Relevant bibliographies by topics / Atherosclerosis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Atherosclerosis'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 November 2024

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Journal articles on the topic "Atherosclerosis"

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Napieralski, Rudolf, Ernst Wagner, Harry Gebhard, Manfred Schmitt, Alexander Zimmermann, Hans-Henning Eckstein, Anna Greißel, Mihaela Culmes, Alma Zernecke, and Jaroslav Pelisek. "Alternation of histone and DNA methylation in human atherosclerotic carotid plaques." Thrombosis and Haemostasis 114, no. 08 (2015): 390–402. http://dx.doi.org/10.1160/th14-10-0852.

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SummaryLittle is known about epigenetics and its possible role in atherosclerosis. We here analysed histone and DNA methylation and the expression of corresponding methyltransferases in early and advanced human atherosclerotic carotid lesions in comparison to healthy carotid arteries. Western Blotting was performed on carotid plaques from our biobank with early (n=60) or advanced (n=60) stages of atherosclerosis and healthy carotid arteries (n=12) to analyse di-methylation patterns of histone H3 at positions K4, K9 and K27. In atherosclerotic lesions, di-methylation of H3K4 was unaltered and that of H3K9 and H3K27 significantly decreased compared to control arteries. Immunohistochemistry revealed an increased appearance of di-methylated H3K4 in smooth muscle cells (SMCs), a decreased expression of di-methylated H3K9 in SMCs and inflammatory cells, and reduced di-methylated H3K27 in inflammatory cells in advanced versus early atherosclerosis. Expression of corresponding histone methyltransferases MLL2 and G9a was increased in advanced versus early atherosclerosis. Genomic DNA hypomethylation, as determined by PCR for methylated LINE1 and SAT-alpha, was observed in early and advanced plaques compared to control arteries and in cell-free serum of patients with high-grade carotid stenosis compared to healthy volunteers. In contrast, no differences in DNA methylation were observed in blood cells. Expression of DNA-methyltransferase DNMT1 was reduced in atherosclerotic plaques versus controls, DNMT3A was undetectable, and DNMT3B not altered. DNA-demethylase TET1 was increased in atherosclerosisc plaques. The extent of histone and DNA methylation and expression of some corresponding methyltransferases are significantly altered in atherosclerosis, suggesting a possible contribution of epigenetics in disease development.
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Li, Junxi, Xinying Fu, Renyi Yang, and Wei Zhang. "Atherosclerosis Vascular Endothelial Secretion Dysfunction and Smooth Muscle Cell Proliferation." Journal of Healthcare Engineering 2022 (March 9, 2022): 1–13. http://dx.doi.org/10.1155/2022/9271879.

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Atherosclerosis is a chronic inflammatory disease of the arterial wall and the main cause of cardiovascular disease and cerebrovascular disease. In recent years, the mortality rate of atherosclerotic diseases has become higher and higher. This article aims to study the dysregulation of atherosclerotic vascular endothelial secretion and smooth muscle cell proliferation, and put forward and practice the pathological research of atherosclerotic disease. This article describes in detail atherosclerosis, endothelial dysfunction, and smooth muscle cell proliferation, and studies the causes of atherosclerosis. Research results indicate that atherosclerotic vascular endothelial dysfunction also has a great influence on the proliferation of smooth muscle cells. Many genes and environmental factors can regulate the functions of endothelial cells, vascular smooth muscle cells, and mononuclear macrophages and affect the formation of atherosclerosis. At the same time, diabetes, hypertension, hyperlipidemia, obesity, etc. are the main causes of atherosclerosis. The number of patients with cardiovascular and cerebrovascular diseases dying from atherosclerosis in the country is increasing, and the proportion is close to 30%.
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Xia, Mingcan, Kangkang Yang, Nadia Guerra, Glina Sukhova, Carla Miller, Guo-Ping Shi, David Raulet, and Na Xiong. "NKG2D/ligands-mediated immune activation promotes atherosclerosis (142.7)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 142.7. http://dx.doi.org/10.4049/jimmunol.184.supp.142.7.

