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=vascular%20damage" title=" vascular damage"> vascular damage</a> </p> <a href="https://publications.waset.org/abstracts/17398/endothelial-progenitor-cell-biology-in-ankylosing-spondylitis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17398.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">438</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3319</span> Expression of uPA, tPA, and PAI-1 in Calcified Aortic Valves</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Abdullah%20M.%20Alzahrani">Abdullah M. Alzahrani</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Our physiopathological assumption is that u-PA, t-PA, and PAI-1 are released by calcified aortic valves and play a role in the calcification of these valves. Sixty-five calcified aortic valves were collected from patients suffering from aortic stenosis. Each valve was incubated for 24 hours in culture medium. The supernatants were used to measure u-PA, t-PA, and PAI-1 concentrations; the valve calcification was evaluated using biphotonic absorptiometry. Aortic stenosis valves expressed normal plasminogen activators concentrations and overexpressed PAI-1 (u-PA, t-PA, and PAI-1 mean concentrations were, resp., 1.69 ng/mL ± 0.80, 2.76 ng/mL ± 1.33, and 53.27 ng/mL ± 36.39). There was no correlation between u-PA and PAI-1 (r = 0.3) but t-PA and PAI-1 were strongly correlated with each other (r = 0.6). Over expression of PAI-1 was proportional to the calcium content of theAS valves. Our results demonstrate a consistent increase of PAI-1 proportional to the calcification. The over expression of PAI-1 may be useful as a predictive indicator in patients with aortic stenosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aortic%20valve" title="aortic valve">aortic valve</a>, <a href="https://publications.waset.org/abstracts/search?q=PAI-1" title=" PAI-1"> PAI-1</a>, <a href="https://publications.waset.org/abstracts/search?q=tPA%20gene" title=" tPA gene"> tPA gene</a>, <a href="https://publications.waset.org/abstracts/search?q=uPA%20gene" title=" uPA gene"> uPA gene</a> </p> <a href="https://publications.waset.org/abstracts/24878/expression-of-upa-tpa-and-pai-1-in-calcified-aortic-valves" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/24878.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">474</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3318</span> Endothelial Progenitor Cells Is a Determinant of Vascular Function and Atherosclerosis in Ankylosing Spondylitis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ashit%20Syngle">Ashit Syngle</a>, <a href="https://publications.waset.org/abstracts/search?q=Inderjit%20Verma"> Inderjit Verma</a>, <a href="https://publications.waset.org/abstracts/search?q=Pawan%20Krishan"> Pawan Krishan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: Endothelial progenitor cells (EPCs) have reparative potential in overcoming the endothelial dysfunction and reducing cardiovascular risk. EPC depletion has been demonstrated in the setting of established atherosclerotic diseases. With this background, we evaluated whether reduced EPCs population are associated with endothelial dysfunction, subclinical atherosclerosis and inflammatory markers in ankylosing spondylitis (AS) patients without any known traditional cardiovascular risk factor in AS patients. Methods: Levels of circulating EPCs (CD34+/CD133+), brachial artery flow-mediated dilatation, carotid intima-media thickness (CIMT) and inflammatory markers i.e erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), tissue necrosis factor (TNF)–α, interleukin (IL)-6, IL-1 were assessed in 30 AS patients (mean age33.41 ± 10.25; 11 female and 19 male) who fulfilled the modified New York diagnostic criteria with 25 healthy volunteers (mean age 29.36± 8.64; 9 female and 16 male) matched for age and sex. Results: EPCs (CD34+/CD133+) cells were significantly (0.020 ± 0.001% versus 0.040 ± 0.010%, p<0.001) reduced in patients with AS compared to healthy controls. Endothelial function (7.35 ± 2.54 versus 10.27 ±1.73, p=0.002), CIMT (0.63 ± 0.01 versus 0.35 ± 0.02, p < 0.001) and inflammatory markers were also significantly (p < 0.01) altered as compared to healthy controls. Specifically, CD34+CD133+cells were inversely multivariate correlated with CRP and TNF-α and endothelial dysfunction was positively correlated with reduced number of EPC. Conclusion: Depletion of EPCs population is an independent predictor of endothelial dysfunction and early atherosclerosis in AS patients and may provide additional information beyond conventional risk factors and inflammatory markers. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=endothelial%20progenitor%20cells" title="endothelial progenitor cells">endothelial progenitor cells</a>, <a href="https://publications.waset.org/abstracts/search?q=atherosclerosis" title=" atherosclerosis"> atherosclerosis</a>, <a href="https://publications.waset.org/abstracts/search?q=ankylosing%20spondylitis" title=" ankylosing spondylitis"> ankylosing spondylitis</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiovascular" title=" cardiovascular "> cardiovascular </a> </p> <a href="https://publications.waset.org/abstracts/17386/endothelial-progenitor-cells-is-a-determinant-of-vascular-function-and-atherosclerosis-in-ankylosing-spondylitis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17386.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">381</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3317</span> Effect of Far Infrared and Endothelial Cell Growth Supplement on Human Umbilical Vascular Endothelial Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ming-Tzu%20Tsai">Ming-Tzu Tsai</a>, <a href="https://publications.waset.org/abstracts/search?q=Jui-Ting%20Hsu"> Jui-Ting Hsu</a>, <a href="https://publications.waset.org/abstracts/search?q=Chia-Chieh%20Lin"> Chia-Chieh Lin</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng-Tsai%20Chiang"> Feng-Tsai Chiang</a>, <a href="https://publications.waset.org/abstracts/search?q=Cheng-Chin%20Huang"> Cheng-Chin Huang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Far infrared (FIR), an invisible and short electromagnetic waves ranges from 6-14 μm also defines as the “growth ray.” Although the mechanism of FIR is still unknown, most data have suggested that FIR could accelerate the skin microcirculation by elevating the blood flow and nitric-oxide (NO) synthesis. In this present work, the effect of FIR irradiation and endothelial cell growth supplement (ECGS) on human umbilical vascular endothelial cells (HUVECs) was evaluated. To understand whether the cell viability and NO production of HUVECs affected by NO, cells with/without ECGS were treated in the presence or absence of L-NAME, an eNOS inhibitor. For FIR exposure, FIR-emitted ceramic powders consisted of a variety of well-mixed metal oxides were developed. The results showed that L-NAME did had a strong effect on the inhibition of NO production, especially in the ECGS-treated group. However, the cell viability of each group was rarely affected in the presence of L-NAME. Cells with the incubation of ECGS showed much higher cell viability compared to the control. Moreover, NO production of HUVECs exposed to FIR irradiation was significantly inhibited in the presence of L-NAME. It suggested that NO could play a role modulating the downstream signals of HUVECs during FIR exposure. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=far-infrared%20irradiation%20%28FIR%29" title="far-infrared irradiation (FIR)">far-infrared irradiation (FIR)</a>, <a href="https://publications.waset.org/abstracts/search?q=nitric%20oxide%20%28NO%29" title=" nitric oxide (NO)"> nitric oxide (NO)</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20nitric%20oxide%20synthase%20%28eNOS%29" title=" endothelial nitric oxide synthase (eNOS)"> endothelial nitric oxide synthase (eNOS)</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20cell%20growth%20supplement%20%28ECGS%29" title=" endothelial cell growth supplement (ECGS)"> endothelial cell growth supplement (ECGS)</a> </p> <a href="https://publications.waset.org/abstracts/25653/effect-of-far-infrared-and-endothelial-cell-growth-supplement-on-human-umbilical-vascular-endothelial-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/25653.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">429</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3316</span> Aerobic Exercise Increases Circulating Hematopoietic Stem Cells and Endothelial Progenitor Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Khaled%20A.%20shady">Khaled A. shady</a>, <a href="https://publications.waset.org/abstracts/search?q=Fagr%20B.%20Bazeed"> Fagr B. Bazeed</a>, <a href="https://publications.waset.org/abstracts/search?q=Nashwa%20K.%20Abousamra"> Nashwa K. Abousamra</a>, <a href="https://publications.waset.org/abstracts/search?q=Ihab%20H.%20Elberawe"> Ihab H. Elberawe</a>, <a href="https://publications.waset.org/abstracts/search?q=Ashraf%20E.%20shaalan"> Ashraf E. shaalan</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohamed%20A.