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1

FOGLI, Eleonora. "Adenosine receptors modulation of inflammatory cells: the foam cells history." Doctoral thesis, Università degli studi di Ferrara, 2010. http://hdl.handle.net/11392/2389328.

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Adenosine is an endogenous purine nucleoside that is constitutively present at low levels outside the cells but might dramatically increase its concentrations following metabolic stress conditions like those induced by hypoxia or ischaemia. After its release adenosine induces its biological effects through the interaction with four cell surface receptors classified by molecular, biochemical and pharmacological data into four subtypes: A1, A2A, A2B and A3. Adenosine through the interaction with A2 and A3 receptors plays a crucial role in inflammation and in the regulation of immune cells. A2A receptors, proposed as “natural” brakes of inflammation, appear to represent a promising pharmacological target to treat a wide variety of diseases characterized by a strong immunoinflammatory component. On the other hand, it may be advantageous in some circumstances to enhance certain aspects of inflammation in order to eliminate the causative agent, as in the case of cancer. In fact, it has to be remarked that tumour defence mechanisms are akin to inflammatory processes. Solid tumours, due to their abnormal vasculature, are often hypoxic and show increased levels of adenosine that may be an important mediator of tumour-associated immunosuppression. It is likely that killer T cells that may be recruited against cancer cells fail to act in an effective manner due to the high level of adenosine in the tumour microenvironment. Because several of these immunosuppressive effects have been attributed to the stimulation of A3 and A2A receptors, expressed on the surface of T cells, adenosine antagonists of these subtypes may be potentially useful in the immunotherapy of cancer. The interest in the elucidation of A3 adenosine receptor involvement in inflammation is evident from the large amount of experimental work carried out in peripheral blood cells of the immune system and in a variety of inflammatory conditions. A3 adenosine receptor subtype play a complex role as both pro and anti-inflammatory effects depending not only on the cell types investigated but also on the model of inflammation used and the species considered. In this study we discuss developments in our understanding of the role of adenosine A3 receptor activation in the function of the different types of cells of the immune system including neutrophils, eosinophils, lymphocytes, monocytes, macrophages and dendritic cells. Then we focused our attention on the role of adenosine in atherosclerosis, a chronic inflammatory disease of the arteries, characterized by an hypoxic region with an high concentration of adenosine and a large number of foam cells. Foam cells formation by oxidized low-density lipoprotein (oxLDL) accumulation in macrophages is crucial for development of atherosclerosis. Hypoxia has been demonstrated in atherosclerosis and hypoxia-inducible factor-1 (HIF-1) has been shown to promote intraplaque angiogenesis and foam cells development. As hypoxia induces HIF-1α stabilization and adenosine accumulation, we investigated whether this nucleoside regulates HIF-1α in FC. Adenosine, under hypoxia, stimulates HIF-1α accumulation by activating all adenosine receptors, while it has only a slight effect in normoxia. HIF-1α modulation involved extracellular signal-regulated kinase 1/2 (ERK 1/2), p38 mitogen-activated protein kinase (p38 MAPK) and protein kinase B (Akt) phosphorylation in the case of A1, A2A, A2B and ERK 1/2 phosphorylation in the case of A3 receptors. Ado, through the activation of A3 and A2B receptors, stimulates vascular endothelial growth factor (VEGF) secretion in a HIF-1α dependent way. Furthermore ado, through the A2B subtype, induces an increase of Interleukin-8 (IL-8) secretion in a ERK 1/2, p38 and Akt kinases-dependent but not HIF-1α-mediated way. Finally, adenosine stimulates FC formation and this effect is strongly reduced by A3 and A2B blockers and by HIF-1α silencing. In conclusion this study provides the first evidence that A3, A2B or mixed A3/A2B antagonists may be useful to block important steps in the atherosclerotic plaque development adoinduced.
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2

Wang, Yenfeng. "The role of mast cells in foam cell formation, growth inhibition, and apoptosis of smooth muscle cells." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/wang/.

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3

Davies, Sian Patricia Mary. "7,8-Dihydroneopterin and its effect on the formation of foam cells." Thesis, University of Canterbury. School of Biological Sciences, 2015. http://hdl.handle.net/10092/10908.

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Atherosclerosis (Heart Disease) is an inflammatory disease caused by the formation of plaque within the arterial wall. In response to inflammation, monocytes enter the artery wall, differentiate into macrophages and take up altered low-density-lipoprotein (such as oxidised-LDL). This oxLDL is taken up into the phagocytotic macrophages via the action of the scavenger receptors. If more oxLDL is engulfed than the cell can process, they further differentiate into lipid-loaded foam cells. These are the main cell type found in atherosclerotic plaques. The scavenger receptor CD36 is responsible for 70% of oxLDL uptake by macrophages. Previous studies show that CD36 expression can be down regulated by the antioxidant, 7,8-dihydroneopterin. This research focuses on the effect of CD36 down regulation by 7,8-dihydroneopterin on foam cell formation. Human macrophages prepared from monocytes purified from human blood were incubated with copper oxidised LDL for up to 48 hours. Macrophage accumulation of the sterols was measured using a high performance chromatograph (HPLC) method developed as part of this project. The HPLC analysis measured: cholesterol, cholesteryl-oleate and -palmitate and 7-ketocholesterol accumulation within human macrophages. A flow cytometry procedure was developed where the strongly adherent macrophages could be lifted from the tissue culture plates before immuno staining for CD36. Effect of incubating macrophages with 7,8-dihydroneopterin on the formation of foam cells was studied by measuring the lipid content by HPLC and flow cytometry measurement of CD36. HPLC analysis showed non-cytotoxic levels of oxLDL produced a large accumulation of cholesterol and cholesteryl esters in the macrophages. Cholesterol, 7-ketocholesterol and cholesteryl-oleate and -palmitate concentrations in the cells rose significantly over the first 24 hours and stayed at a steady level for the following 24 hours. CD36 levels was further analysed on human macrophages. This study shows that foam cell formation can be measured using human macrophages. 7,8-Dihydroneopterin treatment resulted in a reduction of cholesterol and oxysterol uptake back to basal levels. It also reduced CD36 cell surface expression by a third. These results suggest that even a small reduction in CD36 cell surface expression may have a large effect on foam cell formation. This is another mechanism by which 7,8-dihydroneopterin protects against atherosclerosis developing.
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4

Mozgowiec, Mark D. (Mark David). "The use of small cells to reduce radiation heat transfer in foam insulation." Thesis, Massachusetts Institute of Technology, 1990. http://hdl.handle.net/1721.1/26816.

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5

Brown, Bronnwyn Elizabeth. "The role of glycation and glycoxidation of low-density lipoproteins in foam cell formation." University of Sydney. Central Clinical School, 2005. http://hdl.handle.net/2123/682.

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People with diabetes suffer from an increased incidence of atherosclerosis, possibly due to the hyperglycaemia associated with this disease. Glucose may covalently modify proteins via glycation and glycoxidation reactions. Reactive aldehydes (e.g. methylglyoxal and glycolaldehyde) generated from these glycation and glycoxidation reactions, lipid peroxidation and other metabolic pathways may also modify proteins in glycation and glycoxidation reactions. These reactions can result in the formation of advanced glycation end-products, which are increased in diabetes and associated complications such as atherosclerosis. Low-density lipoproteins (LDLs) are the main source of lipid in atherosclerotic plaques, and the lipid-laden foam cells contained within. Modification of the single protein in LDL, apolipoprotein B-100 (apo B) by glucose and aldehydes may result in recognition of these altered LDL particles by macrophage scavenger receptors and cellular accumulation of cholesteryl esters; such accumulation is characteristic of atherosclerotic foam cells. The extent and nature of the modifications of LDLs that give rise to this behaviour have been poorly characterised, especially in regards to modification/oxidation of protein versus lipid components induced by glucose and low-molecular-mass aldehydes. Therefore the aims of this project were to: 1) characterise LDL modification by glucose, methylglyoxal and glycolaldehyde; 2) examine the effect of these modified LDLs on arterial cells by monitoring cellular viability, proliferation and cholesterol and cholesteryl ester levels; and 3) examine macrophage handling of apo B from these modified LDLs. Glycolaldehyde induced more rapid and more extensive changes to LDL than methylglyoxal, which was significantly more modified than LDL exposed to glucose, in the presence or absence of Cu2+. LDL was modified by glycolaldehyde and methylglyoxal in a time- and concentration-dependent manner. These aldehyde-modified LDLs were significantly more negatively charged relative (determined by changes in relative electrophoretic mobility), more aggregated (by SDS-PAGE) and lost more Arg, Lys and Trp residues (assessed by fluorescence-based assays) than glucose-modified and control LDLs. Glucose-modified LDL had more modest increases in net negative charge, aggregation and only significantly lost Arg residues. Under the conditions examined none of the modified LDLs contained significant levels of the protein oxidation products DOPA and o-tyrosine, the lipid oxidation products 7-ketocholesterol and cholesteryl ester hydro(pero)oxides, nor marked depletion of the major antioxidant α-tocopherol or significant radical formation (EPR spectroscopy). Therefore these LDLs were glycated, but not (glyc)oxidised, and so allowed the cellular uptake of glycated LDL, rather than glycoxidised LDL, to be examined. These glycated LDLs had no effect on the cellular viability (assessed by LDH release), cell protein (BCA assay), and cholesterol and cholesteryl ester levels (quantified by reverse-phase HPLC) of endothelial and smooth muscle cells. The glycated LDLs also had no effects on human and mouse macrophage viability, protein and free cholesterol levels. However, exposure of macrophages to some of the glycated LDLs resulted in significant accumulation of cholesteryl esters and apo B. The greatest cellular accumulation of cholesteryl esters was in cells exposed to glycolaldehyde-modified LDL, which occurred in a time- and concentration-dependent manner. Less cholesteryl ester accumulation was observed in cells exposed to methylglyoxal-modified LDL, but some conditions resulted in significantly more cellular cholesteryl esters as compared to control LDLs, unlike glucose-modified LDL. Macrophages endocytosed significantly more apo B from glycolaldehyde-modified LDL labelled with 125I on the apo B, than methylglyoxal-modified 125I-LDL. Apo B from methylglyoxal-modified 125I-LDL was also endocytosed and degraded in greater amounts than control 125I-LDLs, unlike glucose-modified 125I-LDLs. The glycation of LDL by some low-molecular-mass aldehydes have been shown to result in model foam cell formation as characterised by cholesteryl ester and apo B accumulation. This accumulation correlated with increases in net negative charge, aggregation and loss of Lys and Trp residues of the apo B in glycated LDL particles. However, the differences in cellular uptake of glycolaldehyde- versus methylglyoxal-modified LDL were not completely resolved and it is postulated that this may arise from the extent or type of products formed on key amino acid residues, resulting in differential uptake by macrophage scavenger receptors, rather than loss of particular amino acids per se. Therefore these studies provide a potential mechanism to explain the increased atherosclerosis in people with diabetes, and a suitable model to examine the potential inhibition of the effects of glycated LDLs. This could provide potential therapeutic interventions to reduce diabetes-induced atherosclerosis.
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6

Brown, Bronnwyn Elizabeth. "The role of glycation and glycoxidation of low-density lipoproteins in foam cell formation." Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/682.