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Abstract Atherosclerosis, a chronic vascular disease, is characterized by deposition of fatty substances and accumulation of immune cells in susceptible regions of arteries. Increasing evidence show that abnormal metabolic conditions, such as dyslipdemia and diabetes, induce immune cell activation and inflammation, which play crucial roles in progression of atherosclerosis. However, molecular linkers of metabolic disorder, immune activation and atherosclerosis are not well understood. Here we report that ligands for NKG2D, an immune-activating receptor, were upregulated in multiple tissues and organs under atherosclerotic disease condition, particularly in atherosclerotic lesion and liver. Preventing NKG2D/ligands interaction significantly reduced atherosclerotic lesion formation and systemic inflammation. In addition, preventing NKG2D/ligand interaction alleviated abnormal metabolic conditions by suppressing liver inflammation. Our data clearly show that NKG2D/ligand interaction plays critical roles in the progression of atherosclerosis and might be potential targets against atherosclerosis.
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Konstantinova, E. V., A. A. Bogdanova, A. A. Sagatelyan, A. I. Kovaikin, E. S. Pershina, and M. Yu Gilyarov. "Features of atherosclerosis in carotid and coronary arteries." Meditsinskiy sovet = Medical Council, no. 14 (October 18, 2021): 44–53. http://dx.doi.org/10.21518/2079-701x-2021-14-44-53.

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Atherothrombosis is a leading cause of myocardial infarction and ischemic atherothrombotic stroke. It represents a stage of atherosclerosis which is a pathologic process throughout the circulatory system. However, atherosclerosis has specific development characteristics in different vascular beds. Multiple factors contribute to atherosclerosis formation and progression such as genetic factors, vessel hemodynamics, and vessel anatomy. A better understanding of differences in vessels would improve prevention and treatment of atherosclerosis and its complication. In this article we review features of atherosclerosis in carotid and coronary vessels. We discuss specific conditions of local hemodynamics in the areas of bifurcation which promote atherosclerotic plaque progression, and review characteristics of unstable plaques in carotid and coronary vessels. We analyze immunologic and inflammatory processes, extracellular matrix degradation and remodeling, cellular apoptosis and autophagy occurring during atherosclerotic plaque destabilization as well as the possibility of diffuse plaque instability in systemic atherosclerosis. We review association and interaction of atherosclerotic processes in coronary and carotid arteries, and its significance for a patient. Improvement in understanding of atherosclerosis pathogenesis can lead to advances in atherosclerosis prevention. Timely and effective interventions would promote prevention of myocardial infarction and ischemic stroke which is highly important taking into account high mortality and morbidity rates.
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Pakzad, Bahram, Elham Rajae, Saeid Shahrabi, Somayeh Mansournezhad, Nader Davari, Shirin Azizidoost, and Najmaldin Saki. "T-Cell Molecular Modulation Responses in Atherosclerosis Anergy." Laboratory Medicine 51, no. 6 (February 27, 2020): 557–65. http://dx.doi.org/10.1093/labmed/lmaa003.

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Abstract Atherosclerosis continues to be a major cause of death in patients with cardiovascular diseases. The cooperative role of immunity has been recently considered in atherosclerotic plaque inflammation, especially adaptive immune response by T cells. In this review, we examine the possible role of T cells in atherosclerosis-mediated inflammation and conceivable therapeutic strategies that can ameliorate complications of atherosclerosis. The cytokines secreted by T-lymphocyte subsets, different pathophysiological profiles of microRNAs (miRs), and the growth factor/receptor axis have diverse effects on the inflammatory cycle of atherosclerosis. Manipulation of miRNA expression and prominent growth factor receptors involved in inflammatory cytokine secretion in atherosclerosis can be considered diagnostic biomarkers in the induction of anergy and blockade of atherosclerotic development. This manuscript reviews immunomodulation of T cells responses in atherosclerosis anergy.
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Li, Yang, Yi Feng, Genshan Ma, Chengxing Shen, and Naifeng Liu. "Coronary tortuosity is negatively correlated with coronary atherosclerosis." Journal of International Medical Research 46, no. 12 (October 10, 2018): 5205–9. http://dx.doi.org/10.1177/0300060518804723.

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Objective The impact of coronary tortuosity on coronary atherosclerosis remains unclear. This study was performed to determine to the relationship between coronary tortuosity and the presence of coronary atherosclerosis. Methods Tortuosity and the presence of coronary atherosclerosis in the main coronary arteries were evaluated. The coronary artery was divided into non-tortuous and tortuous segments. The incidence of coronary atherosclerosis between the two segments was compared. Results The prevalence of coronary atherosclerotic stenosis was significantly lower in the tortuous than non-tortuous segment. Conclusion The prevalence of coronary atherosclerotic stenosis is lower in the coronary tortuous than non-tortuous segment, indicating that coronary tortuosity might be considered a protective factor for atherosclerosis.
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Yang, Yang, Lixia Yang, Xing Liang, and Guofu Zhu. "MicroRNA-155 Promotes Atherosclerosis Inflammation via Targeting SOCS1." Cellular Physiology and Biochemistry 36, no. 4 (2015): 1371–81. http://dx.doi.org/10.1159/000430303.

