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Relevant bibliographies by topics / Atherosclerosis: pathology

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Academic literature on the topic 'Atherosclerosis: pathology'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Atherosclerosis: pathology"

1

Woolf, N. "Pathology of atherosclerosis." British Medical Bulletin 46, no. 4 (1990): 960–85. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072448.

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Donosepoetro, Marsetio. "MOLECULAR PATHOLOGY OF CEREBROVASCULAR ATHEROSCLEROSIS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 12, no. 1 (2018): 16. http://dx.doi.org/10.24293/ijcpml.v12i1.835.

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Cerebrovascular disease are the third most common cause of death in Western countries. The most frequent manifestation of disease is a sudden episode of neurological deficit termed stroke which is the result of cerebral haemorrhage or cerebral infaction in the mayority of cases. Stroke secondary to atherosclerosis is most common in people over 50 years old.The incidence of stroke rises dramatically with ages, with the risk doubling with each decade after 35 years old. About 5 % of people over 65 years old have at least one stroke. Atherosclerosis is condition where fatty acid deposits occur in

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Watson, Shana R., and Susan M. Lessner. "(Second) Harmonic Disharmony: Nonlinear Microscopy Shines New Light on the Pathology of Atherosclerosis." Microscopy and Microanalysis 22, no. 3 (2016): 589–98. http://dx.doi.org/10.1017/s1431927616000842.

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AbstractThere has been increasing interest in second harmonic generation (SHG) imaging approaches for the investigation of atherosclerosis due to the deep penetration and three-dimensional sectioning capabilities of the nonlinear optical microscope. Atherosclerosis involves remodeling or alteration of the collagenous framework in affected vessels. The disease is often characterized by excessive collagen deposition and altered collagen organization. SHG has the capability to accurately characterize collagen structure, which is an essential component in understanding atherosclerotic lesion devel

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TAKANO, Tatsuya, and Hiroko TAKAHASHI. "Atherosclerosis from Molecular Pathology." Journal of Japan Atherosclerosis Society 17, no. 3 (1989): 407–12. http://dx.doi.org/10.5551/jat1973.17.3_407.

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Rainger, G. Ed, and Gerard B. Nash. "Cellular Pathology of Atherosclerosis." Circulation Research 88, no. 6 (2001): 615–22. http://dx.doi.org/10.1161/01.res.88.6.615.

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6

Wang, Tao, Daniel Palucci, Kelsey Law, Bobby Yanagawa, Jennifer Yam, and Jagdish Butany. "Atherosclerosis: pathogenesis and pathology." Diagnostic Histopathology 18, no. 11 (2012): 461–67. http://dx.doi.org/10.1016/j.mpdhp.2012.09.004.

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Tull, Samantha P., Steve I. Anderson, Sascha C. Hughan, Steve P. Watson, Gerard B. Nash, and G. Ed Rainger. "Cellular Pathology of Atherosclerosis." Circulation Research 98, no. 1 (2006): 98–104. http://dx.doi.org/10.1161/01.res.0000198386.69355.87.

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Maiuri, Maria Chiara, Gianluca Grassia, Andrew M. Platt, Rosa Carnuccio, Armando Ialenti, and Pasquale Maffia. "Macrophage Autophagy in Atherosclerosis." Mediators of Inflammation 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/584715.

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Macrophages play crucial roles in atherosclerotic immune responses. Recent investigation into macrophage autophagy (AP) in atherosclerosis has demonstrated a novel pathway through which these cells contribute to vascular inflammation. AP is a cellular catabolic process involving the delivery of cytoplasmic contents to the lysosomal machinery for ultimate degradation and recycling. Basal levels of macrophage AP play an essential role in atheroprotection during early atherosclerosis. However, AP becomes dysfunctional in the more advanced stages of the pathology and its deficiency promotes vascul

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Kolodgie, Frank D., Gaku Nakazawa, Giuseppe Sangiorgi, Elena Ladich, Allen P. Burke, and Renu Virmani. "Pathology of Atherosclerosis and Stenting." Neuroimaging Clinics of North America 17, no. 3 (2007): 285–301. http://dx.doi.org/10.1016/j.nic.2007.03.006.

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Kozhanova, T. V., E. V. Neudakhin, S. S. Zhilina, et al. "THE GENETIC SUSCEPTIBILITY TO ATHEROSCLEROSIS." Russian Archives of Internal Medicine 8, no. 6 (2018): 407–17. http://dx.doi.org/10.20514/2226-67042018-8-6-407-417.

