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Relevant bibliographies by topics / Atherosclerosis / Dissertations / Theses

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Dissertations / Theses on the topic 'Atherosclerosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Calvert, Patrick Andrew. "Virtual-histology intravascular ultrasound in vulnerable atherosclerosis." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609857.

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2

McCord, Barbara Norton. "Fatigue of atherosclerotic plaque." Diss., Georgia Institute of Technology, 1992. http://hdl.handle.net/1853/15890.

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3

Dennis, Maxine Elizabeth. "Oestrogen and atherosclerosis." University of Western Australia. School of Pathology and Laboratory Medicine, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0134.

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[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative effect of hormone replacement therapy (HRT) on cardiovascular disease (CVD) risk amongst postmenopausal women. It is important to determine how a hormone with numerous positive effects on intermediate pathways of atherosclerosis fails to offer cardioprotection. Further investigation into the actions of oestrogen in the vasculature may add to our current understanding of the pathogenesis of atherosclerosis and oest

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4

Jatta, Ken. "Inflammation in Atherosclerosis." Doctoral thesis, Örebro : Universitetsbiblioteket, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-478.

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5

Shakya, Arvind. "Mechanism of matrix metalloproteinase-14 (mmp-14) regulation during atherosclerosis." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4436.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.<br>"December 2006" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

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6

Crisby, Milita. "Cell death in atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3191-7/.

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7

Ahmed, Ejaz. "Immune mechanisms in atherosclerosis /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4612-4/.

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8

Arno, Gavin. "Chlamydia Pheunomiae and atherosclerosis." Thesis, St George's, University of London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498342.

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9

Kharbanda, Rajesh Kumar. "Endothelial dysfunction in atherosclerosis." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409090.

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10

Alissa, Eman Mokbel. "Micronutrient status and atherosclerosis." Thesis, University of Surrey, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419967.

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11

Johnson-Tidey, Ruth R. "Monocyte adhesion in atherosclerosis." Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387903.

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12

Falck-Hansen, Mika André. "Macrophage regulation in atherosclerosis." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29863.

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Atherosclerosis is the leading cause of cardiovascular disease, topping the mortality list in the United Kingdom and the rest of the world. Macrophage activation and polarisation are key steps in host defence and chronic inflammatory diseases, including atherosclerosis. The myeloid glycoprotein receptor CD200R1 belongs to a family of four isoforms and signals after binding to its cognate ligand, CD200. The CD200/CD200R1 interaction blocks pro-inflammatory cytokines and has never before been studied in atherosclerosis. My work has demonstrated that CD200R is weakly expressed in atherosclerotic

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13

Yaremenko, B., Марина Миколаївна Дунаєва, Марина Николаевна Дунаева, and Maryna Mykolaivna Dunaieva. "Modern look at atherosclerosis." Thesis, Sumy State University, 2020. https://essuir.sumdu.edu.ua/handle/123456789/78062.

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It is known that Atherosclerosis is one of the major cause of mortality in our time, but despite this, the exact therapy and pathogenesis have not been developed. This pathology is caused by local changes of the vascular wall and general disorders of lipid metabolism that cause lipoidosis of the inner lining of the arteries. With slow stenosis of the arteries, there is a gradual replacement of the functional tissue to the connective tissue, which leads to myocardial infarction, ischemic stroke or hypertrophy. Science doesn’t know how to stay and always move from one point to another, so recent

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14

Chalmers, Alexander David. "Mathematical Modelling of Atherosclerosis." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14986.

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In atherosclerosis, the arterial lining undergoes a specific sequence of inflammatory responses to an injury to the cells that line the blood vessel and to low density lipoprotein (LDL) particles from the blood stream that penetrate through this injury into the arterial wall. We model the events that take place inside the blood vessel wall that occur immediately after such an injury with a system of partial differential equations that involve the LDL particles, two proinflammatory cytokines, monocyte-derived macrophages and their lipid-filled counterparts, foam cells. The model includes the ch

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15

Song, Hannah. "Endothelial bone morphogenic protein 4 and bone morphogenic protein receptor II expression in inflammation and atherosclerosis." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/28258.