%20Sobh"> Mohamed A. Sobh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Physical activity activates a variety of adult stem cells which might be released into the circulation or might be activated in their organ-resident state. A variety of stimuli such as metabolic, mechanical, and hormonal stimuli might by responsible for the mobilization. This study was done to know the changes in hematopoietic stem cells and endothelial progenitor in athletes in the 24 hours following 30 min of aerobic exercise. Methods: Ten healthy male's athlete's (age 20.7± 0.61 y) performed moderate running with 30 min at 80% of velocity of The IAT. Blood samples taken pre-, and immediately, 30 min, 2h, 6h and 24h post-exercise were analyzed for hematopoietic stem cells (HSCs ), endothelial progenitor cells (EPCs(, vascular endothelial growth factor (VEGF), nitric oxide (NO), lactic acid (LA), and white blood cells . HSCs and EPCs were quantified by flow cytometry. Results: After 30min of aerobic exercise significant increases in HSCs, EPC, VEGF, NO, LA and WBCs (p ˂ 0.05). This increase will be at different rates according to the timing of taking blood sample and was in the maximum rate of increase after 30 min of aerobic exercise. HSCs, EPC, NO and WBCs were in the maximum rate of increase 2h post exercise. In addition, VEGF was in the maximum rate of increase immediately post exercise and LA concentration not affected after exercise. Conclusion: These data suggest that HSCs and EPCs increased after aerobic exercise due to increase of VEGF which play an important role in mobilization of stem cells and promotes NO increase which contributes to increase EPCs. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=physical%20activity" title="physical activity">physical activity</a>, <a href="https://publications.waset.org/abstracts/search?q=hematopoietic%20stem%20cells" title=" hematopoietic stem cells"> hematopoietic stem cells</a>, <a href="https://publications.waset.org/abstracts/search?q=mobilization" title=" mobilization"> mobilization</a>, <a href="https://publications.waset.org/abstracts/search?q=athletes" title=" athletes"> athletes</a> </p> <a href="https://publications.waset.org/abstracts/158031/aerobic-exercise-increases-circulating-hematopoietic-stem-cells-and-endothelial-progenitor-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/158031.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">117</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3315</span> Plasma Treatment in Conjunction with EGM-2 Medium Can Enhance Endothelial and Osteogenic Marker Expressions of Bone Marrow MSCs</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chih-Hsin%20Lin">Chih-Hsin Lin</a>, <a href="https://publications.waset.org/abstracts/search?q=Shyh-Yuan%20Lee"> Shyh-Yuan Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Yuan-Min%20Lin"> Yuan-Min Lin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> For many tissue engineering applications, an important goal is to create functional tissues in-vitro, and such tissues to be viable, they have to be vascularized. Endothelial cells (EC) and endothelial progenitor cells (EPC) are promising candidates for vascularization. However, both of them have limited expansion capacity and autologous cells currently do not exist for either ECs or EPCs. Therefore, we use bone marrow mesenchymal stem cells (MSC) as a source material for ECs. Growth supplements are commonly used to induce MSC differentiation, and further improvements in differentiation conditions can be made by modifying the cell's growth environment. An example is pre-treatment of the growth dish with gas plasma, in order to modify the surface functional groups of the material that the cells are seeded on. In this work, we compare the effects of different gas plasmas on the growth and differentiation of MSCs. We treat the dish with different plasmas (CO2, N2, and O2) and then induce MSC differentiation with endothelial growth medium-2 (EGM-2). We find that EGM-2 by itself upregulates EC marker CD31 mRNA expression, but not VEGFR2, CD34, or vWF. However, these additional EC marker expressions were increased for cells seeded on plasma treated substrates. Specifically, for EC markers, we found that N2 plasma treatment upregulated CD31 and VEGFR-2 mRNA expressions; CO2 plasma treatment upregulated CD34 and vWF mRNA expressions. The osteogenic markers ALP and osteopontin mRNA expressions were markedly enhanced on all plasma-treated dishes. We also found that plasma treatment in conjunction with EGM-2 growth medium can enhance MSCs differentiation into endothelial-like cells and osteogenic-like cells. Our work shows that the effect of the growth medium (EGM-2) on MSCs differentiation is influenced by the plasma modified surface chemistry of the substrate. In conclusion, plasma surface modification can enhance EGM-2 effectiveness and induced both endothelial and osteogenic differentiation. Our findings provide a method to enhance EGM-2 based cell differentiation, with consequences for tissue engineering and stem cell biology applications. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=endothelial%20differentiation" title="endothelial differentiation">endothelial differentiation</a>, <a href="https://publications.waset.org/abstracts/search?q=EGM-2" title=" EGM-2"> EGM-2</a>, <a href="https://publications.waset.org/abstracts/search?q=osteogenesis" title=" osteogenesis"> osteogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=plasma%20treatment" title=" plasma treatment"> plasma treatment</a>, <a href="https://publications.waset.org/abstracts/search?q=surface%20modification" title=" surface modification"> surface modification</a> </p> <a href="https://publications.waset.org/abstracts/41775/plasma-treatment-in-conjunction-with-egm-2-medium-can-enhance-endothelial-and-osteogenic-marker-expressions-of-bone-marrow-mscs" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41775.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">331</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3314</span> Developing a Tissue-Engineered Aortic Heart Valve Based on an Electrospun Scaffold </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sara%20R.%20Knigge">Sara R. Knigge</a>, <a href="https://publications.waset.org/abstracts/search?q=Sugat%20R.%20Tuladhar"> Sugat R. Tuladhar</a>, <a href="https://publications.waset.org/abstracts/search?q=Alexander%20Becker"> Alexander Becker</a>, <a href="https://publications.waset.org/abstracts/search?q=Tobias%20Schilling"> Tobias Schilling</a>, <a href="https://publications.waset.org/abstracts/search?q=Birgit%20Glasmacher"> Birgit Glasmacher </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Commercially available mechanical or biological heart valve prostheses both tend to fail long-term due to thrombosis, calcific degeneration, infection, or immunogenic rejection. Moreover, these prostheses are non-viable and do not grow with the patients, which is a problem for young patients. As a result, patients often need to undergo redo-operations. Tissue-engineered (TE) heart valves based on degradable electrospun fiber scaffolds represent a promising approach to overcome these limitations. Such scaffolds need sufficient mechanical properties to withstand the hydrodynamic stress of intracardiac hemodynamics. Additionally, the scaffolds should be colonized by autologous or homologous cells to facilitate the in vivo remodeling of the scaffolds to a viable structure. This study investigates how process parameters of electrospinning and degradation affect the mechanical properties of electrospun scaffolds made of FDA-approved, biodegradable polymer polycaprolactone (PCL). Fiber mats were produced from a PCL/tetrafluoroethylene solution by electrospinning. The e-spinning process was varied in terms of scaffold thickness, fiber diameter, fiber orientation, and fiber interconnectivity. The morphology of the fiber mats was characterized with a scanning electron microscope (SEM). The mats were degraded in different solutions (cell culture media, SBF, PBS and 10 M NaOH-Solution). At different time points of degradation (2, 4 and 6 weeks), tensile and cyclic loading tests were performed. Fresh porcine pericardium and heart valves served as a control for the mechanical assessment. The progression of polymer degradation was quantified by SEM and differential scanning calorimetry (DSC). Primary Human aortic endothelial cells (HAECs) and Human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) were seeded on the fiber mats to investigate the cell colonization potential. The results showed that both the electrospinning parameters and the degradation significantly influenced the mechanical properties. Especially the fiber orientation has a considerable impact and leads to a pronounced anisotropic behavior of the scaffold. Preliminary results showed that the polymer became strongly more brittle over time. However, the embrittlement can initially only be detected in the mechanical test. In the SEM and DSC investigations, neither morphological nor thermodynamic changes are significantly detectable. Live/Dead staining and SEM imaging of the cell-seeded scaffolds showed that HAECs and iPSC-ECs were able to grow on the surface of the polymer. In summary, this study's results indicate a promising approach to the development of a TE aortic heart valve based on an electrospun scaffold. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=electrospun%20scaffolds" title="electrospun scaffolds">electrospun scaffolds</a>, <a href="https://publications.waset.org/abstracts/search?q=long-term%20polymer%20degradation" title=" long-term polymer degradation"> long-term polymer degradation</a>, <a href="https://publications.waset.org/abstracts/search?q=mechanical%20behavior%20of%20electrospun%20PCL" title=" mechanical behavior of electrospun PCL"> mechanical behavior of electrospun PCL</a>, <a href="https://publications.waset.org/abstracts/search?q=tissue%20engineered%20aortic%20heart%20valve" title=" tissue engineered aortic heart valve"> tissue engineered aortic heart valve</a> </p> <a href="https://publications.waset.org/abstracts/136128/developing-a-tissue-engineered-aortic-heart-valve-based-on-an-electrospun-scaffold" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/136128.