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People with diabetes suffer from an increased incidence of atherosclerosis, possibly due to the hyperglycaemia associated with this disease. Glucose may covalently modify proteins via glycation and glycoxidation reactions. Reactive aldehydes (e.g. methylglyoxal and glycolaldehyde) generated from these glycation and glycoxidation reactions, lipid peroxidation and other metabolic pathways may also modify proteins in glycation and glycoxidation reactions. These reactions can result in the formation of advanced glycation end-products, which are increased in diabetes and associated complications such as atherosclerosis. Low-density lipoproteins (LDLs) are the main source of lipid in atherosclerotic plaques, and the lipid-laden foam cells contained within. Modification of the single protein in LDL, apolipoprotein B-100 (apo B) by glucose and aldehydes may result in recognition of these altered LDL particles by macrophage scavenger receptors and cellular accumulation of cholesteryl esters; such accumulation is characteristic of atherosclerotic foam cells. The extent and nature of the modifications of LDLs that give rise to this behaviour have been poorly characterised, especially in regards to modification/oxidation of protein versus lipid components induced by glucose and low-molecular-mass aldehydes. Therefore the aims of this project were to: 1) characterise LDL modification by glucose, methylglyoxal and glycolaldehyde; 2) examine the effect of these modified LDLs on arterial cells by monitoring cellular viability, proliferation and cholesterol and cholesteryl ester levels; and 3) examine macrophage handling of apo B from these modified LDLs. Glycolaldehyde induced more rapid and more extensive changes to LDL than methylglyoxal, which was significantly more modified than LDL exposed to glucose, in the presence or absence of Cu2+. LDL was modified by glycolaldehyde and methylglyoxal in a time- and concentration-dependent manner. These aldehyde-modified LDLs were significantly more negatively charged relative (determined by changes in relative electrophoretic mobility), more aggregated (by SDS-PAGE) and lost more Arg, Lys and Trp residues (assessed by fluorescence-based assays) than glucose-modified and control LDLs. Glucose-modified LDL had more modest increases in net negative charge, aggregation and only significantly lost Arg residues. Under the conditions examined none of the modified LDLs contained significant levels of the protein oxidation products DOPA and o-tyrosine, the lipid oxidation products 7-ketocholesterol and cholesteryl ester hydro(pero)oxides, nor marked depletion of the major antioxidant α-tocopherol or significant radical formation (EPR spectroscopy). Therefore these LDLs were glycated, but not (glyc)oxidised, and so allowed the cellular uptake of glycated LDL, rather than glycoxidised LDL, to be examined. These glycated LDLs had no effect on the cellular viability (assessed by LDH release), cell protein (BCA assay), and cholesterol and cholesteryl ester levels (quantified by reverse-phase HPLC) of endothelial and smooth muscle cells. The glycated LDLs also had no effects on human and mouse macrophage viability, protein and free cholesterol levels. However, exposure of macrophages to some of the glycated LDLs resulted in significant accumulation of cholesteryl esters and apo B. The greatest cellular accumulation of cholesteryl esters was in cells exposed to glycolaldehyde-modified LDL, which occurred in a time- and concentration-dependent manner. Less cholesteryl ester accumulation was observed in cells exposed to methylglyoxal-modified LDL, but some conditions resulted in significantly more cellular cholesteryl esters as compared to control LDLs, unlike glucose-modified LDL. Macrophages endocytosed significantly more apo B from glycolaldehyde-modified LDL labelled with 125I on the apo B, than methylglyoxal-modified 125I-LDL. Apo B from methylglyoxal-modified 125I-LDL was also endocytosed and degraded in greater amounts than control 125I-LDLs, unlike glucose-modified 125I-LDLs. The glycation of LDL by some low-molecular-mass aldehydes have been shown to result in model foam cell formation as characterised by cholesteryl ester and apo B accumulation. This accumulation correlated with increases in net negative charge, aggregation and loss of Lys and Trp residues of the apo B in glycated LDL particles. However, the differences in cellular uptake of glycolaldehyde- versus methylglyoxal-modified LDL were not completely resolved and it is postulated that this may arise from the extent or type of products formed on key amino acid residues, resulting in differential uptake by macrophage scavenger receptors, rather than loss of particular amino acids per se. Therefore these studies provide a potential mechanism to explain the increased atherosclerosis in people with diabetes, and a suitable model to examine the potential inhibition of the effects of glycated LDLs. This could provide potential therapeutic interventions to reduce diabetes-induced atherosclerosis.
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7

Baldwin, Zachary D. "Characterization of Anode Conditions and Limitations in Direct Carbon Fuel Cells." Cleveland, Ohio : Case Western Reserve University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1248203858.

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Thesis (M.S.)--Case Western Reserve University, 2009
Title from PDF (viewed on 19 August 2009) Department of Mechanical and Aerospace Engineering Includes abstract Includes bibliographical references Available online via the OhioLINK ETD Center
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8

Conway, James Patrick. "Systems biology analysis of macrophage foam cells finding a novel function for Peroxiredoxin I /." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1156961185.

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Thesis (Ph. D.)--Case Western Reserve University, 2006.
[School of Medicine] Department of Physiology and Biophysics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
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9

Conway, James Patrick. "Systems Biology Analysis of Macrophage Foam Cells: Finding a Novel Function for Peroxiredoxin I." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1156961185.

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10

Ouimet, Mireille. "Regulation of Lipid Droplet Cholesterol Efflux from Macrophage Foam Cells: a Role for Oxysterols and Autophagy." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20399.

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Macrophage foam cells are the major culprits in atherosclerotic lesions, having a prominent role in both lesion initiation and progression. With atherosclerosis being the main factor underlying cardiovascular complications, there is a long-standing interest on finding ways to reverse lipid buildup in plaques. Studies have shown that promoting reverse cholesterol transport (RCT) from macrophage foam cells is anti-atherogenic because it alleviates the cholesterol burden of the plaques. The goal of this thesis was to gain insight into the mechanisms that govern cholesterol efflux from macrophage foam cells. The first part of this study looked at the ability of different oxysterols to promote cholesterol efflux in unloaded as compared to lipid-loaded macrophages, and our major finding here is that epoxycholesterol decreases efflux in lipid-loaded macrophages. It appears that epoxycholesterol does so by impairing the release cholesterol from its cellular storage site, the lipid droplet (LD), where it accumulates in the form of cholesteryl esters (CE). These results highlighted the importance of cholesterol release from LDs for efflux; indeed, this process is increasingly being recognized as the rate-limiting step for RCT in vivo. Subsequent experiments aimed at elucidating the mechanisms that govern LD CE hydrolysis in macrophage foam cells lead to the discovery of a novel pathway involved in cholesterol efflux. Macrophage CE hydrolysis is classically defined as being entirely dependent on neutral CE hydrolases. In the second part of this study, we demonstrate that in addition to the canonical CE hydrolases, which mediate neutral lipid hydrolysis, lysosomal acid lipase (LAL) also participates in the hydrolysis of cytoplasmic CE. Autophagy is specifically triggered in macrophages by atherogenic lipoproteins and delivers LD CE to LAL in lysosomes, thus generating free cholesterol for efflux. This autophagy-mediated cholesterol efflux is a process that is primarily dependant on the ABCA1 transporter and, importantly, is important for whole-body RCT. Overall, the studies presented in this thesis support that macrophage LD CE hydrolysis is rate-limiting for cholesterol efflux and shed light on the mechanisms of cholesterol mobilization for efflux in macrophage foam cells.
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11

Lindstedt, Leena. "Proteolytic modification of high density lipoproteins decreases their ability to induce cholesterol efflux from macrophage foam cells." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/lindstedt/.

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12

Merkel, Matthias. "From cells to tissues." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-156597.