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Thesis (M. S.)--Biomedical Engineering, Georgia Institute of Technology, 2008.<br>Committee Chair: Hanjoong Jo; Committee Member: Ajit P. Yoganathan; Committee Member: Andrew P. Kowalczyk; Committee Member: David G. Harrison; Committee Member: Kathy K. Griendling

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16

Poupel, Lucie. "Rôle des chimiokines dans la mobilisation monocytaire au cours de l’athérosclérose." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T032/document.

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: L’athérosclérose est une maladie inflammatoire chronique des grosses artères à localisation intimale. Elle est probablement la résultante d’une réaction inflammatoire mal contrôlée ayant pour but initial d’éliminer l’accumulation anormale de lipides au niveau de l’intima. Cette élimination est exercé par les monocytes/macrophages, dont l’infiltration et l’accumulation au niveau des lésions sont une étape cruciale de l’inflammation chronique locale provoquant en particulier la production de cytokines.Les mécanismes moléculaires responsables de cette accumulation monocytaire impliquent notamme

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17

Williams, Michelle (Michelle Wing Yin). "The effect of the microenvironment on monocyte differentiation in an atherosclerotic setting using an in vitro model." Thesis, The University of Sydney, 2010. https://hdl.handle.net/2123/28892.

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Atherosclerosis is characterised by the formation of plaques which are composed of a lipid core and a fibrous cap. Pivotal cells in plaque formation are monocytes, which are traditionally known for their ability to engulf excess lipids to become foam cells, a component of the lipid core. In contrast, the principal cells identified in the fibrous cap are SMCs/SM like cells. The potential of a plaque to rupture is determined by its stability which in turn is determined by the ratio of the lipid core to fibrous cap. The rupture of a plaque ultimately leads to heart attacks and strokes often

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18

Zhou, Xinghua. "Immune mechanisms in atherosclerosis : the role of T cells in murine models of atherosclerosis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4217-X/.

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19

Hyder, Joseph Anthony. "Systemic atherosclerosis and bone density." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3211934.

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Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2006.<br>Title from first page of PDF file (viewed June 21, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 121-139).

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20

Wågsäter, Dick. "CXCL16 and CD137 in Atherosclerosis." Doctoral thesis, Örebro University, Institutionen för vårdvetenskap och omsorg, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-115.

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<p>Atherosclerosis is a progressive inflammatory disease that is characterized by the accumulation of lipids, infiltrated cells and fibrous elements in large arteries.</p><p>This thesis focuses on the molecular mechanisms behind foam cell formation and inflammation, two central processes in the development of atherosclerosis. More specific, we studied the effects of proinflammatory cytokines on CXCL16 expression and its role as scavenger receptor on macrophages and smooth muscle cells in atherogenesis. CXCL16 is defined as a chemokine and a scavenger receptor, regulating adhesion and chemoattr

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21

Högberg, Dominika. "Screening for asymptomatic carotid atherosclerosis." Doctoral thesis, Uppsala universitet, Kärlkirurgi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-328803.

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Ischemic stroke is the most common cause of handicap in adults and the third most common cause of death in Sweden. Internal carotid artery atherosclerosis is an important cause and accounts for 20% of ischemic strokes. Screening for carotid atherosclerosis has been debated over the past two decades. The aims of this thesis were (I) to study the prevalence of and risk factors associated with carotid artery atherosclerosis among 65 year old men, (II) to evaluate a simplified ultrasound protocol (the grayscale/mosaic method) for the exclusion of significant carotid artery stenosis for screening p

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22

Rip, Jacob. "Lipoprotein lipase, hypertriglyceridemia and atherosclerosis." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2006. http://dare.uva.nl/document/28665.

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23

Schwartz, Colin J. "Atherosclerosis and occlusive arterial disease /." Title page, contents and foreword only, 1994. http://web4.library.adelaide.edu.au/theses/09SD/09sds399.pdf.

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24

Parums, D. V. "Studies on inflammation in atherosclerosis." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235059.