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Aims: Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155's effects on atherosclerotic inflammation and to explore its mechanism. Methods: MicroRNA-155's effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-κB though microRNA-155 inhibition or overexpression. Results: Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155's functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-κB signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression. Conclusions: microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-κB signaling via targeting SOCS1.
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Kozhanova, T. V., E. V. Neudakhin, S. S. Zhilina, T. I. Mescheryakova, A. A. Abramov, E. N. Lukash, and A. G. Prityko. "THE GENETIC SUSCEPTIBILITY TO ATHEROSCLEROSIS." Russian Archives of Internal Medicine 8, no. 6 (December 3, 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 recent years and their number is rapidly increasing. In recent years, there is significant interest in identifying additional factors of genetic risk for atherosclerosis. In recent years, a large number of genetic studies have been carried out to prove the genetic effect on the atherosclerotic process. Rapid progress in the sequencing of the human genome and molecular genetic methods have helped in the definition of susceptibility loci and associated candidate genes with atherosclerosis and concomitant diseases. The association of a large number of susceptibility genes with atherosclerosis reflects the enormous complexity of the disease. Multiple factors, including endothelial dysfunction, lipid metabolism defects, inflammation and immune responses, oxidative stress, cell proliferation, tissue remodeling and hemostatic defects are involved in the pathogenesis of atherosclerosis. In this review we focus and discuss on some of the major candidate genes and genetic polymorphisms associated with human atherosclerotic vascular diseases.
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Raman Parajuli, Sudhir, Bishwonath Yadav, Prahlad Karki, Paricha Upadhyaya, and Shivendra Jha. "An Autopsy Study of Atherosclerotic Changes in Coronary Arteries at B.P. Koirala Institute of Health Sciences." Annapurna Journal of Health Sciences 1, no. 1 (February 10, 2021): 4–8. http://dx.doi.org/10.52910/ajhs.5.

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Introduction: Atherosclerosis is a giant killer and the incidence of atherosclerosis in coronary arteries is rapidly increasing. The study was designed to assess the atherosclerotic lesions in coronary artery and to correlate the risk factors related to prevalence of atherosclerosis. Methods: Heart from 100 medico legal autopsy cases ranging between ages 15 to 35 years which came to BPKIHS Dharan were taken for this study and processed for coronary arteries using conventional technique. They were then studied,and grading was done based on Modified American Heart Association (AHA) classification of atherosclerosis. Results: Intimal thickening was noted in more than 90% in all three coronary arteries followed by intimal xanthoma whereas intermediate lesion for atherosclerosis was not found. Age, gender, smoking and alcohol in relation to atherosclerosis were found to be of no significance. Conclusion: The study highlights the impact of atherosclerotic lesions in the Eastern region of Nepal. Meticulous postmortem examination along with histopathological study is the best possible way to study atherosclerotic disease in humans and risk factors associated with it.
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Iannuzzi, Arcangelo, Paolo Rubba, Marco Gentile, Vania Mallardo, Ilenia Calcaterra, Alessandro Bresciani, Giuseppe Covetti, et al. "Carotid Atherosclerosis, Ultrasound and Lipoproteins." Biomedicines 9, no. 5 (May 6, 2021): 521. http://dx.doi.org/10.3390/biomedicines9050521.

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Carotid artery plaques are considered a measure of atherosclerosis and are associated with an increased risk of atherosclerotic cardiovascular disease, particularly ischemic strokes. Monitoring of patients with an elevated risk of stroke is critical in developing better prevention strategies. Non-invasive imaging allows us to directly see atherosclerosis in vessels and many features that are related to plaque vulnerability. A large body of evidence has demonstrated a strong correlation between some lipid parameters and carotid atherosclerosis. In this article, we review the relationship between lipids and atherosclerosis with a focus on carotid ultrasound, the most common method to estimate atherosclerotic load.
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Dissertations / Theses on the topic "Atherosclerosis"