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An essential prerequisite for the existence of multi-cellular life is the organization of cells into tissues. In this thesis, we theoretically study how large-scale tissue properties can emerge from the collective behavior of individual cells. To this end, we focus on the properties of epithelial tissue, which is one of the major tissue types in animals. We study how rheological properties of epithelia emerge from cellular processes, and we develop a physical description for the dynamics of an epithelial cell polarity. We apply our theoretical studies to observations in the developing wing of the fruit fly, Drosophila melanogaster. In order to study epithelial mechanics, we first develop a geometrical framework that rigorously describes the deformation of two-dimensional cellular networks. Our framework decomposes large-scale deformation into cellular contributions. For instance, we show how large-scale tissue shear decomposes into contributions by cell shape changes and into contributions by different kinds of topological transitions. We apply this framework in order to quantify the time-dependent deformation of the fruit fly wing, and to decompose it into cellular contributions. We also use this framework as a basis to study large-scale rheological properties of epithelia and their dependence on cellular fluctuations. To this end, we represent epithelial tissues by a vertex model, which describes cells as elastic polygons. We extend the vertex model by introducing fluctuations on the cellular scale, and we develop a method to perform perpetual simple shear simulations. Analyzing the steady state of such simple shear simulations, we find that the rheological behavior of vertex model tissue depends on the fluctuation amplitude. For small fluctuation amplitude, it behaves like a plastic material, and for high fluctuation amplitude, it behaves like a visco-elastic fluid. In addition to analyzing mechanical properties, we study the reorientation of an epithelial cell polarity. To this end, we develop a simple hydrodynamic description for polarity reorientation. In particular, we account for polarity reorientation by tissue shear, by another polarity field, and by local polarity alignment. Furthermore, we develop methods to quantify polarity patterns based on microscopical images of the fly wing. We find that our hydrodynamic description does not only account for polarity reorientation in wild type fly wings. Moreover, it is for the first time possible to also account for the observed polarity patterns in a number of genetically altered flies
Eine wesentliche Voraussetzung für die Existenz mehrzelligen Lebens ist, dass sich einzelne Zellen sinnvoll zu Geweben ergänzen können. In dieser Dissertation untersuchen wir, wie großskalige Eigenschaften von Geweben aus dem kollektiven Verhalten einzelner Zellen hervorgehen. Dazu konzentrieren wir uns auf Epitheliengewebe, welches eine der Grundgewebearten in Tieren darstellt. Wir stellen theoretische Untersuchungen zu rheologischen Eigenschaften und zu zellulärer Polarität von Epithelien an. Diese theoretischen Untersuchungen vergleichen wir mit experimentellen Beobachtungen am sich entwickelnden Flügel der schwarzbäuchigen Taufliege (Drosophila melanogaster). Um die Mechanik von Epithelien zu untersuchen, entwickeln wir zunächst eine geometrische Beschreibung für die Verformung von zweidimensionalen zellulären Netzwerken. Unsere Beschreibung zerlegt die mittlere Verformung des gesamten Netzwerks in zelluläre Beitrage. Zum Beispiel wird eine Scherverformung des gesamten Netzwerks auf der zellulären Ebene exakt repräsentiert: einerseits durch die Verformung einzelner Zellen und andererseits durch topologische Veränderungen des zellulären Netzwerks. Mit Hilfe dieser Beschreibung quantifizieren wir die Verformung des Fliegenflügels während des Puppenstadiums. Des Weiteren führen wir die Verformung des Flügels auf ihre zellulären Beiträge zurück. Wir nutzen diese Beschreibung auch als Ausgangspunkt, um effektive rheologische Eigenschaften von Epithelien in Abhängigkeit von zellulären Fluktuationen zu untersuchen. Dazu simulieren wir Epithelgewebe mittels eines Vertex Modells, welches einzelne Zellen als elastische Polygone abstrahiert. Wir erweitern dieses Vertex Modell um zelluläre Fluktuationen und um die Möglichkeit, Schersimulationen beliebiger Dauer durchzuführen. Die Analyse des stationären Zustands dieser Simulationen ergibt plastisches Verhalten bei kleiner Fluktuationsamplitude und visko-elastisches Verhalten bei großer Fluktuationsamplitude. Neben mechanischen Eigenschaften untersuchen wir auch die Umorientierung einer Zellpolarität in Epithelien. Dazu entwickeln wir eine einfache hydrodynamische Beschreibung für die Umorientierung eines Polaritätsfeldes. Wir berücksichtigen dabei insbesondere Effekte durch Scherung, durch ein anderes Polaritätsfeld und durch einen lokalen Gleichrichtungseffekt. Um unsere theoretische Beschreibung mit experimentellen Daten zu vergleichen, entwickeln wir Methoden um Polaritätsmuster im Fliegenflügel zu quantifizieren. Schließlich stellen wir fest, dass unsere hydrodynamische Beschreibung in der Tat beobachtete Polaritätsmuster reproduziert. Das gilt nicht nur im Wildtypen, sondern auch in genetisch veränderten Tieren
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13

Venable, Andrea Henning. "Implications of Diet in Cardiovascular Disease Risk: Postprandial Changes in Circulating Monocytes and Endotoxemia." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1248401/.

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It is well established that continual consumption of a diet high in fat leads to the development of chronic conditions such as obesity, cardio metabolic syndrome, and atherosclerosis that are associated with high incidence of cardiovascular disease. Recent studies have identified endotoxin-derived inflammation as a major diving force for the development of these conditions. Our laboratory has recently demonstrated that consumption of a single high-fat meal results in acute postprandial endotoxemia and alters monocyte cell surface adhesion molecule expression and scavenger receptor CD36 expression. These collective projects describe our efforts to understand the physiological significance of these postprandial changes and if supplementation with spore-based probiotics are able to provide any form of protection against these responses that are associated with the onset of atherogenesis.
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14

Kazuma, Soraya Megumi. "Expressão de fragmentos variáveis de cadeia simples anti-LDL eletronegativa (scFv) em Pichia pastoris e seu efeito sobre a formação de células espumosas." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-08072010-141439/.

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Os produtos de modificação de lipoproteínas de baixa densidade (LDL) como a subfração eletronegativa [LDL(-)] desempenham um importante papel na progressão da aterosclerose. O acúmulo massivo de LDL modificada captada por macrófagos resulta em células espumosas que liberam mediadores inflamatórios e contribuem para a aterogênese. O scFv (single chain fragment variable) é um fragmento de anticorpo recombinante que contém o sítio completo de ligação ao antígeno. Diante do papel da LDL(-) na aterogênese e da necessidade de novas intervenções terapêuticas que possam inibir o acúmulo de lipídeos em macrófagos, este trabalho objetivou a expressão do scFv anti-LDL(-) 2C7 em Pichia pastoris, bem como a avaliação do efeito deste fragmento de anticorpo sobre a formação de células espumosas em cultura de macrófagos RAW 264.7. O vetor inicial de expressão pPIgLE apresentava como estratégia de detecção e purificação o fusionamento com a proteína A. No entanto, a alta imunogenicidade da proteína A inviabilizaria o estudo da proteína de fusão em cultura de macrófagos, o que determinou a substituição da estratégia de purificação anterior pela cromatografia com resina de níquel através da inserção de hexahistidina na região C-terminal da proteína. A análise de sequenciamento confirmou a presença da inserção e das regiões determinantes de complementariedade. O cassete de expressão com hexahistidina foi inserido no vetor pPIgLE de P. pastoris e transformado na linhagem SMD1168 (Invitrogen®). Testes preliminares de expressão em pequena escala permitiram a análise entre sete clones diferentes, demonstrando uma banda correspondente ao peso molecular de 28 KDa em SDS-PAGE, confirmado por Western Blot. A separação do scFv 2C7 através de resina de níquel obteve uma proteína pura, conforme foi analisado em SDS-PAGE corado com prata. A afinidade do scFv 2C7 a 9 LDL(-) foi confirmada por Dot Blot. O ensaio de captação de LDL(-) demonstrou que o scFv 2C7 foi eficaz na redução de células espumosas e este efeito foi acompanhado pela diminuição na expressão gênica de CD36, TLR-4 e COX-2. Baseado nestes dados, o scFv 2C7 demonstra uma propriedade importante para uma futura intervenção terapêutica para a aterosclerose.
The modification products of low-density lipoprotein (LDL), as the electronegative subfraction [LDL(-)], play an important role in the progression of atherosclerosis. The massive accumulation of modified LDL uptake by macrophages results in foam cells that release inflammatory mediators and contribute to atherogenesis. The scFv (singlechain fragment variable) is a recombinant antibody fragment that contains the complete site antigen-binding. Considering the role of LDL(-) in atherogenesis and the need for new therapeutic interventions that may inhibit the accumulation of lipids in macrophages, this study aimed the expression of anti-LDL(-) 2C7 scFv in Pichia pastoris and the evaluation of the effect of this recombinant antibody fragment on foam cells formation in cultured RAW 264.7 macrophages. The pPIgLE expression initial vector presented as a strategy for detection and purification the fusion with protein A. However, the high immunogenicity of the protein impairs the study of the fusion protein in cultured macrophages, leading to the replacement of the previous strategy of purification by chromatography with nickel resin by inserting hexahistidine tag at the C-terminus of the protein. The sequence analysis confirmed the presence of insertion and the complementary determining regions. The expression cassete with hexahistidine was inserted into the pPIgLE vector of P. pastoris and transformed in the SMD1168 strain (Invitrogen®). Preliminary tests of expression in small-scale allowed the analysis of seven different clones, showing a band corresponding to the molecular weight of 28KDa on SDS-PAGE, confirmed by Western Blot. The separation of 2C7 scFv by the nickel resin yield a pure protein, as it was shown by SDS-PAGE stained with silver. The affinity of 2C7 scFv was confirmed by Dot Blot. The assay of LDL(-) uptake showed that the 2C7 scFv was effective in reducing foam cells and this effect was determined by the decrease in gene expression of CD36, TLR-4 and COX-2. Based on these data, the 2C7 scFv demonstrates an important property for future therapeutic intervention for atherosclerosis
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15

Joffre, Jérémie. "Exploration du rôle de TREM-1 dans l'athérosclérose." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB109.

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Les cellules myéloïdes jouent un rôle majeur dans le développement et les complications de l’athérosclérose. TREM (Triggering Receptor Expressed on Myeloid cells)-1 est un récepteur, exprimé par les cellules myéloïdes, impliqué dans l’amplification de la réponse inflammatoire en réponse à une stimulation de la voie des TLRs. Notre objectif était d’étudier les conséquences de l’inhibition de TREM-1 sur le développement de l’athérosclérose expérimentale.Matériel et résultats : Dans un modèle de souris chimères Ldlr-/- retransplantées avec une moelle de souris Trem-1+/+ ou Trem-1-/-, nous avons montré que la déficience hématopoïétique en Trem-1 induisait une réduction de 42% de la taille des plaques d’athérosclérose au niveau du sinus aortique après 6 semaines de régime gras et une réduction de 60% après 14 semaines. De plus, la déficience hématopoïétique en Trem-1 induisait un phénotype lésionnel plus stable avec une moindre accumulation macrophagique, un centre nécrotique moins volumineux. Ces résultats ont été confirmés dans un modèle de souris ApoE-/-/Trem1-/-. Parallèlement, l’inhibition pharmacologique de TREM-1 par des injections répétées de peptide LR12 induisait une réduction significative de la taille des plaques au niveau du sinus et de l’aorte thoracique chez la souris ApoE-/- sous un régime riche en matières grasses. En utilisant différentes approches in vitro et in vivo, nous avons montré que l’invalidation génique de Trem-1 ou son inhibition pharmacologique induisait une déviation de la réponse immune vers un profil moins inflammatoire, réduisait le recrutement des monocytes non classiques dans la plaque d’athérosclérose et enfin limitait l’endocytose des lipides oxydés en régulant l’expression du CD36. Ces données de modulation de la réponse immune et de l’endocytose des lipides ont été confirmées sur des macrophages humains. Nous avons enfin montré que TREM-1 est exprimé dans des plaques d’athérosclérose humaines essentiellement par les macrophages spumeux. L’expression de TREM-1 est significativement plus importante dans les plaques athéromateuses par rapport aux plaques fibreuses. Conclusion : Nous avons montré que TREM-1 est impliqué dans le développement de l’athérosclérose à différents stades de la maladie, en modulant la réponse immune systémique et l’endocytose des lipides oxydés. L’inhibition de TREM-1 pourrait constituer une nouvelle cible thérapeutique des maladies cardiovasculaires
Innate immune responses activated through myeloid cells contribute to the initiation, progression and complications of atherosclerosis in experimental models. However, the critical upstream pathways that link innate immune activation to foam cell formation are still poorly identified.Objectives: We hypothesized that activation of TREM (Triggering Receptor Expressed on Myeloid cells)-1 plays a determinant role in macrophage atherogenic responses. Methods and Results: Ldlr-/- mice reconstituted with bone marrow deficient for Trem-1 (Trem-1-/-) showed a strong reduction of atherosclerotic plaque size in both the aortic sinus and the thoraco-abdominal aorta, and were less inflammatory compared to plaques of Trem-1+/+ chimeric mice. Genetic invalidation of Trem-1 led to alteration of monocyte recruitment into atherosclerotic lesions and inhibited Tlr4-initiated pro-inflammatory macrophage responses. Furthermore, we identified a critical role for Trem-1 in the upregulation of Cd36, thereby promoting the formation of inflammatory foam cells. Genetic invalidation of Trem-1 in Apoe-/-/Trem-1-/- mice or pharmacological blockade of Trem-1 in Apoe-/- mice using LR-12 peptide also significantly reduced the development of atherosclerosis throughout the vascular tree, and lessened plaque inflammation. TREM-1 was expressed in human atherosclerotic lesions mainly in lipid-rich areas, with significantly higher levels of expression in atheromatous compared to fibrous plaques. Conclusion: We identify TREM-1 as a major upstream pro-atherogenic receptor. We propose that TREM-1 activation orchestrates monocyte/macrophage pro-inflammatory responses and foam cell formation through coordinated and combined activation of CD36 and TLR4. Blockade of TREM-1 signaling may constitute an attractive novel and double-hit approach for the treatment of atherosclerosis
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Ackers, Ian. "Characterization and Mechanisms of WNT Signaling in Macrophages and Vascular Smooth Muscle Cells in the Atherosclerotic Plaque." Ohio University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1556702578855203.