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A spectrum of chronic inflammation is commonly seen in association with advanced human atherosclerosis. This local complication of advanced atherosclerosis is termed '<i>chronic periaortitis</i>'. This may be seen sub-clinically in necropsy samples or may present clinically, in more severe cases, as the conditions previously termed 'idiopathic retroperitoneal fibrosis', 'inflammatory aneurysm' or 'peri-aneurysmal retroperitoneal fibrosis'. The inflammatory cells consist of lymphocytes and plasma cells. Thinning or breaching of the media is common to all forms. A histological survey of necropsy

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25

Ramshaw, Anna Louise. "Immunological aspects of human atherosclerosis." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305549.

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26

Lindsay, Alistair. "Magnetic resonance imaging of atherosclerosis." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526491.

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27

Smith, Cheryl. "Reactive oxygen species in atherosclerosis." Thesis, King's College London (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302549.

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28

Hegyi, Laszlo. "Macrophage apoptosis and human atherosclerosis." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627017.

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29

Smith, Dr David Andrew. "Chlamydia pneumoniae infection and atherosclerosis." Thesis, University of London, 2004. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539377.

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30

Qing, Hua. "TELOMERASE REVERSE TRANSCRIPTASE IN ATHEROSCLEROSIS." UKnowledge, 2017. http://uknowledge.uky.edu/pharmacol_etds/19.

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Telomerase reverse transcriptase (TERT) is the catalytic subunit of telomerase and the limiting factor for the enzyme activity. The expression of TERT and telomerase activity is increased in atherosclerotic plaques. However, the role of TERT dysregulation during atherosclerosis formation remains unknown. The work herein first identified a multi-tiered regulation of TERT expression in smooth muscle cells (SMC) through histone deacetylase (HDAC) inhibition. HDAC inhibition induces TERT transcription and promoter activation. At the protein level in contrast, HDAC inhibition decreases TERT protein

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31

Davenport, Carolyn Marie Connor. "Multispectral fluorescence imaging of atherosclerosis." Diss., The University of Arizona, 1992. http://hdl.handle.net/10150/186077.

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Multispectral fluorescence imaging is a new diagnostic technique with the potential to provide improved detection and classification of atherosclerotic disease. This technique involves imaging the fluorescence response of a tissue region through a tunable band-pass filtering device. The result is a set of images in which each individual image is composed of the fluorescence emission within a specified band of wavelengths. Multispectral imaging combined with angioscopic technology allows direct access to important spectral information and spatial attributes providing the potential for more info

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32

Zhu, Chengcheng. "High resolution black blood magnetic resonance imaging of atherosclerotic plaque." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648792.

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33

Persson, Jerker. "Ultrasound and atherosclerosis evaluation of methods, risk factors and intervention /." Malmö : Lund : Malmö University Hospital ; Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945104.html.

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34

Dunn, Erin Kristine. "Endothelial nuclear hormone receptors in atherosclerosis." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3402333.

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Thesis (Ph. D.)--University of California, San Diego, 2010.<br>Title from first page of PDF file (viewed May 19, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (leaves 50-56).

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35

Hägg, Sara. "Gene Expression Profiling of Human Atherosclerosis." Doctoral thesis, Linköpings universitet, Biologiska Beräkningar, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-52085.

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Atherosclerosis is a progressive inflammatory disease that causes lipid accumulation in the arterial wall, leading to the formation of plaques. The clinical manifestations of plaque rupture—stroke and myocardial infarction—are increasing worldwide and pose an enormous economic burden for society. Atherosclerosis development reflects a complex interaction between environmental exposures and genetic predisposition. To understand this complexity, we hypothesized that a top-down approach—one in which all molecular activities that drive atherosclerosis are examined simultaneously—is necessary to hi

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36

Neuger, Lucyna. "Aspects on lipoprotein lipase and atherosclerosis." Doctoral thesis, Umeå : Univ, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-564.

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37

Wuttge, Dirk Marcus. "Cellular immunity and inflammation in atherosclerosis /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-051-2/.

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38

Sluimer, Judith Christina. "Hypoxia, HIF and angiogenesis in atherosclerosis." Maastricht : Maastricht : Universitaire pers Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=10707.