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">143</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3313</span> Angiogenesis and Blood Flow: The Role of Blood Flow in Proliferation and Migration of Endothelial Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hossein%20Bazmara">Hossein Bazmara</a>, <a href="https://publications.waset.org/abstracts/search?q=Kaamran%20Raahemifar"> Kaamran Raahemifar</a>, <a href="https://publications.waset.org/abstracts/search?q=Mostafa%20Sefidgar"> Mostafa Sefidgar</a>, <a href="https://publications.waset.org/abstracts/search?q=Madjid%20Soltani"> Madjid Soltani</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Angiogenesis is formation of new blood vessels from existing vessels. Due to flow of blood in vessels, during angiogenesis, blood flow plays an important role in regulating the angiogenesis process. Multiple mathematical models of angiogenesis have been proposed to simulate the formation of the complicated network of capillaries around a tumor. In this work, a multi-scale model of angiogenesis is developed to show the effect of blood flow on capillaries and network formation. This model spans multiple temporal and spatial scales, i.e. intracellular (molecular), cellular, and extracellular (tissue) scales. In intracellular or molecular scale, the signaling cascade of endothelial cells is obtained. Two main stages in development of a vessel are considered. In the first stage, single sprouts are extended toward the tumor. In this stage, the main regulator of endothelial cells behavior is the signals from extracellular matrix. After anastomosis and formation of closed loops, blood flow starts in the capillaries. In this stage, blood flow induced signals regulate endothelial cells behaviors. In cellular scale, growth and migration of endothelial cells is modeled with a discrete lattice Monte Carlo method called cellular Pott's model (CPM). In extracellular (tissue) scale, diffusion of tumor angiogenic factors in the extracellular matrix, formation of closed loops (anastomosis), and shear stress induced by blood flow is considered. The model is able to simulate the formation of a closed loop and its extension. The results are validated against experimental data. The results show that, without blood flow, the capillaries are not able to maintain their integrity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=angiogenesis" title="angiogenesis">angiogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20cells" title=" endothelial cells"> endothelial cells</a>, <a href="https://publications.waset.org/abstracts/search?q=multi-scale%20model" title=" multi-scale model"> multi-scale model</a>, <a href="https://publications.waset.org/abstracts/search?q=cellular%20Pott%27s%20model" title=" cellular Pott's model"> cellular Pott's model</a>, <a href="https://publications.waset.org/abstracts/search?q=signaling%20cascade" title=" signaling cascade"> signaling cascade</a> </p> <a href="https://publications.waset.org/abstracts/37304/angiogenesis-and-blood-flow-the-role-of-blood-flow-in-proliferation-and-migration-of-endothelial-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/37304.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">425</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3312</span> Right Atrial Tissue Morphology in Acquired Heart Diseases</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Edite%20Kulmane">Edite Kulmane</a>, <a href="https://publications.waset.org/abstracts/search?q=Mara%20Pilmane"> Mara Pilmane</a>, <a href="https://publications.waset.org/abstracts/search?q=Romans%20Lacis"> Romans Lacis</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Acquired heart diseases remain one of the leading health care problems in the world. Changes in myocardium of the diseased hearts are complex and pathogenesis is still not fully clear. The aim of this study was to identify appearance and distribution of apoptosis, homeostasis regulating factors, and innervation and ischemia markers in right atrial tissue in different acquired heart diseases. Methods: During elective open heart surgery were taken right atrial tissue fragments from 12 patients. All patients were operated because of acquired heart diseases- aortic valve stenosis (5 patients), coronary heart disease (5 patients), coronary heart disease and secondary mitral insufficiency (1 patient) and mitral disease (1 patient). The mean age was (mean±SD) 70,2±7,0 years (range 58-83 years). The tissues were stained with haematoxylin and eosin methods for routine light-microscopical examination and for immunohistochemical detection of protein gene peptide 9.5 (PGP 9.5), human atrial natriuretic peptide (hANUP), vascular endothelial growth factor (VEGF), chromogranin A and endothelin. Apoptosis was detected by TUNEL method. Results: All specimens showed degeneration of cardiomyocytes with lysis of myofibrils, diffuse vacuolization especially in perinuclear region, different size of cells and their nuclei. The severe invasion of connective tissue was observed in main part of all fragments. The apoptotic index ranged from 24 to 91%. One specimen showed region of newly performed microvessels with cube shaped endotheliocytes that were positive for PGP 9.5, endothelin, chromogranin A and VEGF. From all fragments, taken from patients with coronary heart disease, there were observed numerous PGP 9.5-containing nerve fibres, except in patient with secondary mitral insufficiency, who showed just few PGP 9.5 positive nerves. In majority of specimens there were regions observed with cube shaped mixed -VEGF immunoreactive endocardial and epicardial cells. Only VEGF positive endothelial cells were observed just in few specimens. There was no significant difference of hANUP secreting cells among all specimens. All patients operated due to the coronary heart disease moderate to numerous number of chromogranin A positive cells were seen while in patients with aortic valve stenosis tissue demonstrated just few factor positive cells. Conclusions: Complex detection of different factors may indicate selectively disordered morphopathogenetical event of heart disease: decrease of PGP 9.5 nerves suggests the decreased innervation of organ; increased apoptosis indicates the cell death without ingrowth of connective tissue; persistent presence of hANUP proves the unchanged homeostasis of cardiomyocytes probably supported by expression of chromogranins. Finally, decrease of VEGF detects the regions of affected blood vessels in heart affected by acquired heart disease. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=heart" title="heart">heart</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a>, <a href="https://publications.waset.org/abstracts/search?q=protein-gene%20peptide%209.5" title=" protein-gene peptide 9.5"> protein-gene peptide 9.5</a>, <a href="https://publications.waset.org/abstracts/search?q=atrial%20natriuretic%20peptide" title=" atrial natriuretic peptide"> atrial natriuretic peptide</a>, <a href="https://publications.waset.org/abstracts/search?q=vascular%20endothelial%20growth%20factor" title=" vascular endothelial growth factor"> vascular endothelial growth factor</a>, <a href="https://publications.waset.org/abstracts/search?q=chromogranin%20A" title=" chromogranin A"> chromogranin A</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelin" title=" endothelin"> endothelin</a> </p> <a href="https://publications.waset.org/abstracts/24903/right-atrial-tissue-morphology-in-acquired-heart-diseases" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/24903.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">295</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3311</span> Hybrid Polymer Microfluidic Platform for Studying Endothelial Cell Response to Micro Mechanical Environment</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mitesh%20Rathod">Mitesh Rathod</a>, <a href="https://publications.waset.org/abstracts/search?q=Jungho%20Ahn"> Jungho Ahn</a>, <a href="https://publications.waset.org/abstracts/search?q=Noo%20Li%20Jeon"> Noo Li Jeon</a>, <a href="https://publications.waset.org/abstracts/search?q=Junghoon%20Lee"> Junghoon Lee</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Endothelial cells respond to cues from both biochemical as well as micro mechanical environment. Significant effort has been directed to understand the effects of biochemical signaling, however, relatively little is known about regulation of endothelial cell biology by the micro mechanical environment. Numerous studies have been performed to understand how physical forces regulate endothelial cell behavior. In this regard, past studies have majorly focused on exploring how fluid shear stress governs endothelial cell behavior. Parallel plate flow chambers and rectangular microchannels are routinely employed for applying fluid shear force on endothelial cells. However, these studies fall short in mimicking the in vivo like micro environment from topological aspects. Few studies have only used circular microchannels to replicate in vivo like condition. Seldom efforts have been directed to elucidate the combined effect of topology, substrate rigidity and fluid shear stress on endothelial cell response. In this regard, we demonstrate a facile fabrication process to develop a hybrid polydimethylsiloxane microfluidic platform to study endothelial cell biology. On a single chip microchannels with different cross sections i.e., circular, rectangular and square have been fabricated. In addition, our fabrication approach allows variation in the substrate rigidity along the channel length. Two different variants of polydimethylsiloxane, namely Sylgard 184 and Sylgard 527, were utilized to achieve the variation in rigidity. Moreover, our approach also enables in creating Y bifurcation circular microchannels. Our microfluidic platform thus facilitates for conducting studies pertaining to endothelial cell morphology with respect to change in topology, substrate rigidity and fluid flow on a single chip. The hybrid platform was tested by culturing Human Umbilical Vein Endothelial Cells in circular microchannels with varying substrate rigidity, and exposed to fluid shear stress of 12 dynes/cm² and static conditions. Results indicate the cell area response to flow induced shear stress was governed by the underlying substrate mechanics. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hybrid" title="hybrid">hybrid</a>, <a href="https://publications.waset.org/abstracts/search?q=microfluidic%20platform" title=" microfluidic platform"> microfluidic platform</a>, <a href="https://publications.waset.org/abstracts/search?q=PDMS" title=" PDMS"> PDMS</a>, <a href="https://publications.waset.org/abstracts/search?q=shear%20flow" title=" shear flow"> shear flow</a>, <a href="https://publications.waset.org/abstracts/search?q=substrate%20rigidity" title=" substrate rigidity"> substrate rigidity</a> </p> <a href="https://publications.waset.org/abstracts/80807/hybrid-polymer-microfluidic-platform-for-studying-endothelial-cell-response-to-micro-mechanical-environment" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/80807.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">275</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3310</span> Impact of Cytokines Alone and Primed with Macrophages on Balamuthia mandrillaris Interactions with Human Brain Microvascular Endothelial Cells in vitro</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Abdul%20Matin">Abdul Matin</a>, <a href="https://publications.waset.org/abstracts/search?q=Salik%20Nawaz"> Salik Nawaz</a>, <a href="https://publications.waset.org/abstracts/search?q=Suk-Yul%20Jung"> Suk-Yul Jung</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Balamuthia mandrillaris is well known to cause fatal Balamuthia amoebic encephalitis (BAE). Amoebic transmission into the central nervous system (CNS), haematogenous spread is thought to be the prime step, followed by blood-brain barrier (BBB) dissemination. Macrophages are considered to be the foremost line of defense and present in excessive numbers during amoebic infections. The aim of the present investigation was to evaluate the effects of macrophages alone or primed with cytokines on the biological characteristics of Balamuthia in vitro. Using human brain microvascular endothelial cells (HBMEC), which constitutes the BBB, we have shown that Balamuthia demonstrated > 90% binding and > 70% cytotoxicity to host cells. However, macrophages further increased amoebic binding and Balamuthia-mediated cell cytotoxicity. Furthermore, macrophages exhibited no amoebicidal effect against Balamuthia. Zymography assay demonstrated that macrophages exhibited no inhibitory effect on proteolytic activity of Balamuthia. Overall, to our best knowledge, we have shown for the first time macrophages has no inhibitory effects on the biological properties of Balamuthia in vitro. This also strengthened the concept that how and why Balamuthia can cause infections in both immuno-competent and immuno-compromised individuals. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Balamuthia%20mandrillaris" title="Balamuthia mandrillaris">Balamuthia mandrillaris</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophages" title=" macrophages"> macrophages</a>, <a href="https://publications.waset.org/abstracts/search?q=cytokines" title=" cytokines"> cytokines</a>, <a href="https://publications.waset.org/abstracts/search?q=human%20brain%20microvascular%20endothelial%20cells" title=" human brain microvascular endothelial cells"> human brain microvascular endothelial cells</a>, <a href="https://publications.waset.org/abstracts/search?q=Balamuthia%20amoebic%20encephalitis" title=" Balamuthia amoebic encephalitis"> Balamuthia amoebic encephalitis</a> </p> <a href="https://publications.waset.org/abstracts/86213/impact-of-cytokines-alone-and-primed-with-macrophages-on-balamuthia-mandrillaris-interactions-with-human-brain-microvascular-endothelial-cells-in-vitro" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/86213.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">156</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3309</span> Effects of Anti-FGL2 Monoclonal Antibody SPF89 on Vascular Inflammation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ying%20Sun">Ying Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Biao%20Cheng"> Biao Cheng</a>, <a href="https://publications.waset.org/abstracts/search?q=Qing%20Lu"> Qing Lu</a>, <a href="https://publications.waset.org/abstracts/search?q=Xuefei%20Tao"> Xuefei Tao</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiaoyu%20Lai"> Xiaoyu Lai</a>, <a href="https://publications.waset.org/abstracts/search?q=Cheng%20Guo"> Cheng Guo</a>, <a href="https://publications.waset.org/abstracts/search?q=Dan%20Wang"> Dan Wang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Fibrinogen-like protein 2 (FGL2) has recently been identified to play an important role in inflammatory diseases such as atherosclerosis through a thrombin-dependent manner. Here, a murine monoclonal antibody was raised against the critical residue Ser(89) of FGL2, and the effects of the anti-FGL2 mAb (SPF89) were analyzed in human umbilical vein endothelial cells (HUVECs) and THP-1 cells. Firstly, it was proved that SPF89, which belongs to the IgG1 subtype with a KD value of 44.5 pM, could specifically show the expression levels of protein FGL2 in different cell lines of known target gene status. The lipopolysaccharide (LPS)-mediated endothelial cell proliferation was significantly inhibited with a decline of phosphorylation nuclear factor-κB (NF-κB) in a dose-dependent manner after SPF89 treatment. Furthermore, SPF89 reduced LPS-induced expression of adhesion molecules and inflammatory cytokines such as vascular cell adhesion molecule-1, tumor necrosis factor-α, Matrix metalloproteinase MMP-2, Integrin αvβ3, and interleukin-6 in HUVECs. In macrophage-like THP-1 cells, SPF89 effectively inhibited LPS and low-density lipoprotein-induced foam cell formation. However, these anti-inflammatory and anti-atherosclerotic effects of anti-FGL2 mAb in HUVECs and THP-1 cells were significantly reduced after treatment with an NF-κB inhibitor PDTC. All the above suggest, by efficiently inhibiting LPS-induced pro-inflammatory effects in vascular endothelial cells by attenuating NF-κB dependent pathway, the new anti-FGL2 mAb SPF89 could to be a potential therapeutic candidate for protecting the vascular endothelium against inflammatory diseases such as atherosclerosis. This work was supported by the Program of Sichuan Science and Technology Department (2017FZ0069) and Collaborative Innovation Program of Sichuan for Elderly Care and Health(YLZBZ1511). <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=monoclonal%20antibody" title="monoclonal antibody">monoclonal antibody</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrinogen%20like%20protein%202" title=" fibrinogen like protein 2"> fibrinogen like protein 2</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20cells" title=" endothelial cells"> endothelial cells</a> </p> <a href="https://publications.waset.org/abstracts/79816/effects-of-anti-fgl2-monoclonal-antibody-spf89-on-vascular-inflammation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/79816.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">271</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3308</span> Detection, Isolation, and Raman Spectroscopic Characterization of Acute and Chronic Staphylococcus aureus Infection in an Endothelial Cell Culture Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Astrid%20Tannert">Astrid Tannert</a>, <a href="https://publications.waset.org/abstracts/search?q=Anuradha%20Ramoji"> Anuradha Ramoji</a>, <a href="https://publications.waset.org/abstracts/search?q=Christina%20Ebert"> Christina Ebert</a>, <a href="https://publications.waset.org/abstracts/search?q=Frederike%20Gladigau"> Frederike Gladigau</a>, <a href="https://publications.waset.org/abstracts/search?q=Lorena%20Tuchscherr"> Lorena Tuchscherr</a>, <a href="https://publications.waset.org/abstracts/search?q=J%C3%BCrgen%20Popp"> Jürgen Popp</a>, <a href="https://publications.waset.org/abstracts/search?q=Ute%20Neugebauer"> Ute Neugebauer</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Staphylococcus aureus is a facultative intracellular pathogen, which by entering host cells may evade immunologic host response as well as antimicrobial treatment. In that way, S. aureus can cause persistent intracellular infections which are difficult to treat. Depending on the strain, S. aureus may persist at different intracellular locations like the phagolysosome. The first barrier invading pathogens from the blood stream that they have to cross are the endothelial cells lining the inner surface of blood and lymphatic vessels. Upon proceeding from an acute to a chronic infection, intracellular pathogens undergo certain biochemical and structural changes