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Atherosclerosis is a complex multifocal arterial disease involving interactions of multiple genetic and environmental factors. Atherosclerosis is the main cause of death and disability in developed countries, while in developing countries the incidence of this pathology is growing rapidly. Advances in techniques of molecular genetics have revealed that genetic polymorphisms significantly influence susceptibility to atherosclerotic vascular diseases. A large number of candidate genes, genetic polymorphisms and susceptibility loci associated with atherosclerotic diseases have been identified in

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Dissertations / Theses on the topic "Atherosclerosis: pathology"

1

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

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Stuart, Persoons Maria Cornelia Johanna. "Cytomegalovirus and vascular pathology." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8496.

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Li, Wei. "Oxidized lipids and lysosomal pathology in atherogenesis /." Linköping : Univ, 2000. http://www.bibl.liu.se/liupubl/disp/disp2000/med652s.pdf.

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Murphy, Deirdre. "Investigating the BAFF/APRIL cytokine system in atherosclerosis pathology." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709281.

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Gough, Peter Joseph. "The molecular pathology of the macrophage scavenger receptor." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301397.

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6

Wang, He 1965. "Extracellular matrix metabolism in injury-induced atherosclerosis." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40277.

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Remodelling of extracellular matrix (ECM) is a prominent feature of atherosclerotic lesions and contributes to lipoprotein retention as well as smooth muscle cell (SMC) activation. To gain further knowledge about ECM, certain ECM components and their degrading enzymes were studied in injury-induced arterial neointima, which shares features with early atherosclerotic lesions.<br>It has been shown that synthesis of collagen and syndecan-1, a hybrid heparan/chondroitin sulfate proteoglycan, is enhanced. In situ hybridization indicates that syndecan positive cells are restricted to the arterial ne

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Wasty, S. Fasahat. "Changes in the human aortic glycosaminoglycans in atherosclerosis and diabetes." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61187.

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Arterial Glycosaminoglycans (GAGs) have gained importance in artherogenesis due to their ability to trap lipid inside the vessel wall. Atherosclerotic lesions have displayed an altered GAG content and distribution. Diabetes is a recognized risk factor for atherosclerosis, but no information is available on the arterial GAGs in human diabetes. To improve our understanding of the atherogenic proccss we examined GAGs in normal and atherosclerotic intima of nondiabetic and type-II diabetic humans. Intima was stripped from the autopsy samples of thoracic aortas, normal and plaque areas were separat

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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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Sheikine, Yuri. "Chemoattractants as causative agents, biomarkers and therapeutic targets in vascular pathology /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-884-3/.

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Bousette, Nicolas. "The role of urotensin-II in atherosclerosis and ischemic cardiomyopathy /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111848.

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Atherosclerosis, a vascular disease which may lead to coronary artery occlusion and consequent myocardial infarction is primarily caused by dyslipidemia. Ischemic cardiomyopathy due to atherosclerosis is the leading cause of morbidity and mortality in the western world today. Vasoactive factors are increasingly being recognized not only as contributors to atherosclerotic plaque formation, but also to cardiac function and remodeling following ischemic cardiac injury. Urotensin II (UII) is one such vasoactive factor. UII possesses a wide range of cardiovascular effects, from contraction of the r

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Books on the topic "Atherosclerosis: pathology"

1

Chlamydia atherosclerosis lesion: Discovery, diagnosis and treatment. Springer, 2007.

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2

J, Halpern M., ed. Lipid metabolism and its pathology: Proceedings of the IVth International Colloquium on Lipid Metabolism and its Pathology, Lisbon, 18-22 November 1984. Excerpta Medica, 1986.

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3

Cellular dysfunction in atherosclerosis and diabetes: Reports from bench to bedside. Romanian Academy Pub. House, 2004.

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4

Tracy, Richard E. The role of aging in atherosclerosis: The sequestration hypothesis. Kluwer Academic Publishers, 2003.

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5

Altschul Symposium (1st 1990 Saskatoon, Sask.). Atherosclerosis: Cellular and molecular interactions in the artery wall. Plenum Press, 1991.

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6

Yen, Ho Siew, ed. Atlas of coronary artery disease. Lippincott Raven, 1998.

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7

NATO Advanced Research Workshop on Progress, Problems, and Promises for an Effective Quantitative Evaluation of Atherosclerosis in Living and Autopsied Experimental Animals and Man (1990 Siena, Italy). Atherosclerotic plaques: Advances in imaging for sequential quantitative evaluation. Edited by Wissler Robert W. 1917- and North Atlantic Treaty Organization. Scientific Affairs Division. Plenum Press, 1991.

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8

S, Edgington Thomas, Ross Russell, and Silverstein Samuel C, eds. Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of the Triton Biosciences-UCLA Symposium, held in Park City, Utah, February 2-8, 1985. Liss, 1987.