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39

Leeuw, Karina de. "Premature atherosclerosis in systemic autoimmune diseases." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.

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40

Rafatian, Naimeh. "Role of Cathepsin G in Atherosclerosis." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23641.

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Angiotensin II (Ang II) is an important modulator for development of atherosclerosis from early stage foam cell formation to advanced stage plaque rupture. Recently, the importance of locally generated Ang II, especially in macrophages, has become more evident. Generation of Ang II by several enzymes other than ACE and renin has been shown mainly in vitro. Cathepsin G is one these enzymes which is expressed in neutrophils and macrophages. Macrophages are one of the primary and crucial cells in atherosclerotic lesions which become lipid-laden foam cells through lipoprotein uptake. We hypoth

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41

Pierides, C. "Immune responses against atherosclerosis-related antigens." Thesis, University of Surrey, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529425.

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42

Milioti, Natalia. "Immunomodulation of atherosclerosis using dendritic cells." Thesis, University of Surrey, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608344.

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Inflammation plays a crucial role in atherosclerotic plaque generation/progression. Dendritic cells (DCs). cellular immune-response components linking innate and adaptive immune systems, have been found in atherosclerotic plaques. In this study, Des were examined as a possible therapeutic tool to modulate the inflammatory immune response underlying plaque formation. Apolipoprotein (apo) B-100 derived antigens are believed to modulate humoral immune responses to achieve atheroprotection, but their role in cellular immunity remains unclear. Therefore, one objective was to characterise the immuno

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43

Tai, Daven C. H. "STAT6 and STAT4 in murine atherosclerosis." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45653.

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Atherosclerosis is a chronic inflammatory condition and the major underlying cause of heart attacks and strokes. Since the immune system is paramount in all stages of atherosclerosis, modulating the immune response is an attractive therapeutic strategy for atherosclerotic disease. Signal transducers and activators of transcription (STAT) 6 and STAT4 are essential orchestrators of the anti-inflammatory Th2 response and the pro-inflammatory Th1 response, respectively. Using bone marrow transplantation to deplete STAT6 and STAT4 expression in specific immune compartments in low density lipoprotei

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44

Satterthwaite, Gemma. "Discovery of diagnostic markers for atherosclerosis." Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274961.

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45

Grahame-Clarke, Christine Naomi Ellinor. "The role of herpesviruses in atherosclerosis." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252101.

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46

Overed-Sayer, Catherine Lucy. "Inflammation in atherosclerosis : modulation by tamoxifen." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611124.

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47

Raftis, Jennifer. "Nanoparticles and atherosclerosis : resolving the paradox." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8796.

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Air pollution is increasingly recognised as an important and modifiable risk factor for cardiovascular disease. Exposure is associated with a range of adverse cardiovascular events including hospital admissions with angina and myocardial infarction, and with cardiovascular death. The main arbiter of these adverse health effects appears to be combustion-derived nanoparticles that incorporate reactive organic and transition metal components. Through the induction of cellular oxidative stress and pro-inflammatory pathways, these nanoparticles exert detrimental effects on platelets, vasculature an

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48

Yu, Emma Pei Kuen. "Mitochondrial DNA damage, dysfunction and atherosclerosis." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648537.

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49

Seibel, Yasmine. "The Role of Serotonin in Atherosclerosis." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21818.

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Atherosklerose ist eine verbreitete Krankheit deren Pathogenese unzureichend erforscht ist. Bekannt ist jedoch, dass externe und interne Faktoren eine Rolle spielen. Die zugrunde liegenden Prozesse müssen genauer untersucht werden, um neue Therapieansätze zu entwickeln. Als Allroundtalent könnte Serotonin (5-HT) ein Kandidat sein, der eine entscheidende Rolle bei der atherosklerotischen Pathogenese spielt. Ob und wie dieses Hormon die Bildung atherosklerotischer Plaques, Makrophageninvasion, Verkalkung und Fibrose beeinflusst, war Gegenstand dieser Studie. Die vorliegende Studie ist die erst

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50

Scalzi, Lisabeth Victoria. "Subclinical Atherosclerosis in Systemic Lupus Erythematosus." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1212695307.

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