including a deceleration of metabolic processes to adopt for long-term intracellular survival and the development of a special phenotype designated as small colony variant. In this study, the endothelial cell line Ea.hy 926 was used as a model for acute and chronic S. aureus infection. To this end, Ea.hy 926 cells were cultured on QIAscout™ Microraft Arrays, a special graded cell culture substrate that contains around 12,000 microrafts of 200 µm edge length. After attachment to the substrate, the endothelial cells were infected with GFP-expressing S. aureus for 3 weeks. The acute infection and the development of persistent bacteria was followed by confocal laser scanning microscopy, scanning the whole Microraft Array for the presence and for detailed determination of the intracellular location of fluorescent intracellular bacteria every second day. After three weeks of infection representative microrafts containing infected cells, cells with protruded infections and cells that did never show any infection were isolated and fixed for Raman micro-spectroscopic investigation. For comparison, also microrafts with acute infection were isolated. The acquired Raman spectra are correlated with the fluorescence microscopic images to give hints about a) the molecular alterations in endothelial cells during acute and chronic infection compared to non-infected cells, and b) metabolic and structural changes within the pathogen when entering a mode of persistence within host cells. We thank Dr. Ruth Kläver from QIAGEN GmbH for her support regarding QIAscout technology. Financial support by the BMBF via the CSCC (FKZ 01EO1502) and from the DFG via the Jena Biophotonic and Imaging Laboratory (JBIL, FKZ PO 633/29-1, BA 1601/10-1) is highly acknowledged. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=correlative%20image%20analysis" title="correlative image analysis">correlative image analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=intracellular%20infection" title=" intracellular infection"> intracellular infection</a>, <a href="https://publications.waset.org/abstracts/search?q=pathogen-host%20adaption" title=" pathogen-host adaption"> pathogen-host adaption</a>, <a href="https://publications.waset.org/abstracts/search?q=Raman%20micro-spectroscopy" title=" Raman micro-spectroscopy"> Raman micro-spectroscopy</a> </p> <a href="https://publications.waset.org/abstracts/79133/detection-isolation-and-raman-spectroscopic-characterization-of-acute-and-chronic-staphylococcus-aureus-infection-in-an-endothelial-cell-culture-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/79133.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">181</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3307</span> Intrastromal Donor Limbal Segments Implantation as a Surgical Treatment of Progressive Keratoconus: Clinical and Functional Results</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mikhail%20Panes">Mikhail Panes</a>, <a href="https://publications.waset.org/abstracts/search?q=Sergei%20Pozniak"> Sergei Pozniak</a>, <a href="https://publications.waset.org/abstracts/search?q=Nikolai%20Pozniak"> Nikolai Pozniak</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Purpose: To evaluate the effectiveness of intrastromal donor limbal segments implantation for treatment of progressive keratoconus considering on main characteristics of corneal endothelial cells. Setting: Outpatient ophthalmic clinic. Methods: Twenty patients (20 eyes) with progressive keratoconus II-III of Amsler classification were recruited. The worst eye was treated with the transplantation of donor limbal segments in the recipient corneal stroma, while the fellow eye was left untreated as a control of functional and morphological changes. Furthermore, twenty patients (20 eyes) without progressive keratoconus was used as a control of corneal endothelial cells changes. All patients underwent a complete ocular examination including uncorrected and corrected distance visual acuity (UDVA, CDVA), slit lamp examination fundus examination, corneal topography and pachymetry, auto-keratometry, Anterior Segment Optical Coherence Tomography and Corneal Endothelial Specular Microscopy. Results: After two years, statistically significant improvement in the UDVA and CDVA (on the average on two lines for UDVA and three-four lines for CDVA) were noted. Besides corneal astigmatism decreased from 5.82 ± 2.64 to 1.92 ± 1.4 D. Moreover there were no statistically significant differences in the changes of mean spherical equivalent, keratometry and pachymetry indicators. It should be noted that after two years there were no significant differences in the changes of the number and form of corneal endothelial cells. It can be regarded as a process stabilization. In untreated control eyes, there was a general trend towards worsening of UDVA, CDVA and corneal thickness, while corneal astigmatism was increased. Conclusion: Intrastromal donor segments implantation is a safe technique for keratoconus treatment. Intrastromal donor segments implantation is an efficient procedure to stabilize and improve progressive keratoconus. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=corneal%20endothelial%20cells" title="corneal endothelial cells">corneal endothelial cells</a>, <a href="https://publications.waset.org/abstracts/search?q=intrastromal%20donor%20limbal%20segments" title=" intrastromal donor limbal segments"> intrastromal donor limbal segments</a>, <a href="https://publications.waset.org/abstracts/search?q=progressive%20keratoconus" title=" progressive keratoconus"> progressive keratoconus</a>, <a href="https://publications.waset.org/abstracts/search?q=surgical%20treatment%20of%20keratoconus" title=" surgical treatment of keratoconus"> surgical treatment of keratoconus</a> </p> <a href="https://publications.waset.org/abstracts/50386/intrastromal-donor-limbal-segments-implantation-as-a-surgical-treatment-of-progressive-keratoconus-clinical-and-functional-results" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/50386.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">281</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3306</span> Validation of a Fluid-Structure Interaction Model of an Aortic Dissection versus a Bench Top Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=K.%20Khanafer">K. Khanafer</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The aim of this investigation was to validate the fluid-structure interaction (FSI) model of type B aortic dissection with our experimental results from a bench-top-model. Another objective was to study the relationship between the size of a septectomy that increases the outflow of the false lumen and its effect on the values of the differential of pressure between true lumen and false lumen. FSI analysis based on Galerkin’s formulation was used in this investigation to study flow pattern and hemodynamics within a flexible type B aortic dissection model using boundary conditions from our experimental data. The numerical results of our model were verified against the experimental data for various tear size and location. Thus, CFD tools have a potential role in evaluating different scenarios and aortic dissection configurations. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aortic%20dissection" title="aortic dissection">aortic dissection</a>, <a href="https://publications.waset.org/abstracts/search?q=fluid-structure%20interaction" title=" fluid-structure interaction"> fluid-structure interaction</a>, <a href="https://publications.waset.org/abstracts/search?q=in%20vitro%20model" title=" in vitro model"> in vitro model</a>, <a href="https://publications.waset.org/abstracts/search?q=numerical" title=" numerical"> numerical</a> </p> <a href="https://publications.waset.org/abstracts/74636/validation-of-a-fluid-structure-interaction-model-of-an-aortic-dissection-versus-a-bench-top-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/74636.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">271</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3305</span> Finite Element Modeling of Aortic Intramural Haematoma Shows Size Matters</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aihong%20%20Zhao">Aihong Zhao</a>, <a href="https://publications.waset.org/abstracts/search?q=Priya%20Sastry"> Priya Sastry</a>, <a href="https://publications.waset.org/abstracts/search?q=Mark%20L%20Field"> Mark L Field</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohamad%20Bashir"> Mohamad Bashir</a>, <a href="https://publications.waset.org/abstracts/search?q=Arvind%20Singh"> Arvind Singh</a>, <a href="https://publications.waset.org/abstracts/search?q=David%20Richens"> David Richens</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objectives: Intramural haematoma (IMH) is one of the pathologies, along with acute aortic dissection, that present as Acute Aortic Syndrome (AAS). Evidence suggests that unlike aortic dissection, some intramural haematomas may regress with medical management. However, intramural haematomas have been traditionally managed like acute aortic dissections. Given that some of these pathologies may regress with conservative management, it would be useful to be able to identify which of these may not need high risk emergency intervention. A computational aortic model was used in this study to try and identify intramural haematomas with risk of progression to aortic dissection. Methods: We created a computational model of the aorta with luminal blood flow. Reports in the literature have identified 11 mm as the radial clot thickness that is associated with heightened risk of progression of intramural haematoma. Accordingly, haematomas of varying sizes were implanted in the modeled aortic wall to test this hypothesis. The model was exposed to physiological blood flows and the stresses and strains in each layer of the aortic wall were recorded. Results: Size and shape of clot were seen to affect the magnitude of aortic stresses. The greatest stresses and strains were recorded in the intima of the model. When the haematoma exceeded 10 mm in all dimensions, the stress on the intima reached breaking point. Conclusion: Intramural clot size appears to be a contributory factor affecting aortic wall stress. Our computer simulation corroborates clinical evidence in the literature proposing that IMH diameter greater than 11 mm may be predictive of progression. This preliminary report suggests finite element modelling of the aortic wall may be a useful process by which to examine putative variables important in predicting progression or regression of intramural haematoma. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=intramural%20haematoma" title="intramural haematoma">intramural haematoma</a>, <a href="https://publications.waset.org/abstracts/search?q=acute%20aortic%20syndrome" title=" acute aortic syndrome"> acute aortic syndrome</a>, <a href="https://publications.waset.org/abstracts/search?q=finite%20element%20analysis" title=" finite element analysis"> finite element analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=" title=""></a> </p> <a href="https://publications.waset.org/abstracts/27846/finite-element-modeling-of-aortic-intramural-haematoma-shows-size-matters" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/27846.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">431</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3304</span> The Prodomain-Bound Form of Bone Morphogenetic Protein 10 is Biologically Active on Endothelial Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Austin%20Jiang">Austin Jiang</a>, <a href="https://publications.waset.org/abstracts/search?q=Richard%20M.%20Salmon"> Richard M. Salmon</a>, <a href="https://publications.waset.org/abstracts/search?q=Nicholas%20W.%20Morrell"> Nicholas W. Morrell</a>, <a href="https://publications.waset.org/abstracts/search?q=Wei%20Li"> Wei Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> BMP10 is highly expressed in the developing heart and plays essential roles in cardiogenesis. BMP10 deletion in mice results in embryonic lethality due to impaired cardiac development. In adults, BMP10 expression is restricted to the right atrium, though ventricular hypertrophy is accompanied by increased BMP10 expression in a rat hypertension model. However, reports of BMP10 activity in the circulation are inconclusive. In particular it is not known whether in vivo secreted BMP10 is active or whether additional factors are required to achieve its bioactivity. It has been shown that high-affinity binding of the BMP10 prodomain to the mature ligand inhibits BMP10 signaling activity in C2C12 cells, and it was proposed that prodomain-bound BMP10 (pBMP10) complex is latent. In this study, we demonstrated that the BMP10 prodomain did not inhibit BMP10 signaling activity in multiple endothelial cells, and that recombinant human pBMP10 complex, expressed in mammalian cells and purified under native conditions, was fully active. In addition, both BMP10 in human plasma and BMP10 secreted from the mouse right atrium were fully active. Finally, we confirmed that active BMP10 secreted from mouse right atrium was in the prodomain-bound form. Our data suggest that circulating BMP10 in adults is fully active and that the reported vascular quiescence function of BMP10 in vivo is due to the direct activity of pBMP10 and does not require an additional activation step. Moreover, being an active ligand, recombinant pBMP10 may have therapeutic potential as an endothelial-selective BMP ligand, in conditions characterized by loss of BMP9/10 signaling. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bone%20morphogenetic%20protein%2010%20%28BMP10%29" title="bone morphogenetic protein 10 (BMP10)">bone morphogenetic protein 10 (BMP10)</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20cell" title=" endothelial cell"> endothelial cell</a>, <a href="https://publications.waset.org/abstracts/search?q=signal%20transduction" title=" signal transduction"> signal transduction</a>, <a href="https://publications.waset.org/abstracts/search?q=transforming%20growth%20factor%20beta%20%28TGF-B%29" title=" transforming growth factor beta (TGF-B)"> transforming growth factor beta (TGF-B)</a> </p> <a href="https://publications.waset.org/abstracts/46841/the-prodomain-bound-form-of-bone-morphogenetic-protein-10-is-biologically-active-on-endothelial-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/46841.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">273</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3303</span> The Differences of Vascular Endothelial Growth Factor Levels in Serum to Determine Follicular Adenoma and Follicular Carcinoma of Thyroid</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Tery%20Nehemia%20Nugraha%20Joseph">Tery Nehemia Nugraha Joseph</a>, <a href="https://publications.waset.org/abstracts/search?q=J.%20D.%20P.%20Wisnubroto"> J. D. P. Wisnubroto</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Thyroid cancer is a healthcare problem with high morbidity and mortality. Follicular adenoma and follicular carcinoma are thyroid tumors from the thyroid follicular cells differentiation with a microfollicular pattern that consists of follicular cuboidal cells. vascular endothelial growth factor (VEGF) is a potent and powerful mitogen for endothelial cells and increases vascular permeability. Therefore, due to an increase in thyroid-stimulating hormone (TSH), VEGF production is activated in the thyroid that leads to the end of mitogenic TSH stimulation and initiation of angiogenesis. The differences in VEGF levels in the follicular carcinoma of thyroid tissue with follicular adenoma thyroid can be used as a basis in differentiating the two types of neoplasms. This study aims to analyze VEGF in the serum so that it can be used to differentiate the types of thyroid carcinoma before surgery. This study uses a cross-sectional research design. Samples were carried out by taking serum samples, and the VEGF levels were calculated. Data were analyzed using the Mann-Whitney test. The results found a significant difference between VEGF levels in the follicular carcinoma thyroid group and VEGF levels in the follicular adenoma thyroid group with a value of p = 0.007 (p < 0.05). The results obtained are 560,427 ± 160,506 ng/mL in the type of follicular carcinoma thyroid and 320.943 ± 134.573 ng/mL in the type of follicular adenoma thyroid. VEGF levels between follicular adenoma and follicular carcinoma are different. VEGF levels are higher in follicular carcinoma thyroid than follicular adenoma thyroid. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=follicular%20adenoma%20thyroid" title="follicular adenoma thyroid">follicular adenoma thyroid</a>, <a href="https://publications.waset.org/abstracts/search?q=follicular%20carcinoma%20thyroid" title=" follicular carcinoma thyroid"> follicular carcinoma thyroid</a>, <a href="https://publications.waset.org/abstracts/search?q=thyroid" title=" thyroid"> thyroid</a>, <a href="https://publications.waset.org/abstracts/search?q=VEGF" title=" VEGF"> VEGF</a> </p> <a href="https://publications.waset.org/abstracts/136980/the-differences-of-vascular-endothelial-growth-factor-levels-in-serum-to-determine-follicular-adenoma-and-follicular-carcinoma-of-thyroid" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/136980.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">143</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3302</span> Determining the Threshold for Protective Effects of Aerobic Exercise on Aortic Structure in a Mouse Model of Marfan Syndrome Associated Aortic Aneurysm</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Christine%20P.%20Gibson">Christine P. Gibson</a>, <a href="https://publications.waset.org/abstracts/search?q=Ramona%20Alex"> Ramona Alex</a>, <a href="https://publications.waset.org/abstracts/search?q=Michael%20Farney"> Michael Farney</a>, <a href="https://publications.waset.org/abstracts/search?q=Johana%20Vallejo-Elias"> Johana Vallejo-Elias</a>, <a href="https://publications.waset.org/abstracts/search?q=Mitra%20Esfandiarei"> Mitra Esfandiarei </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aortic aneurysm is the leading cause of death in Marfan syndrome (MFS), a connective tissue disorder caused by mutations in fibrillin-1 gene (FBN1). MFS aneurysm is characterized by weakening of the aortic wall due to elastin fibers fragmentation and disorganization. The above-average height and distinct physical features make young adults with MFS desirable candidates for competitive sports; but little is known about the exercise limit at which they will be at risk for aortic rupture. On the other hand, aerobic cardiovascular exercise has been shown to have protective effects on the heart and aorta. We have previously reported that mild aerobic exercise can delay the formation of aortic aneurysm in a mouse model of MFS. In this study, we aimed to investigate the effects of various levels of exercise intensity on the progression of aortic aneurysm in the mouse model. Starting at 4 weeks of age, we subjected control and MFS mice to different levels of exercise intensity (8m/min, 10m/min, 15m/min, and 20m/min, corresponding