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Triton Biosciences-UCLA Symposium (1985 Park City, Utah). Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of a Triton Biosciences-UCLA Symposium, held in Park City, Utah, February 2-8, 1985. Edited by Edgington Thomas S, Ross Russell, and Silverstein Samuel C. A.R. Liss, 1987.

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10

Tousoulis, Dimitris. Risk factors and vascular endothelium. Nova Science Publishers, 2011.

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Book chapters on the topic "Atherosclerosis: pathology"

1

Vuong, Phat N., and Colin Berry. "Atherosclerosis." In The Pathology of Vessels. Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0786-7_4.

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2

Trotter, Simon, and Mufeed Ali. "Pathology of atherosclerosis." In Developments in Cardiovascular Medicine. Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-5406-2_2.

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3

Song, Ping, and Ming-Hui Zou. "Roles of Reactive Oxygen Species in Physiology and Pathology." In Atherosclerosis. John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch30.

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4

Marsico, Andrea. "Pathology of Atherosclerotic Disease." In Atherosclerosis Disease Management. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7222-4_4.

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5

Fattah, Aseel N., and Abdul-Kadir Abdulla. "The pathology of atherosclerosis." In Occult Atherosclerotic Disease. Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3404-0_2.

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6

Thim, Troels, Mette Kallestrup Hagensen, Jacob Fog Bentzon, and Erling Falk. "Pathology of Vulnerability Caused by High-Risk (Vulnerable) Arteries and Plaques." In Asymptomatic Atherosclerosis. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-179-0_3.

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7

Munro, J. Michael, and Ramzi S. Cotran. "The Pathogenesis of Atherosclerosis: Atherogenesis and Inflammation." In Pathology Reviews · 1989. Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4502-5_10.

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8

Rose, A. G., and C. J. Uys. "Pathology of Graft Atherosclerosis (Chronic Rejection)." In The Transplantation and Replacement of Thoracic Organs. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0711-9_18.

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9

van der Wal, Allard C., Onno J. de Boer, and Anton E. Becker. "Pathology of acute coronary syndromes." In Inflammatory and Infectious Basis of Atherosclerosis. Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8239-2_3.

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Carter-Monroe, Naima, Saami K. Yazdani, Elena Ladich, Frank D. Kolodgie, and Renu Virmani. "Introduction to the Pathology of Carotid Atherosclerosis: Histologic Classification and Imaging Correlation." In Atherosclerosis Disease Management. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7222-4_1.

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Conference papers on the topic "Atherosclerosis: pathology"

1

Richardson, William J., Dennis D. van der Voort, and James E. Moore. "A Device to Subject Cells to Longitudinal Stretch Gradients on a Tube In Vitro." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80941.

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In the US, cardiovascular disease accounts for more than 800,000 deaths and an economic burden of nearly $300 billion per year. A major pathology afflicting the cardiovascular system is atherosclerosis, characterized by intraluminal plaque formation, producing a stenosis and obstructing flow. Balloon angioplasty, often coupled with the implantation of either a bare-metal or drug-eluting stent, has become a standard treatment of atherosclerosis. However, the host tissue’s response to stenting is frequently maladaptive, leading to intimal hyperplasia via smooth muscle cell (SMC) division and mig

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2

Ferdous, Zannatul, Hanjoong Jo, and Robert M. Nerem. "Differential Osteogenic Marker Expression by Human Vascular and Valvular Cells in Tissue-Engineered Collagen Constructs." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19424.

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Atherosclerosis and aortic stenosis are two of the most prevalent cardiovascular disorders and a major cause of death in elderly population. In atherosclerosis, plaques and calcium deposits build up inside major arteries, which lead to narrowing of the vessel lumens and limits or completely blocks blood flow. Similarly, in calcific aortic stenosis, calcium deposits on valve cusps and valve ring result in narrowing of valve lumen, eventually leading to impaired function and even valve failure. As the disease progresses, both diseases thus require expensive replacement/repair surgeries in most p

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3

Hewlin, Rodward L., and John P. Kizito. "Comparison of Carotid Bifurcation Hemodynamics in Patient-Specific Geometries at Rest and During Exercise." In ASME 2013 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/fedsm2013-16248.

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The ultimate goal of the present study is to determine whether investigations of flow patterns (flow reversal and flow branching) and mechanical factors (wall shear stress and normal stress) have a role in local risk factors and if flow modeling can truly rely on surrogate geometric sites (simplified geometries). Cardiovascular disease is considered to be the leading cause of morbidity and mortality across the world and improved methods of disease management are desperately needed. One of the main forms of cardiovascular disease is atherosclerosis. The presence of atherosclerotic plaques has b

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Fukui, Tomohiro, Kim H. Parker, Yohsuke Imai, et al. "Wall Shear Stress Change Due to Arterial Wall Stiffness; Fluid-Solid Interactions Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176102.