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17

Mussard, Chase W. "In Vitro Investigation of the Effect of Exogenous Ubiquitin on Processes Associated with Atherosclerosis." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/honors/327.

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Atherosclerosis, characterized by the build-up of cholesterol, immune cells and cellular debris within arterial walls, is accelerated following myocardial infarction by poorly understood mechanisms. Ubiquitin, a small, well-studied intracellular protein involved in protein turnover via the proteasome pathway, has recently been shown to exert extracellular effects on cardiac myocytes, in vitro, and in mice undergoing myocardial remodeling. This study investigates the potential role of extracellular ubiquitin in atherosclerosis by determining its effects on two critical atherosclerotic processes: the migration of vascular smooth muscles cells and the uptake of modified LDL by monocyte/macrophages in foam cell formation. In the presence of ubiquitin, smooth muscle cell migration was accelerated and foam cell formation was enhanced, suggesting that ubiquitin has an active role in atherosclerosis.
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Covizzi, Luiz Gustavo [UNESP]. "Seleção de um suporte sintético para imobilizar células do Botryospaheria rhodina e comparação da produção de lacase por células livres e imobilizadas." Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/88405.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
O uso de células microbianas imobilizadas para aumentar a produção de metabólitos fúngicos em processos fermentativos tem mostrado altos rendimentos. Nesse trabalho foi avaliado pela primeira vez, a imobilização de células do Botryosphaeria rhodina, um fungo ligninolitico produtor constitutivo de lacases. Três suportes foram avaliados: Fibra Acrílica Fina (FAF); Espuma de Poliuretano Expandido (EPE); Espuma de Poliuretano Fibroso (EPF). O EPF foi o melhor suporte por ter mostrado uma imobilização mais homogenia das células. Um planejamento fatorial foi desenvolvido para otimizar a produção de lacases por células livres, na presença de álcool veratrílico (AV). A análise da superfície de resposta mostrou que 18mM como a melhor concentração de AV para a produção de lacases, usando-se 3 mL de homogeinato de células como inóculo (DOλ400nm 0.4-0.6) para 25 mL de meio de cultura em frascos de 125mL, a 180 rmp, durante 126 horas a 28ºC. O perfil de crescimento do fungo, associado a produção de lacase foram comparados na presença e na ausência de AV, usando-se células livres e células imobilizadas do B. rhodina. A imobilização aumentou aproximadamente 3 vezes a produção de lacases e manteve estável o nível de produção durante 6 reciclos. A imobilização de células do B. rhodina mostrou-se útil uma vez que economizou 72horas para atingir a maior produção de lacase, quando comparada com células livres e também aumentou a tolerância do fungo a concentrações mais altas de AV (500mM)
The use of microbial immobilized cells to increase the production of fungal metabolites in fermentation processes has showed higher yields. This work evaluated by the first time, the immobilization of Botryosphaeria rhodina cells, a ligninolytic fungus that produces laccase. Three carriers were evaluated: acrylic fine fiber (FAF), expanded polyurethane foam (EPE), and fiber polyurethane foam (EPF). The EPF was the best carrier because showed a homogeneous immobilization cells. A factorial design was developed in order to optimize the laccase production by free cells in the presence of the laccase inducer veratryl alcohol (VA). The analysis by response surface answer showed 18 mM as the best VA concentration to produce laccase using 3 mL of a cell homogenate (ODλ400nm 0.4-0.6) as inoculum, to 25 mL of culture medium in shaked flasks (125 mL) at 180 rpm, during 126 hours at 28 °C. A growth profile for laccase and fungal biomass production were compared with and without VA using free and immobilized cells of B. rhodina. The cell immobilization increased approximately 3 folds the laccase production and maintained it stable during 6 consecutive recycles. The cell immobilization of B. rhodina showed to be useful once saved 72 hours to achieve the higher laccase production when compared to the one with free cells, and also increased the fungal cell tolerance at higher VA concentrations (500 mM)
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Covizzi, Luiz Gustavo. "Seleção de um suporte sintético para imobilizar células do Botryospaheria rhodina e comparação da produção de lacase por células livres e imobilizadas /." São José do Rio Preto : [s.n.], 2007. http://hdl.handle.net/11449/88405.

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Orientador: Roberto da Silva
Banca: Crispin Humberto Garcia Cruz
Banca: Aneli de Melo Barbosa
Resumo: O uso de células microbianas imobilizadas para aumentar a produção de metabólitos fúngicos em processos fermentativos tem mostrado altos rendimentos. Nesse trabalho foi avaliado pela primeira vez, a imobilização de células do Botryosphaeria rhodina, um fungo ligninolitico produtor constitutivo de lacases. Três suportes foram avaliados: Fibra Acrílica Fina (FAF); Espuma de Poliuretano Expandido (EPE); Espuma de Poliuretano Fibroso (EPF). O EPF foi o melhor suporte por ter mostrado uma imobilização mais homogenia das células. Um planejamento fatorial foi desenvolvido para otimizar a produção de lacases por células livres, na presença de álcool veratrílico (AV). A análise da superfície de resposta mostrou que 18mM como a melhor concentração de AV para a produção de lacases, usando-se 3 mL de homogeinato de células como inóculo (DOλ400nm 0.4-0.6) para 25 mL de meio de cultura em frascos de 125mL, a 180 rmp, durante 126 horas a 28ºC. O perfil de crescimento do fungo, associado a produção de lacase foram comparados na presença e na ausência de AV, usando-se células livres e células imobilizadas do B. rhodina. A imobilização aumentou aproximadamente 3 vezes a produção de lacases e manteve estável o nível de produção durante 6 reciclos. A imobilização de células do B. rhodina mostrou-se útil uma vez que economizou 72horas para atingir a maior produção de lacase, quando comparada com células livres e também aumentou a tolerância do fungo a concentrações mais altas de AV (500mM)
Abstract: The use of microbial immobilized cells to increase the production of fungal metabolites in fermentation processes has showed higher yields. This work evaluated by the first time, the immobilization of Botryosphaeria rhodina cells, a ligninolytic fungus that produces laccase. Three carriers were evaluated: acrylic fine fiber (FAF), expanded polyurethane foam (EPE), and fiber polyurethane foam (EPF). The EPF was the best carrier because showed a homogeneous immobilization cells. A factorial design was developed in order to optimize the laccase production by free cells in the presence of the laccase inducer veratryl alcohol (VA). The analysis by response surface answer showed 18 mM as the best VA concentration to produce laccase using 3 mL of a cell homogenate (ODλ400nm 0.4-0.6) as inoculum, to 25 mL of culture medium in shaked flasks (125 mL) at 180 rpm, during 126 hours at 28 °C. A growth profile for laccase and fungal biomass production were compared with and without VA using free and immobilized cells of B. rhodina. The cell immobilization increased approximately 3 folds the laccase production and maintained it stable during 6 consecutive recycles. The cell immobilization of B. rhodina showed to be useful once saved 72 hours to achieve the higher laccase production when compared to the one with free cells, and also increased the fungal cell tolerance at higher VA concentrations (500 mM)
Mestre
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20

Pop-Iliev, Remon. "Processing of fine-cell polypropylene foams in compounding-based rotational foam molding." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0001/MQ45622.pdf.

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21

Santos, José André Bernardino dos. "Estudo da aterosclerose induzida por diferentestipos de dieta hiperlipídica em coelhos albinos(Oryctolagus cuniculus)." Universidade Federal de Alagoas, 2008. http://repositorio.ufal.br/handle/riufal/912.