to 55%, 65%, 75%, and 85% of VO2 max, respectively) on a treadmill for 30 minutes per day, five days a week for the duration of the study. At 24 weeks of age, aortic tissue were isolated and subjected to structural and functional studies using histology and wire myography in order to evaluate the effects of different exercise routines on elastin fragmentation and organization and aortic wall elasticity/stiffness. Our data shows that exercise training at the intensity levels between 55%-75% significantly reduces elastin fragmentation and disorganization, with less recovery observed in 85% MFS group. The reversibility of elasticity was also significantly restored in MFS mice subjected to 55%-75% intensity; however, the recovery was less pronounced in MFS mice subjected to 85% intensity. Furthermore, our data shows that smooth muscle cells (SMCs) contractilion in response to vasoconstrictor agent phenylephrine (100nM) is significantly reduced in MFS aorta (54.84 ± 1.63 mN/mm2) as compared to control (95.85 ± 3.04 mN/mm2). At 55% of intensity, exercise did not rescue SMCs contraction (63.45 ± 1.70 mN/mm2), while at higher intensity levels, SMCs contraction in response to phenylephrine was restored to levels similar to control aorta [65% (81.88 ± 4.57 mN/mm2), 75% (86.22 ± 3.84 mN/mm2), and 85% (83.91 ± 5.42 mN/mm2)]. This study provides the first time evidence that high intensity exercise (e.g. 85%) may not provide the most beneficial effects on aortic function (vasoconstriction) and structure (elastin fragmentation, aortic wall elasticity) during the progression of aortic aneurysm in MFS mice. On the other hand, based on our observations, medium intensity exercise (e.g. 65%) seems to provide the utmost protective effects on aortic structure and function in MFS mice. These findings provide new insights into the potential capacity, in which MFS patients could participate in various aerobic exercise routines, especially in young adults affected by cardiovascular complications particularly aortic aneurysm. This work was funded by Midwestern University Research Fund. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aerobic%20exercise" title="aerobic exercise">aerobic exercise</a>, <a href="https://publications.waset.org/abstracts/search?q=aortic%20aneurysm" title=" aortic aneurysm"> aortic aneurysm</a>, <a href="https://publications.waset.org/abstracts/search?q=aortic%20wall%20elasticity" title=" aortic wall elasticity"> aortic wall elasticity</a>, <a href="https://publications.waset.org/abstracts/search?q=elastin%20fragmentation" title=" elastin fragmentation"> elastin fragmentation</a>, <a href="https://publications.waset.org/abstracts/search?q=Marfan%20syndrome" title=" Marfan syndrome"> Marfan syndrome</a> </p> <a href="https://publications.waset.org/abstracts/47433/determining-the-threshold-for-protective-effects-of-aerobic-exercise-on-aortic-structure-in-a-mouse-model-of-marfan-syndrome-associated-aortic-aneurysm" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/47433.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">381</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3301</span> Angiomotin Regulates Integrin Beta 1-Mediated Endothelial Cell Migration and Angiogenesis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yuanyuan%20Zhang">Yuanyuan Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yujuan%20Zheng"> Yujuan Zheng</a>, <a href="https://publications.waset.org/abstracts/search?q=Giuseppina%20Barutello"> Giuseppina Barutello</a>, <a href="https://publications.waset.org/abstracts/search?q=Sumako%20Kameishi"> Sumako Kameishi</a>, <a href="https://publications.waset.org/abstracts/search?q=Kungchun%20Chiu"> Kungchun Chiu</a>, <a href="https://publications.waset.org/abstracts/search?q=Katharina%20Hennig"> Katharina Hennig</a>, <a href="https://publications.waset.org/abstracts/search?q=Martial%20Balland"> Martial Balland</a>, <a href="https://publications.waset.org/abstracts/search?q=Federica%20Cavallo"> Federica Cavallo</a>, <a href="https://publications.waset.org/abstracts/search?q=Lars%20Holmgren"> Lars Holmgren</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Angiogenesis describes that new blood vessels migrate from pre-existing ones to form 3D lumenized structure and remodeling. During directional migration toward the gradient of pro-angiogenic factors, the endothelial cells, especially the tip cells need filopodia to sense the environment and exert the pulling force. Of particular interest are the integrin proteins, which play an essential role in focal adhesion in the connection between migrating cells and extracellular matrix (ECM). Understanding how these biomechanical complexes orchestrate intrinsic and extrinsic forces is important for our understanding of the underlying mechanisms driving angiogenesis. We have previously identified Angiomotin (Amot), a member of Amot scaffold protein family, as a promoter for endothelial cell migration in vitro and zebrafish models. Hence, we established inducible endothelial-specific Amot knock-out mice to study normal retinal angiogenesis as well as tumor angiogenesis. We found that the migration ratio of the blood vessel network to the edge was significantly decreased in Amotec- retinas at postnatal day 6 (P6). While almost all the Amot defect tip cells lost migration advantages at P7. In consistence with the dramatic morphology defect of tip cells, there was a non-autonomous defect in astrocytes, as well as the disorganized fibronectin expression pattern correspondingly in migration front. Furthermore, the growth of transplanted LLC tumor was inhibited in Amot knockout mice due to fewer vasculature involved. By using MMTV-PyMT transgenic mouse model, there was a significantly longer period before tumors arised when Amot was specifically knocked out in blood vessels. In vitro evidence showed that Amot binded to beta-actin, Integrin beta 1 (ITGB1), Fibronectin, FAK, Vinculin, major focal adhesion molecules, and ITGB1 and stress fibers were distinctly induced by Amot transfection. Via traction force microscopy, the total energy (force indicater) was found significantly decreased in Amot knockdown cells. Taken together, we propose that Amot is a novel partner of the ITGB1/Fibronectin protein complex at focal adhesion and required for exerting force transition between endothelial cell and extracellular matrix. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=angiogenesis" title="angiogenesis">angiogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=angiomotin" title=" angiomotin"> angiomotin</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20cell%20migration" title=" endothelial cell migration"> endothelial cell migration</a>, <a href="https://publications.waset.org/abstracts/search?q=focal%20adhesion" title=" focal adhesion"> focal adhesion</a>, <a href="https://publications.waset.org/abstracts/search?q=integrin%20beta%201" title=" integrin beta 1"> integrin beta 1</a> </p> <a href="https://publications.waset.org/abstracts/72725/angiomotin-regulates-integrin-beta-1-mediated-endothelial-cell-migration-and-angiogenesis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/72725.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">237</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3300</span> Type A Quadricuspid Aortic Valve; Rarer than a Four-Leaf Clover, an Example of Availability Heuristic</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Frazer%20Kirk">Frazer Kirk</a>, <a href="https://publications.waset.org/abstracts/search?q=Rohen%20Skiba"> Rohen Skiba</a>, <a href="https://publications.waset.org/abstracts/search?q=Pankaj%20Saxena"> Pankaj Saxena</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The natural history of the QAV is poorly understood due to the exceeding rarity of the condition. Incidence rates vary between 0.00028-1%. Classically patients present with Aortic Regurgitation (AR) between 40-60 years of age experiencing palpitations, chest pain, or heart failure. (1, 2) Echocardiography is the mainstay of diagnosis for this condition; however, given the rarity of this condition, it can easily be overlooked, as demonstrated here. The case report that follows serves as a reminder of the condition to reduce the innate cognitive bias to overlook the diagnosis due to the availability heuristic. Intraoperative photography, echocardiographic and magnetic resonance imaging from this case for reference to demonstrate that while the diagnosis of Aortic regurgitation was recognized early, the valve morphology was underappreciated. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=quadricuspid%20aortic%20valve" title="quadricuspid aortic valve">quadricuspid aortic valve</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiac%20surgery" title=" cardiac surgery"> cardiac surgery</a>, <a href="https://publications.waset.org/abstracts/search?q=echocardiography" title=" echocardiography"> echocardiography</a>, <a href="https://publications.waset.org/abstracts/search?q=congenital" title=" congenital"> congenital</a> </p> <a href="https://publications.waset.org/abstracts/142246/type-a-quadricuspid-aortic-valve-rarer-than-a-four-leaf-clover-an-example-of-availability-heuristic" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/142246.