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Blood flow plays an important role in regulating blood vessel structure and developing vascular pathology such as atherosclerosis. Of particular importance is the role of the shear stress on a surface of the blood vessel, which is known as wall shear stress (WSS). It is recognized today that atherosclerosis develops in areas where the WSS is low, i.e., low-shear hypothesis by Caro et al., therefore, many researchers have been studying WSS distribution in time and space in order to predict the precise region where atherosclerosis occurs by CFD simulations. Practically, however, most of the stud

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Massai, Diana, Raffaele Ponzini, Diego Gallo, et al. "Effects of Blood Rheology on Flow Topology and Blood-Vessel Interaction in Image-Based Carotid Bifurcation Numerical Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206154.

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In recent years, interest is growing on compact measures for assessing the role of local hemodynamics in the pathogenesis of atherosclerosis and atherogenesis. CFD and its power in evaluating and predicting the effect of some hemodynamic variables in vascular disease is becoming a key factor in clinical research. Recently, Lee and Steinman [1] assessed the importance of blood rheology assumptions to ascertain the effect of constitutive relation for blood on local wall shear stress (WSS) and on the correlated vascular pathology. We present a preliminary in silico investigation on the sensitivit

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Szczeklik, A., K. Sladek, and J. Dropinski. "IgE-MEDIATED IMMUNOLOGICAL RESPONSE IN MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643022.

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Mast cells have been described in adventitia of coronary arteries; their number increases with progression of atherosclerosis. We reasoned that, if these cells were to contribute to cardiac pathology, the signals turning them on should be detectable in the blood. We, therefore, measured systematically serum IgE in 25 patients (18 men and 7 women, mean age 55 years) with unequivocal diagnosis of recent transmural myocardial infarction. All patients survived. When specifically interviewed, only two gave a history compatible with atopy. In 14 patients, whose initial values ranged from 44-750 IU/m

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7

Haskett, Darren, Marie Fouts, Urs Utzinger, Doug Larson, Mohamad Azhar, and Jonathan Vande Geest. "The Effects of Angiotensin II Infusion on the Mechanical Response and Microstructural Organization of Mouse Aorta." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19635.

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Vascular diseases such as aneurysm and aortic dissection account for almost 16,000 deaths in the United States annually. In both of these diseases vascular inflammation is a common pathogenic factor. Another common pathologic feature of vascular disease includes structural matrix remodeling. It is also increasingly believed that inflammation may play a key role in the formation and progression of atherosclerotic vascular disease. Angiotensin II (AngII), a potent vasopressor, is also a strong inducer of vascular inflammation and aortic remodeling in atherosclerosis-prone mice. Based on this kno

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Bini, A., R. Mesa-Tejada, J. Fenoglio, B. Kudryk, and K. L. Kaplan. "SPECIFIC DETECTION OF FIBRIN IN HUMAN TISSUES BY A NEW IMMUNOHISTOCHEMICAL TECHNIQUE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643316.

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Human biopsy (30), surgical (50) and autopsy (14) specimens of different embryonic origin (skin, blood vessel, kidney, lymph nodes, prostate, lung, liver, and intestine) were stained by the avidin-biotin complex immunoperoxidase technique (ABC-IP) with monoclonal antibodies (MAbs). MAb T2G1 (recognizes 315-42 and detects fibrin II in tissues), MAb I8C6 (recognizes BS1-42 and indicates fibrinogen and fibrin I), MAb GC4 (specific for fragments D and D-D), and a polyclonal antiserum for fibrinogen. The method can be applied to frozen or Boilin’s fixed paraffin embedded tissues with good preservat

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Stocchino, Alessandro, Domenico Palombo, Bianca Pane, and Giovanni Spinella. "In Vivo Echo-PIV Measurements of the Flow Within Abdominal Aortic Aneurisms (AAA)." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19331.

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The incidence of Abdominal Aortic Aneurysms (AAA) varies between 3% and 6% of the elder population, especially men over sixty years of age. Moreover, familiarity, smoking and peripherical atherosclerosis are known to be important risk factors. In the United States AAA ruptures cause about 9000 deaths every year. About 33000 elective surgical treatments per year are performer with a mortality of 1400–2800 patients. The percentage of success of surgical treatment remains strictly related to the diagnosis of the stage of the AAA. Mortality rate for elective surgical intervention (asymptomatic ane

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Lewis, William, Maura Williams, and Walfre Franco. "Ex-vivo UV autofluorescence imaging and fluorescence spectroscopy of atherosclerotic pathology in human aorta." In SPIE BiOS, edited by Guillermo J. Tearney, Kenton W. Gregory, and Laura Marcu. SPIE, 2017. http://dx.doi.org/10.1117/12.2252590.

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