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The egg yolk chicken and pork lard as compared with other foods, have high cholesterol. 20 ml of gem shows on average 200 mg cholesterol and 20 ml of lard average value of 14 mg of cholesterol. Good food for experiences concerning cholesterol, are low cost compared them with cholesterol powder. Method: We used rabbits of New Zealand (n = 42) adults from 7 to 8 months of age divided into groups of 4: control group diet with 200 g and water ad libitum (G1), the group treated with 1 g of cholesterol (G2); group treated with 20 ml egg yolk (G3); group treated with 20 ml of lard (G4); group (G5) treated with 40 ml of yolk and the group (G6) treated with 40 ml of lard. All groups were fed during the period of 100 days with the aim of verifying which of the diet is best for induction of atherosclerosis. The blood collection for the dosages of the lipid profile of animals occurred at times 0, 30, 60 and 100 days. At the end of the trial period, the animals were subjected to euthanasia. Segments of the aortic arch, the right carotid artery and right femoral artery were collected for analysis histological. Results: As expected the group G1 not noticed amendment, the group G2 training light of atherosclerosis, the group returned G3 significant increase (p <0,05) in total cholesterol levels, the group G4 were not identified histological changes and G5 and G6 is not adapted the diet administered. By microscopic examination, were observed foam cells in the aortic arch, and femoral and carotid thickening of endothelium in the group G3 so significant comparing them with the G2. Conclusion: The diet enriched with egg yolk, chicken is the best option for formation of foam cells and thickening of endothelium, is practical and low cost for research on cholesterol and atherosclerosis.
A gema de ovo de galinha e a banha do porco, em relação aos outros alimentos, têm alto índice de colesterol total. 20 ml de gema apresenta em média 200 mg de colesterol total e 20 ml de banha valor médio de 14 mg de colesterol total. São bons alimentos para experiências referentes à colesterolemia, são de baixo custo comparando-os com colesterol puro. Métodos: Foram utilizados coelhos da Nova Zelândia (n=42) adultos entre 7 a 8 meses de idade divididos em grupos de 4: grupo controle com ração 200 g e água ad libitum (G1); o grupo tratado com 1 g de colesterol (G2); grupo tratado com 20 ml gema de ovo (G3); grupo tratado com 20 ml de banha (G4); grupo (G5) tratado com 40 ml de gema e o grupo (G6) tratado com 40 ml de banha. Todos os grupos foram alimentados durante o período de 100 dias tendo como objetivo verificar qual das dietas é melhor para indução da aterosclerose. A coleta de sangue para as dosagens do perfil lipídico dos animais aconteceram nos momentos 0, 30, 60 e 100 dias. Ao término do período experimental, os animais foram submetidos à eutanásia. Segmentos do arco aórtico, da artéria carótida direita e artéria femoral direita foram coletados para análise histológica. Resultados: Como esperado o grupo G1 não observou alteração, o grupo G2 formação leve de aterosclerose, o grupo G3 obteve aumento significante (p<0,05) nos níveis de colesterol total, o grupo G4 não foram identificada alterações histológicas e o G5 e G6 não se adaptaram a dieta administrada. Ao exame microscópico, foram observadas células espumosas no arco aórtico, femoral e carótida e espessamento de endotélio no grupo G3 de forma significante comparando-os ao G2. Conclusão: A dieta enriquecida com gema de ovo de galinha é a melhor opção para formação de células espumosas e espessamento de endotélio, é prática e de baixo custo para pesquisas com colesterolemia e aterosclerose.
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22

Guilherme, Daniel Ferreira. "Obtenção de GFP5-scFv recombinante reativo à LDL(-): possíveis aplicações na investigação da aterosclerose." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-16102012-144328/.

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A aterosclerose é a doença de base das principais complicações cardiovasculares. Os produtos de modificação das lipoproteínas de baixa densidade, como a subfração eletronegativa LDL (-), exercem um importante papel na progressão da aterosclerose. O objetivo do presente trabalho foi expressar a proteína de fusão, GFP5-scFv anti-LDL (-), desenvolver um método para detecção de LDL (-), assim como avaliar a possível utilização desta proteína como uma ferramenta para monitorar os ensaios de formação de células espumosas. A proteína GFP5-scFv anti-LDL (-) foi expressa em E. coli BL21DE3. Esta proteína de fusão foi desnaturada com 7M de ureia, purificada por cromatografia de afinidade e reenovelada por gradiente de diálise na presença de poliestireno sulfonado. A massa molecular da proteína foi confirmada por SDS-PAGE e sua afinidade de ligação à LDL (-) confirmada pelo dot blot e ELISA. O espectro de emissão de fluorescência da GFP5-scFv anti-LDL (-) é qualitativamente equivalente ao da GFP5, porém com intensidade de emissão mais baixa. Na tentativa de superar essa limitação tentou-se realizar a inserção de um peptídeo ligante flexível entre os domínios de ligação da GFP5 e do scFv anti-LDL (-) para melhorar a eficiência de emissão de fluorescência da quimera. Os ensaios in vitro com macrófagos RAW 264.7 demonstraram que a GFP5-scFv anti-LDL (-) não apresentou toxicidade significante e não reduziu a captação de LDL (-) pelos macrófagos. Demonstrou-se por microscopia confocal, que a GFP5-scFv anti-LDL é internalizada pelos macrófagos e pode ser visualizada no interior destas células. Portanto, a proteína recombinante GFP5-scFv anti-LDL (-) é uma ferramenta que poderá ser utilizada em ensaios in vitro com macrófagos para o estudo da aterosclerose.
Atherosclerosis is the most important cause of the cardiovascular diseases. The modifications of low density lipoproteins that induces the formation of modified particles, like the electronegative LDL subfraction, - LDL (-), are know to play a key role in the progression of atherosclerosis. The aim of the present work was to express a fusion protein, GFP5-scFv anti LDL (-), to develop a method to assess LDL (-), as well as to evaluate the use of this protein as a tool for in vitro assay in the investigation of atherosclerosis. The protein GFP5-scFv anti LDL (-) was expressed in E. Coli BL21DE3. The fusion protein was denatured with 7M urea, purified by affinity chromatografy and refolded by gradient dialysis in the presence of PSS. The molecular mass of the protein was confirmed by SDS-PAGE and its affinity for LDL (-) was confirmed by dot blot and ELISA. The emission spectrum of GFP5-scFv is qualitatively equivalent to that of GFP5, although with a lower fluorescence emission intensity. In an attempt to overcome this limitation we tried to perform the insertion of a flexible linker between the binding domains of GPF5 and scFv was done in order to increase the fluorescence emission of this fusion protein. The in vitro assays with RAW 264.7 macrophages showed that the GFP5-scFv anti-LDL (-) has no significant toxicity to these cells and did not decrease the uptake of LDL (-) by these macrophages. It was demonstrated by confocal microscopy that the GFP5-scFv anti-LDL (-) is internalized by macrophages and can be visualized inside these cells. Thus, GFP5-scFv anti-LDL (-) fusion proteins is a useful to that can be used for in vitro assays with macrophages in the investigation of atherosclerosis.
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Barra, Quaglia Carolina M. 1982. "Sinusoid-lining cells are novel myeloid-endothelial innate cells that form splenic niches for marginal zone B cell activation and plasma cell survival." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/328415.

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Los sinusoides del bazo humano promueven la lenta percolación de la sangre, favoreciendo la captura de antígeno por los fagocitos y linfocitos del sistema inmune local. Estratégicamente posicionadas delimitando los vasos, e históricamente conocidas como células retículo-endoteliales, las células que delinean los sinusoides (SLCs), tienen una biología enigmática y podrían ser vistas como un componente desconocido del sistema inmunológico. En esta tesis hemos observado que las SLCs poseían un fenotipo simil-endotelial, eran específicas de humano y expresaban moléculas típicamente asociadas al linaje endotelial como el factor de von Willenbrand, y las moléculas CD31, CD54, CD102, CD105 y CD141. Sin embargo, a diferencia de las células endoteliales, las SLCs también expresaban moléculas típicamente asociadas al linaje estromal como la vimentina y la actina de músculo liso, junto con varias moléculas del linaje mieloide como CD14, CD36, CD163, MR, DEC-205 y TLR4. A si mismo, las SLCs evidenciaron una huella genética típicamente macrofágica que incluía sensores microbianos, receptores de tipo “scavenger”, mediadores de la respuesta inmunitaria y reguladores de la fagocitosis y la presentación antigénica. Además de fagocitar antígenos a través de un mecanismo actina-dependiente, las SLCs secretaban BAFF, APRIL, IL-6 y CXCL10, induciendo el reclutamiento, la activación y la supervivencia de células B de la zona marginal, un subtipo celular especializado en la respuesta de anticuerpos frente a antígenos provenientes de la sangre. Por lo tanto, las SLCs son células endoteliomieloides que funcionan como centinelas dotados de funciones fagocíticas y que ayudan en la producción de anticuerpos.
Sinusoid vessels promote the slow percolation of venous blood through the red pulp of the spleen, thereby favoring antigen capture by phagocytes and lymphocytes of the local immune system. Strategically positioned around sinusoids and historically known as reticulo-endothelial cells, sinusoid-lining cells (SLCs) have an enigmatic biology and thus can be viewed as an orphan component of our immune system. We found here that SLCs were a human-specific population of endothelial-like cells that expressed typical endothelial molecules such as von Willenbrand factor, CD31 (PECAM-1), CD54 (ICAM-1), CD102 (ICAM-2), CD105 (endoglin) and CD141 (thrombomodulin). However, unlike endothelial cells, SLCs also expressed the stromal molecules vimentin and smooth muscle actin along with several myeloid molecules such as CD14, CD36, CD163, MR, DEC-205 and TLR4. Accordingly, SLCs showed a prominent macrophage-like gene signature that included microbial sensors, scavanger receptors, immune mediators, and regulators of phagocytosis and antigen presentation. Besides phagocytosing particulate antigens through an actin-dependent mechanism, SLCs released BAFF, APRIL, IL-6 and CXCL10, which enhanced the recruitment, activation and survival of marginal zone (MZ) B cells, a splenic lymphocyte subset specialized in innate-like antibody responses to blood-borne antigens. Thus, SLCs are endothelialmyeloid cells that serve as sentinels endowed with phagocytic and antibody-enhancing functions.
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Yin, Min. "Vésicules extracellulaires et régulation de la réponse inflammatoire dans les pathologies cardiovasculaires." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05S009.