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">162</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3299</span> An Accurate Computer-Aided Diagnosis: CAD System for Diagnosis of Aortic Enlargement by Using Convolutional Neural Networks</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mahdi%20Bazarganigilani">Mahdi Bazarganigilani</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aortic enlargement, also known as an aortic aneurysm, can occur when the walls of the aorta become weak. This disease can become deadly if overlooked and undiagnosed. In this paper, a computer-aided diagnosis (CAD) system was introduced to accurately diagnose aortic enlargement from chest x-ray images. An enhanced convolutional neural network (CNN) was employed and then trained by transfer learning by using three different main areas from the original images. The areas included the left lung, heart, and right lung. The accuracy of the system was then evaluated on 1001 samples by using 4-fold cross-validation. A promising accuracy of 90% was achieved in terms of the F-measure indicator. The results showed using different areas from the original image in the training phase of CNN could increase the accuracy of predictions. This encouraged the author to evaluate this method on a larger dataset and even on different CAD systems for further enhancement of this methodology. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=computer-aided%20diagnosis%20systems" title="computer-aided diagnosis systems">computer-aided diagnosis systems</a>, <a href="https://publications.waset.org/abstracts/search?q=aortic%20enlargement" title=" aortic enlargement"> aortic enlargement</a>, <a href="https://publications.waset.org/abstracts/search?q=chest%20X-ray" title=" chest X-ray"> chest X-ray</a>, <a href="https://publications.waset.org/abstracts/search?q=image%20processing" title=" image processing"> image processing</a>, <a href="https://publications.waset.org/abstracts/search?q=convolutional%20neural%20networks" title=" convolutional neural networks"> convolutional neural networks</a> </p> <a href="https://publications.waset.org/abstracts/145129/an-accurate-computer-aided-diagnosis-cad-system-for-diagnosis-of-aortic-enlargement-by-using-convolutional-neural-networks" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/145129.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">162</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3298</span> A Mathematical Analysis of a Model in Capillary Formation: The Roles of Endothelial, Pericyte and Macrophages in the Initiation of Angiogenesis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Serdal%20Pamuk">Serdal Pamuk</a>, <a href="https://publications.waset.org/abstracts/search?q=Irem%20Cay"> Irem Cay</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Our model is based on the theory of reinforced random walks coupled with Michealis-Menten mechanisms which view endothelial cell receptors as the catalysts for transforming both tumor and macrophage derived tumor angiogenesis factor (TAF) into proteolytic enzyme which in turn degrade the basal lamina. The model consists of two main parts. First part has seven differential equations (DE’s) in one space dimension over the capillary, whereas the second part has the same number of DE’s in two space dimensions in the extra cellular matrix (ECM). We connect these two parts via some boundary conditions to move the cells into the ECM in order to initiate capillary formation. But, when does this movement begin? To address this question we estimate the thresholds that activate the transport equations in the capillary. We do this by using steady-state analysis of TAF equation under some assumptions. Once these equations are activated endothelial, pericyte and macrophage cells begin to move into the ECM for the initiation of angiogenesis. We do believe that our results play an important role for the mechanisms of cell migration which are crucial for tumor angiogenesis. Furthermore, we estimate the long time tendency of these three cells, and find that they tend to the transition probability functions as time evolves. We provide our numerical solutions which are in good agreement with our theoretical results. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=angiogenesis" title="angiogenesis">angiogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=capillary%20formation" title=" capillary formation"> capillary formation</a>, <a href="https://publications.waset.org/abstracts/search?q=mathematical%20analysis" title=" mathematical analysis"> mathematical analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=steady-state" title=" steady-state"> steady-state</a>, <a href="https://publications.waset.org/abstracts/search?q=transition%20probability%20function" title=" transition probability function"> transition probability function</a> </p> <a href="https://publications.waset.org/abstracts/74388/a-mathematical-analysis-of-a-model-in-capillary-formation-the-roles-of-endothelial-pericyte-and-macrophages-in-the-initiation-of-angiogenesis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/74388.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">156</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3297</span> The Combination Of Aortic Dissection Detection Risk Score (ADD-RS) With D-dimer As A Diagnostic Tool To Exclude The Diagnosis Of Acute Aortic Syndrome (AAS)</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mohamed%20Hamada%20Abdelkader%20Fayed">Mohamed Hamada Abdelkader Fayed</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: To evaluate the diagnostic accuracy of (ADD-RS) with D-dimer as a screening test to exclude AAS. Methods: We conducted research for the studies examining the diagnostic accuracy of (ADD- RS)+ D-dimer to exclude the diagnosis of AAS, We searched MEDLINE, Embase, and Cochrane of Trials up to 31 December 2020. Results: We identified 3 studies using (ADD-RS) with D-dimer as a diagnostic tool for AAS, involving 3261 patients were AAS was diagnosed in 559(17.14%) patients. Overall results showed that the pooled sensitivities were 97.6 (95% CI 0.95.6, 99.6) at (ADD-RS)≤1(low risk group) with D-dimer and 97.4(95% CI 0.95.4,, 99.4) at (ADD-RS)>1(High risk group) with D-dimer., the failure rate was 0.48% at low risk group and 4.3% at high risk group respectively. Conclusions: (ADD-RS) with D-dimer was a useful screening test with high sensitivity to exclude Acute Aortic Syndrome. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aortic%20dissection%20detection%20risk%20score" title="aortic dissection detection risk score">aortic dissection detection risk score</a>, <a href="https://publications.waset.org/abstracts/search?q=D-dimer" title=" D-dimer"> D-dimer</a>, <a href="https://publications.waset.org/abstracts/search?q=acute%20aortic%20syndrome" title=" acute aortic syndrome"> acute aortic syndrome</a>, <a href="https://publications.waset.org/abstracts/search?q=diagnostic%20accuracy" title=" diagnostic accuracy"> diagnostic accuracy</a> </p> <a href="https://publications.waset.org/abstracts/142780/the-combination-of-aortic-dissection-detection-risk-score-add-rs-with-d-dimer-as-a-diagnostic-tool-to-exclude-the-diagnosis-of-acute-aortic-syndrome-aas" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/142780.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">215</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3296</span> Warning about the Risk of Blood Flow Stagnation after Transcatheter Aortic Valve Implantation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aymen%20Laadhari">Aymen Laadhari</a>, <a href="https://publications.waset.org/abstracts/search?q=G%C3%A1bor%20Sz%C3%A9kely"> Gábor Székely</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In this work, the hemodynamics in the sinuses of Valsalva after Transcatheter Aortic Valve Implantation is numerically examined. We focus on the physical results in the two-dimensional case. We use a finite element methodology based on a Lagrange multiplier technique that enables to couple the dynamics of blood flow and the leaflets’ movement. A massively parallel implementation of a monolithic and fully implicit solver allows more accuracy and significant computational savings. The elastic properties of the aortic valve are disregarded, and the numerical computations are performed under physiologically correct pressure loads. Computational results depict that blood flow may be subject to stagnation in the lower domain of the sinuses of Valsalva after Transcatheter Aortic Valve Implantation. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hemodynamics" title="hemodynamics">hemodynamics</a>, <a href="https://publications.waset.org/abstracts/search?q=simulations" title=" simulations"> simulations</a>, <a href="https://publications.waset.org/abstracts/search?q=stagnation" title=" stagnation"> stagnation</a>, <a href="https://publications.waset.org/abstracts/search?q=valve" title=" valve"> valve</a> </p> <a href="https://publications.waset.org/abstracts/63534/warning-about-the-risk-of-blood-flow-stagnation-after-transcatheter-aortic-valve-implantation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/63534.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">291</span> </span> </div> </div> <ul class="pagination"> <li class="page-item disabled"><span class="page-link">&lsaquo;</span></li> <li class="page-item active"><span class="page-link">1</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=aortic%20endothelial%20cells&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=aortic%20endothelial%20cells&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=aortic%20endothelial%20cells&page=4">4</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=aortic%20endothelial%20cells&page=5">5</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=aortic%20endothelial%20cells&page=6">6</a></li> 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