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Les vésicules extracellulaires telles que les microvésicules et les exosomes sont libérées lors de l’apoptose ou de l’activation cellulaire. Ce sont des médiateurs importants dans la communication intercellulaire, suggérant que ces vésicules pourraient jouer un rôle physiopathologique, en particulier dans les maladies cardiovasculaires. L'athérosclérose est une maladie inflammatoire chronique de la paroi artérielle qui résulte de l’interaction entre les lipoprotéines, les cellules inflammatoires, et les cellules vasculaires. L'infarctus du myocarde est une complication aiguë et grave de l'athérosclérose. La réaction inflammatoire post-infarctus joue un rôle central dans la formation de néovaisseaux sanguins et la cicatrisation. Cependant, les mécanismes de l’inflammation sont encore mal connus dans ces pathologies. Mon travail de thèse a porté sur les effets des vésicules extracellulaires isolées de tissus pathologiques sur les cellules inflammatoires. Nous avons montré dans un premier travail que les microvésicules s’accumulant dans les lésions d’athérosclérose humaines contribuent à la surcharge en cholestérol et en triglycérides des macrophages et facilitent la formation de cellules spumeuses. L’accumulation des lipides intracellulaires induite par ces microvésicules est contrebalancée par une augmentation de l’efflux du cholestérol associée à une activation d’ABCA1. Dans un deuxième travail, nous avons examiné les effets des vésicules produites dans le cœur post-infarctus sur la réponse inflammatoire. Nos résultats montrent : 1- une augmentation de la libération in situ des microvésicules majoritairement d’origine cardiomyocytaire et des exosomes 15 heures après infarctus ; 2- la stimulation de la production de VEGF monocytaire par les vésicules extracellulaires ; 3- l’incapacité en ce qui concerne les vésicules isolées de cœur diabétique infarci à reproduire cet effet sur les monocytes des souris contrôles. Afin de clarifier les déterminants de l’angiogenèse post-ischémique, nous avons également étudié les profils de miARNs des vésicules contrôles et diabétiques. Après infarctus du myocarde, l’expression de miR-126-3p et de miR-92a-3p est significativement diminuée dans les vésicules diabétiques en comparaison avec les vésicules contrôles. Par ailleurs, nous avons observé une augmentation de miR-126-3p et de miR-92a-3p respectivement dans les microvésicules et les exosomes chez les souris contrôles post-infarctus. En conclusion, ce travail apporte des éléments nouveaux sur les fonctions des vésicules extracellulaires générées localement dans les tissus inflammatoires, en particulier leur capacité à promouvoir la transformation des macrophages en cellules spumeuses dans la plaque. Par ailleurs, les vésicules isolées du cœur ischémique pourraient favoriser l’angiogenèse post-infarctus en stimulant la production de VEGF monocytaire. La disparition de cet effet bénéfique dans le diabète pourrait être associée à des modifications d’adressage des miARNs dans les vésicules extracellulaires au cours de cette pathologie
Extracellular vesicles, such as microvesicles and exosomes, are released during cell apoptosis or activation. They are important mediators of intercellular communication, suggesting that these vesicles could play a pathophysiological role, especially in cardiovascular diseases. Atherosclerosis is a chronic inflammatory disease of the arterial wall which results from the interaction between lipoproteins, inflammatory cells, and vascular cells. Myocardial infarction is an acute and severe complication of atherosclerosis. The postinfarction inflammatory response plays a central role in the formation of new blood vessels and scarring. However, the mechanisms of inflammation are still poorly known in these pathologies. My thesis concerned the effects of extracellular vesicles isolated from pathological tissues on inflammatory cells. We showed in the first work that microvesicles accumulating in human atherosclerotic lesions contribute to cholesterol and triglyceride overload in macrophages and facilitate foam cell formation. The accumulation of the intracellular lipids induced by those microvesicles is offset by an increase in cholesterol efflux associated with activation of ABCA1. In the second study, we examined the effect of vesicles produced in the infarcted heart on the inflammatory response. Our results showed : 1- an increased release in situ of microvesicles mostly of cardiomyocyte origin and exosomes 15 hours after infarction ; 2- the stimulation of monocyte VEGF production by extracellular vesicles ; 3- the incapacity of diabetic vesicles isolated from infarcted heart to reproduce that effect on control mice monocytes. In order to clarify the determinants of postischemic angiogenesis, we also studied miRNA profiles of control and diabetic vesicles. After myocardial infarction, the expression level of miR-126-3p and miR-92a-3p was significantly decreased in diabetic vesicles compared to control vesicles. Furthermore, we observed an increased expression of miR-126-3p and miR-92a-3p respectively in the microvesicles and the exosomes isolated from control mice heart after myocardial infarction. In conclusion, this work provides new information on the functions of extracellular vesicles locally generated in inflamed tissues, particularly in promoting macrophage transformation into foam cells in the atherosclerotic plaque. Furthermore, vesicles isolated from ischemic heart could enhance postinfarction angiogenesis by stimulating monocyte VEGF production. The loss of this beneficial effect in diabetes may be associated with changes of miRNA cargo in extracellular vesicles in this pathology
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Fox, Timothy J. "Aging in closed-cell phenolic foam." Thesis, Massachusetts Institute of Technology, 1986. http://hdl.handle.net/1721.1/15025.

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Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 1986.
MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING
Bibliography: leaves 126-127.
by Timothy J. Fox.
M.S.
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26

Pope, Ellen Grace. "Sepiolite/polyurethane open cell foam composites." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.738272.

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27

Kabani, Sarah. "Lifecycle progression in Trypanosoma brucei : genome-wide expression profiling and role of the cell cycle in this process." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/3929.

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The bloodstream form of Trypanosoma brucei differentiates into the stumpy form in the mammalian bloodstream, completing differentiation into the procyclic form on uptake by the tsetse fly. The underlying genetic events occurring during this differentiation process in pleomorphic cell lines were investigated through whole-genome microarray studies of key time points during differentiation from stumpy form cells to the procyclic form found in the insect midgut. The microarray was extensively validated and bioinformatic experiments conducted to detect motifs over represented in stumpy form or slender form cells. A positional-dependent motif was identified that was over represented in stumpy form cells, possibly representing a regulatory domain. The transcripts found to be enriched in stumpy form cells included a chloride channel, although RNAi directed against this gene showed no phenotype, suggesting the protein is redundant, as three other homologous proteins exist in the genome and showed similar mRNA profiles on the microarray. Stumpy form cells are G0 arrested and two proteins implicated in G0/G1 regulation in other organisms, Target of Rapamycin (Tor) and Cdh1, were investigated in T. brucei to determine whether these proteins were involved in differentiation. The result of depletion of either protein was rapid cell death in bloodstream form cells, although treatment with the drug rapamycin did not have any effect on the cells in contrast to other eukaryotes where this drug causes G1 arrest. A method for synchronisation of bloodstream form cells was also designed using a supravital dye and flow cytometry to allow investigation into cell cycle-dependent processes. This method was particularly suitable for harvesting populations enriched in G0/G1 stage cells, however differentiation of the isolated G0/G1 and G2/M populations did not show significantly different differentiation kinetics.
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Sue, Ji Woong. "Effect of microstructure of closed cell foam on strength and effective stiffness." Texas A&M University, 2006. http://hdl.handle.net/1969.1/4986.

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This research is concerned with the modeling and failure analysis of closed cell foam with various scales of microstructure that is disordered due to defects. This foam material is used for the forward bipod closeout on the space shuttle external tank. Three dimensional finite element simulations of closed cell foams with various microstructures are performed to study the influence of the geometric character of the microstructure (eg. defect size and distribution) on the stiffness and failure behavior of the foam. First, regularly arrayed cells are modeled for a reference to compare with the disordered microstructure. For studying the effect of cellular microstructure, a discrete model is developed where in every edge and face of each cell are modeled. Two types of defects, point defects (void) and area defects (knot), are indicated from the examination of BX250 and BX265 polyurethane foams. However, this research is focused on the point defect. Analyzing a material with such complex microstructure is especially challenging in terms of computation power as well as required modeling techniques. A finite element model consisting of only beam and shell elements was developed. Certain complications that arise from using beam and shell elements were resolved using novel techniques. Stiffness predictions from the model agreed with data from the literature for a wide range of relative densities. Parametric studies were performed to examine the effect of different properties, such as relative densities and edge fraction, on the effective stiffness, Von Mises stress, and buckling stress. The thickness of the face plays an important role in the behavior of the foam material. Linear buckling and postbuckling analyses were performed to understand the effect of local buckling on the effective properties of the foam and stress concentrations. A distorted multicell model was developed to analyze the effect of point defects on the foam behavior. In particular, two geometric parameters, the defect size and the defect density (or the distance between two defects) were varied to find their effect on the stress concentrations and the effective stiffness of the foam. It is seen that the discrete model that accounts for the foam microstructure reveals much more about the foam behavior than a homogenous model.
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Kachurina, Nadezda. "Morphogenesis of opaque form «Candida albicans» cells." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40831.

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ABSTRACT We followed the localization of GFP-tagged myosin I (Myo5), septin (Cdc12) and rhodamin-stained actin during bud and shmoo formation in opaque-phase cells of Candida albicans, and monitored the mating-associated processes of cell fusion, zygote budding, septum formation, daughter cell development and the dynamics of nuclear migration and division. The localization of Myo5p, Cdc12p and actin during budding in opaque and white cells is similar. In pheromone-stimulated cells, these proteins localize in shmoos in patterns consistent with hyphal formation in white-phase cells. MTLa cells generate shmoos 5-7 hours earlier than MTLα cells in mixed populations. In the daughter cell generated after mating, Cdc12p, Myo5p and actin localize as they do under vegetative budding conditions. Intriguingly, isogenicity for the mating type locus is involved in the positioning of the nuclear division; in MTLa cells the nucleus divides within the mother cell up to 70% of the time, rather than across the mother-bud neck.
RÉSUMÉ Nous avons déterminé la localisation de l'actine ainsi que de la myosine I (Myo5) et de la septine (Cdc12) modifiées avec la protéine fluorescente verte (GFP) chez Candida albicans en phase opaque (reproductive) et blanche (végétative). Plus particulièrement, nous avons porté notre attention sur les processus associé à la reproduction tel le bourgeonnement et l'expansion cellulaire (shmoo), la conjugaison et la fusion cellulaire, le bourgeonnement et le développement des zygotes (cellules -filles issues de la conjugaison). Nous avons aussi observé la configuration subcellulaire de Myo5p, Cdc12p et de l’actine lors de la migration et de la division nucléaire en phase blanche. Que ce soit en phase opaque ou en phase blanche, la localisation de Myo5p, Cdc12p et de l'actine reste similaire lors du bourgeonnement. Lors d’une stimulation à la phéromone, en phase opaque, ces trois protéines ont le même patron d’organisation cellulaire que lors de la formation d'hyphes en phase blanche. Les cellules de type MTLa produisent des shmoo entre 5 et 7 heures plus tôt que les cellules de type MTLα dans une population mixte. Dans les zygotes, Cdc12p, Myo5p et l'actine ont la même localisation que celle observée dans les cellule-filles issues du bourgeonnement en mode végétatif. Étonnamment, l'isogénicité du locus génétique déterminant le type sexuel de la cellule influence la position du noyau lors de la division; Ainsi, dans 70% des cas, le noyau des cellules de type MTLa se divise à l'intérieur de la cellule-mère plutôt qu'au travers du col entre la cellule-mère et le bourgeon.
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Zamanishourabi, Solmaz. "Effect of cell size on the quasi-static compressive properties of silicone foams with spherical closed cells." Master's thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/69515.

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Dans ce travail, l'effet de la taille des cellules sur les propriétés de compression des mousses de caoutchouc de silicone avec des cellules sphériques a été étudié expérimentalement. Les mousses ont été fabriquées en utilisant une résine de silicone et des billes de polystyrène expansé (EPS) par une nouvelle technique. Les billes ont été mélangées avec la résine réactive et le mélange a été laissé à température ambiante jusqu'à ce que la résine soit durcie. Ensuite, le matériau solidifié a été chauffé pour rétracter les billes et former la structure cellulaire. Trois mousses différentes avec des tailles de cellules différentes, allant d'environ 1 mm à environ 2 mm, ont été fabriquées et testées sous compression quasi-statique. Pour chaque échantillon, le module de compression par rapport au poids et la résistance à la compression par rapport au poids ont été obtenus. Enfin, ces valeurs ont été comparées entre elles pour déterminer l'effet de la taille des cellules sur les propriétés de compression. Les résultats montrent que l'augmentation de la taille des cellules augmente la rigidité. Par exemple, l'augmentation de la taille des cellules de 1 mm à 1,5 mm à densité constante (480 kg/m³) augmente le module de compression de 17%, tandis que la contrainte de compression à 50% de déformation augmente de14%. De tous les résultats obtenus, on peut conclure que parmi les mousses de caoutchouc à cellules fermées ayant la même composition de matrice et des densités similaires, mais des tailles d'alvéoles différentes, celle ayant la plus petite taille d'alvéole donne les propriétés de compression les plus faibles par rapport au poids, tandis que celle ayant la plus grande taille d'alvéole donne le rapport le plus élevé lorsqu'elles sont lentement comprimées.
In this work, the effect of cell size on the compressive properties of silicone rubber foams with spherical cells was experimentally studied. The foams were made using a silicone resin and expanded polystyrene beads (EPS) through a novel technique. The beads were mixed with the reactive resin and the mixture was left at room temperature until the resin was cured. Then, the solidified material was heated up to shrink down the beads to form the cellular structure. Three different foams with different cell sizes, ranging from about 1 mm to about 2 mm,were made and tested under quasi-static compression. For each sample, the compressive modulus to weight ratio and compressive strength to weight ratio were obtained. Finally, these values were compared between them to determine the effect of cell size on the compressive properties. The results show that increasing the cell size increases the stiffness. For example, increasing the cell size from 1 mm to 1.5 mm at constant density (480 kg/m³) increases the compressive modulus by 17%, while the compressive stress at 50% strain increasesby 14%. From all the results obtained, it can be concluded that among the closed cell rubber foams having the same matrix composition and similar densities,but different cell sizes, the one having the smallest cell size gives the lowest compressive properties to weight ratio, while the one with the largest cell size gives the highest ratio when they are slowly compressed.
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31

Dissmore, Tixieanna. "The role of P2Y[subscript]2 nucleotide receptor in lipoprotein receptor-related protein 1 expression and aggregated low density lipoprotein uptake in vascular smooth muscle cells." Diss., Kansas State University, 2012. http://hdl.handle.net/2097/15180.

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Doctor of Philosophy
Department of Human Nutrition
Denis M. Medeiros
Laman Mamedova
The internalization of aggregated low-­density lipoprotein (agLDL) may involve the actin cytoskeleton in ways that differ from the endocytosis of soluble LDL. Based on previous findings the P2Y[subscript]2 receptor (P2Y[subscript]2R) mediates these effects through interaction with filamin‐A (FLN‐A), an actin binding protein. Our findings also showed that uridine 5’‐ triphosphate (UTP), a preferential agonist of the P2Y[subscript]2R, stimulates the uptake of agLDL, and increases expression of low‐density lipoprotein receptor related protein 1 (LRP 1) in cultured mouse vascular smooth muscle cells (SMCs). The strategy of this research was to define novel mechanisms of LDL uptake through the modulation of the actin cytoskeleton in order to identify molecular targets involved in foam cell formation in vascular SMCs. For this project, we isolated aortic SMCs from wild type (WT) and P2Y[subscript]2R‐/‐ mice to investigate whether UTP and the P2Y[subscript]2R modulate expression of LRP 1 and low‐density lipoprotein receptor (LDLR). We also investigated the effects of UTP on uptake of DiI‐labeled agLDL in WT and P2Y[subscript]2R‐/‐ vascular SMCs. For LRP1 expression, cells were stimulated in the presence or absence of 10 [mu]M UTP. To determine LDLR mRNA expression, and for agLDL uptake, cells were transiently transfected for 24 h with cDNA encoding hemagglutinin-­tagged (HA-­tagged) WT P2Y[subscript]2R or a mutant P2Y[subscript]2R that does not bind FLN‐A, and afterwards treated with 10 [mu]M UTP. Total RNA was isolated, reversed transcribed to cDNA, and mRNA relative abundance determined by RT-­PCR using the delta-­delta Ct method with GAPDH as control gene. Results show SMCs expressing the mutant P2Y[subscript]2R that lacks the FLN‐A binding domain exhibit 3‐fold lower LDLR expression than SMCs expressing the WT P2Y[subscript]2R. There was also decrease in LRP1 mRNA expression in response to UTP in P2Y[subscript]2R‐/‐ SMCs compared to WT. Actinomycin‐D (20 [mu]g/ml) significantly reduced UTP-­induced LRP1 mRNA expression in P2Y[subscript]2R‐/‐ SMCs (P < 0.05). Compared to cells transfected with mutant P2Y[subscript]2R, cells transfected with WT P2Y[subscript]2R showed greater agLDL uptake in both WT VSMC and P2Y[subscript]2R-­/-­ cells. Together these results show that both LRP 1 and LDLR expressions are dependent on an intact P2Y[subscript]2R, and P2Y[subscript]2R/ FLN‐ A interaction is necessary for agLDL uptake.
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32

Jenkins, Nicholas Paul. "Metalloproteinases and foam-cell macrophage phenotypes in atherosclerotic plaques." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535202.

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33

Harrison, Jillian A. "Regulation of hormone-sensitive lipase in mouse macrophages." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287805.

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34

Mullarkey, Peter Gerard. "The modelling of variable geometry honeycombs and foam." Thesis, University of Exeter, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341164.

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35

Brückner, Karoline. "Charakterisierung des mechanischen Verformungsverhaltens von weichelastischen Schaumstoffen unter impulsartigen sportspezifischen Belastungen." Doctoral thesis, Universitätsbibliothek Chemnitz, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:ch1-qucosa-118947.

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Im Rahmen dieser Arbeit wird ein physikalisches Modell für weichelastische EVA-Schaumstoffe entwickelt, das das mechanische Verformungsverhalten (Spannungs-Verformungs-Kurve) bei der Interaktion zwischen Sportler und Sportgerät am Beispiel eines Laufschuhs anwendungsgerecht – d.h. bei hoher Verformung und Belastungsgeschwindigkeit – kennzeichnet. Im Stand der Technik werden als Einflussfaktoren auf das mechanische Verformungsverhalten von Weichschäumen die Parameter Schaumdichte, Zellgröße bzw. Zelldurchmesser, Schaumhärte und Verformungsgeschwindigkeit ermittelt. Diese werden für die vorliegenden vier Versuchsmaterialien analysiert, wobei die letzten zwei Parameter im Modell Berücksichtigung finden. Das Modell setzt sich aus einem Matrix- und einem Gasphasenanteil zusammen. Der Matrixphasenanteil wird experimentell bei der jeweiligen Verformungsgeschwindigkeit bestimmt, wohingegen der Gasphasenanteil der in den Zellen komprimierten Luft auf einem physikalischen Zusammenhang beruht und anhand der gemessenen Schaumhärte und des Atmosphärendrucks bei der jeweiligen Verformung berechnet wird. Die Voraussetzungen für die Verwendung des Modells, zu denen inkompressible Matrixphase, Geschlossenzelligkeit und keine Querausdehnung des Schaums zählen, werden vorab umfangreich geprüft. Zusammenfassend lässt sich aussagen, dass das gewählte Modell eine gute Übereinstimmung mit den experimentell bestimmten Ergebnissen erzielt. Dies wird anhand der Mittelwertes der Differenz von experimentell ermittelten zu modellierten Daten bestimmt, für den ein Wert von 7 % berechnet wird
The purpose of this doctoral thesis is developing a physical model for flexible foam materials (e.g. ethylene/vinyl acetate foam) characterizing the mechanical deformation behavior (stress-strain-curve) at the interaction between athlete and sports equipment (e.g. running footwear) during high deformation and high loading rate. Previous studies described various parameters influencing the mechanical deformation behavior of flexible foams: foam density, cell size / cell diameter, foam hardness and loading rate. These parameters are being analyzed for the four present foams whereof the last two parameters were considered in the model. The model consists of a matrix phase measured experimentally at required loading rate multiplied with a correction factor and a gas phase of the air compressed in the foam cells which is calculated by atmospheric pressure and foam hardness. The requirements (incompressible matrix phase, closed cells and zero Poisson ratio) for using the model are verified first of all. In conclusion, the developed model presents a good accordance with the experimental data calculated by a mean difference between experimental and modeled data of 7 %
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36

Smith, P. A. "Electrophysiology of #beta#-cells form the islets of Langerhans." Thesis, University of East Anglia, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380117.

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37

Zhao, C. Y. "Thermal transport in cellular metal foams with open cells." Thesis, University of Cambridge, 2003. https://www.repository.cam.ac.uk/handle/1810/272087.

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38

Ranade, Aditya Prakash. "Structure Property Relationships in Various Layered Polymeric Systems." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1157753371.

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39

Han, Xiangmin. "CONTINUOUS PRODUCTION OF MICROCELLULAR FOAMS." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1041275301.

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40

Charlton, Susan. "The particulate form of the enzyme methane monooxygenase." Thesis, University of Warwick, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323371.

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41

Bortolomai, Ileana. "Identification and characterization of tumour initiating cells form gynaecological malignancies." Thesis, Open University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534378.

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42

Tiwari, Housila. "INVESTIGATION OF THE FEASIBILTY OF METALS, POLYMERIC FOAMS, AND COMPOSITE FOAM FOR ON-BOARD VEHICULAR HYDROGEN STORAGE VIA HYDROSTATIC PRESSURE RETAINMENT (HPR) USING IDEAL BCC MICROSTRUCTURE." Ohio University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1186967436.

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43

Rodrigues, Tiago Alexandre Morais. "Tubes reinforced with foams with density gradients." Master's thesis, Universidade de Aveiro, 2016. http://hdl.handle.net/10773/17994.

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Mestrado em Engenharia Mecânica
Estudos na área dos materiais têm desempenhado um importante papel na indústria automóvel. Com o tempo, a utilização de materiais pesados tem vindo a ser substítuido por materiais mais leves como ligas de aço avançados, ligas de alumínio e compósitos. Quanto mais leves forem as estruturas, melhor o seu desempenho em termos de consumo de combustível e emissão de gases. No entanto, as estruturas necessitam de manter a sua integridade, assegurando a segurança activa e passiva dos ocupantes. Sendo assim, este estudo concentra-se em estudar o comportamento mecânico à compressão de tubos de alumínio preenchidos com espumas de alumínio. As espumas fechadas são produzidas através do método de pulverotecnologia ao passo que as espumas abertas são fabricadas com recurso à técnica de fundição de precisão. Este estudo passa também pela análise de espumas abertas preenchidas com polímeros, neste caso silicone e epóxido, comummente chamadas espumas híbridas. Os testes de compressão foram realizados em condições quasi-estáticas e dinâmicas, sendo analisados com recurso a uma técnica não destrutiva (Termografia Infravermelha), na qual se obtêm imagens térmicas (termogramas), utilizados no estudo dos modos de deformação. A análise dos resultados passa não só pelo estudo dos modos de deformação mas também da sua influência na capacidade de absorção de energia, mas também na ocurrência de fendas e fracturas. Os resultados demonstram que os tubos preenchidos com espumas de alumínio de porosidade fechada durante a etapa de formação da própria espuma, designados in-situ, são aqueles que garantem melhor resposta mecânica, tendo um comportamento mais estável e prevísivel.
Research in materials has been playing and important role in automotive industry. With time, the use of heavier material is being replaced by lighter materials such as advanced steel alloys, aluminium alloys and composites. The lighter the structures the better in terms of fuel consumptions and gas emission’s reduction. However, these structures have to maintain their reliability, ensuring active and passive security to vehicles passengers. Therefore, this study concentrates on studying the mechanical behaviour of aluminium tubes filled with aluminium foams under compression. The closed foams are produced through a powder metallurgical method, while the open-cell foams are produced through investment casting. This study also focuses on the study of open-cell foams embedded with polymers, silicone and epoxy, commonly called ’Hybrid Foams’. Compression tests are made under quasi-static and dynamic conditions, and analysed with non-destructive technique (Infrared Thermography), which allows to obtain thermal images (thermogrames), used to study the deformation modes. The analyses of the results passes not only through the study of the deformation modes but also focuses on its influence in energy absorption capability, as well as in the occurrence of cracks and fractures. The results show that foam filled tubes with closed-cell, expanded inside the tube itself ( designated as in-situ), ensures a better mechanical response, due to its more stable and predictable behaviour.
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44

Nagel, Adam Richard. "Closed cell steel foams from oxide reduction." Thesis, Georgia Institute of Technology, 1997. http://hdl.handle.net/1853/19569.

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45

Wikström, Jakob D. "Mitochondrial form and function in pancreatic β-cells and brown adipocytes." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-39336.

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This thesis is focused on the role of mitochondria in pancreatic β-cells and brown adipose tissue (BAT). Two main aspects of mitochondria were explored; mitochondrial functional efficiency and the interrelationship between mitochondrial shape and function. Mitochondria in β-cells were found to exhibit heterogeneity in mitochondrial membrane potential. This functional diversity decreased when cells were challenged with glucose stimuli, suggesting that at higher fuel levels low-activity mitochondria are recruited into a pool of high-activity mitochondria. Glucolipotoxic conditions increased the functional diversity suggesting that this may be of importance for diabetes pathophysiology. To examine mitochondrial efficiency in intact islets a high throughput islet respirometry method was developed. Due to increased uncoupling, islets from a diabetic animal model exhibit lower respiratory efficiency. Glucose, free fatty acids and amino acids all decreased respiratory efficiency. A large portion of the respiratory efficiency was mediated by reactive oxygen species and the adenine nucleotide translocase. In β-cells mitochondria were found to undergo cycles of fusion and fission. During glucolipotoxicity mitochondria fragmented and lost their fusion ability. Knock down of the fission protein Fis1 rescued the β-cells from glucolipotoxic induced cell death. BAT mitochondria also showed fusion and fission. The mitochondrial dynamics proteins Mfn2 and Drp1 were shown to strongly affect BAT mitochondrial morphology. In response to a combination of adrenergic and free fatty acid stimuli mitochondria drastically changed from long filamentous structures to fragmented spheres. Inhibiting fission by the negative form of Drp1 decreased BAT response to adrenergic stimuli by half. In conclusion, mitochondrial efficiency may be of importance for normal as well as compromised β-cell and islet function. Mitochondrial morphology appears critical for mitochondrial function in β-cells and BAT.
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.
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46

Xu, Leilei. "Influence of In-filledTrench as Wave Barrier on Ground Vibrations." Thesis, KTH, Jord- och bergmekanik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-102879.

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With the development and expansion of traffic systems, problems associated with ground vibrations have required increased attention. Increasing vehicle loads,traffic volumes, and aging roads and railways,vibrations induced by traffic are gradually becoming acrucialproblem.Traffic induced vibrations have much smaller amplitude than those considered in seismic design, but may nevertheless cause annoyance for humans, damage to building, disturb sensitive equipment such as measurements devices, automated manufacturing in factories, etc. It is the purposeto study the effects of the in-filled trench (cell foamis usedas in-filled material in the test)as a wave barrieron the ground vibrationunder excitation of amechanicalvibrator(with an electric motor) in small scale laboratory tests. Laboratory methods are utilized for investigating the influence of cell foam on vibrations in sand by conducting vertical vibration tests with different thickness of cell foam.It is concluded that cell foam used as a wave barriermaterialis significantly working forhighfrequency rangeand for low frequency range the effect is not so effective and obvious.
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47

Herring, Jessica A. "Mechanical and electrical characterization of carbon Black-doped closed-cell Polydimethylsiloxane (PDMS) foam." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/98652.

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Thesis: S.B., Massachusetts Institute of Technology, Department of Materials Science and Engineering, 2015.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 51-52).
Carbon Black-doped Polydimethylsiloxane (CB-PDMS) can be used as a pressure sensing material due to its piezoresistive properties. The sensitivity of such a sensor is in part dependent on the stiffness of the material. A closed-cell CB-PDMS foam is being explored as a possible flexible, lightweight, and waterproof underwater sensing material for use in unmanned underwater vehicles and other hydrodynamic sensing purposes. The percolation threshold for conduction through the CB-PDMS foam is theorized, and a number of different concentrations based on the theorized threshold are explored in order to determine the optimum weight percent of Carbon Black dopant to achieve a high sensitivity, low stiffness sensing CB-PDMS foam. Sinusoidal mechanical pressure patterns were applied and voltage response measured. An optimum dopant weight percent out of the concentrations tested was found at 5.5 wt% CB-PDMS.
by Jessica A. Herring.
S.B.
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48

Page, Melissa C. (Melissa Catherine). "Effects of alternate blowing agents on the aging of closed-cell foam insulation." Thesis, Massachusetts Institute of Technology, 1991. http://hdl.handle.net/1721.1/13280.

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49

Betts, Charles. "Structural integrity of open-cell aluminium foam sandwich panels for lightweight wing structures." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/17995.

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The overarching aim of this work was to concentrate on the mechanical modelling and experimental characterisation of novel open-cell aluminium foam core sandwich panels for prospective use as an airplane wing skin material. A repeating unit cell 2D FE model was created to assess the mechanical behaviour of infinitely long, regularly tessellated honeycomb core sandwich panels. An analytical model using Timoshenko beam theory was developed to predict the Young’s modulus of a hexagonal honeycomb core; there is good agreement between the two models. A microtensile test procedure was developed to determine the mechanical properties of individual foam struts. A FE model of the as-tested struts was created, using XMT scans of the undeformed struts to define the geometry, to establish a method that compensates for grip slippage inherent in the testing of the struts. Strut deformation was described by a calibrated continuum viscoplastic damage model. The damage model was implemented into 3D FE models of an open-cell aluminium alloy foam core sandwich panel subjected to uniform compression to study the effect of varying the strut aspect ratio on the mechanical properties of the core. FE models of the panel subjected to three and four point bending were created to provide a virtual standardised test to assess the core elastic properties. The extent of structural damage in the panels was simulated for indentation loading indicative of a tool strike; an optimal strut aspect ratio was identified providing the best energy absorption per unit mass whilst ensuring core damage is detectable. The effect of morphological imperfections on the mechanical properties and extent of detectable damage of the core was studied. The shear modulus of the core was greatly reduced under the presence of both fractured cell walls and missing cells. The extent of visible damage was largely unaffected by either type of defect.
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50

Lu, Kuo-Yun, and 呂國昀. "Erythropoietin Suppresses the Formation of Macrophage Foam Cells." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/69255868128995983110.

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博士
國立陽明大學
生理學研究所
99
In addition to the hematopoietic effect of erythropoietin (EPO), abundant evidence suggests that EPO also performs cardiovascular protective effects which utilize a distinct receptor complex that composes of EPO receptor and the beta common receptor (bCR). However, the role of EPO and its underlying mechanism in macrophage foam cell formation are poorly understood. Compared to wild-type specimens, EPO was increased in atherosclerotic aortas of apolipoprotein E-deficient mice, mainly in the macrophage foam cells of the lesions. In addition, both the macrophage foam cells of the lesions and bone marrow-derived macrophages also express ?毧R. EPO levels in culture medium and macrophages were significantly elevated in response to oxidized low density lipoprotein (oxLDL) treatment in a dose-dependent manner, and EPO markedly attenuated lipid accumulation in oxLDL-treated macrophages, a result that was due to an increase in cholesterol efflux through a bCR pathway. Furthermore, EPO treatment significantly increased ATP-binding cassette transporter (ABC)-A1 and G1 (ABCA1 and ABCG1) mRNA and protein levels without affecting protein expression of scavenger receptors (SRs) including SR-A, CD36 and SR-BI. The up-regulation of ABCA1 and ABCG1 by EPO resulted from liver X receptor (LXR)alpha activation via a bCR pathway, which was confirmed by their prevention on expression of ABCA1 and ABCG1 after pharmacological or siRNA inhibition. Moreover, the EPO-mediated attenuation on lipid accumulation was abolished by such inhibition. Finally, reduced lipid accumulation and marked increase of ABCA1 and ABCG1 were demonstrated in EPO-overexpressed macrophages. Our data suggest that EPO suppresses foam cell formation via the bCR pathway to activate the LXRa-dependent up-regulation of ABCA1 and ABCG1.
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