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

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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 oestrogen biology. The primary aim of this thesis was to investigate involvement of the oestrogen receptors (ERs) in atherosclerotic CVD and to provide further insight into the actions of oestrogen on the vasculature by studying the actions of oestrogen on the regulation of an oestrogen-responsive gene within human vascular cells. Following confirmation of ERa and ERß expression at the RNA and protein level in human aorta sections, correlations of receptor expression with age and atherosclerosis were examined. Significantly strong negative relationships of ERa, androgen receptor (AR), and progesterone receptor (PR) with age in both males and females were detected. No trend was detected between ERß expression and age. These findings suggest that the receptor-mediated actions of hormones in the vasculature may change with age. Further, this thesis compared for the first time sex hormone receptor expression in normal and adjacent atherosclerotic aortic tissue providing a critical assessment of receptor differences due to atherosclerosis. Results revealed reductions of all hormone receptors in early atherosclerotic versus normal aorta tissue. ... These results suggest that the 3'-UTR SNPS may have more of an influence on carotid thickening when oestrogen levels are lower, suggesting the importance of both genetic variation of the ERß gene and oestrogen status on carotid thickening. Finally, this was the first study to investigate oestrogen-induced regulation of angiotensinogen (AGT), a candidate gene for CVD, in human vascular cells. Oestrogen influenced AGT transcription in a cell specific manner. The overall influence of oestrogen on AGT transcription in the vasculature is unknown. This thesis adds to the knowledge of oestrogen and atherosclerosis by suggesting the involvement of the sex hormone receptors (ERa, ERß, PR and AR) in atherosclerosis, presenting ERß as a potentially important candidate gene for atherosclerosis, revealing interactions between estrogen status and associations of ERß SNPs with carotid thickening, and demonstrating vascular cell-specific actions of oestrogen on the regulation of a candidate gene for CVD. These factors may have contributed to the lack of cardio-protection following HRT, as revealed by large clinical trials.
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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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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.
"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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Crisby, Milita. "Cell death in atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3191-7/.

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

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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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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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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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Books on the topic "Atherosclerosis"

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Drew, Angela F. Atherosclerosis. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/159259073x.

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Ramji, Dipak, ed. Atherosclerosis. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1924-7.

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Gotlieb, Avrum I., B. Lowell Langille, and Sergey Fedoroff, eds. Atherosclerosis. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3754-0.

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Wang, Hong, and Cam Patterson, eds. Atherosclerosis. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.

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T, Lee K., Albany Medical College. Dept. of Pathology., and Saratoga Springs Conference on Atherosclerosis (1984), eds. Atherosclerosis. New York, NY: New York Academy of Sciences, 1985.

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Saratoga International Conference on Atherosclerosis (4th 1996 Hawaii). Atherosclerosis IV: Recent advances in atheroslcerosis research : the fourth Saratoga International Conference on Atherosclerosis. New York, N.Y: The New York Academy of Sciences, 1997.

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George, Sarah J., and Johnson Jason. Atherosclerosis: Molecular and cellular mechanisms. Weinheim: Wiley-VCH, 2010.

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Kim, Jong S., Louis R. Caplan, and K. S. Lawrence Wong, eds. Intracranial Atherosclerosis. Oxford, UK: Wiley-Blackwell, 2008. http://dx.doi.org/10.1002/9781444300673.

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Naghavi, Morteza, ed. Asymptomatic Atherosclerosis. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-179-0.

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S, Kim Jong, Caplan Louis R, and Wong K. S. Lawrence, eds. Intracranial atherosclerosis. Chichester: Wiley-Blackwell, 2008.

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Book chapters on the topic "Atherosclerosis"

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Carlson, Lars A. "Atherosclerosis and clinical atherosclerosis." In Comprehensive lipid testing and management, 1–9. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-33-3_1.

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Hristov, Michael, and Christian Weber. "Atherosclerosis." In Arterial Disorders, 49–55. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14556-3_3.

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Roth, Elliot J. "Atherosclerosis." In Encyclopedia of Clinical Neuropsychology, 383–84. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_2159.

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Paeng, Jin-Chul. "Atherosclerosis." In Clinical PET and PET/CT, 249–55. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0802-5_21.

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Roth, Elliot J. "Atherosclerosis." In Encyclopedia of Clinical Neuropsychology, 278–79. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_2159.

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Carter, Jennifer. "Atherosclerosis." In Encyclopedia of Behavioral Medicine, 168. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1213.

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Abrams, David B., J. Rick Turner, Linda C. Baumann, Alyssa Karel, Susan E. Collins, Katie Witkiewitz, Terry Fulmer, et al. "Atherosclerosis." In Encyclopedia of Behavioral Medicine, 144–45. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1213.

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Vuong, Phat N., and Colin Berry. "Atherosclerosis." In The Pathology of Vessels, 69–88. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0786-7_4.

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Roth, Elliot J. "Atherosclerosis." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_2159-2.

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Kaltenbach, Martin, and Ronald E. Vlietstra. "Atherosclerosis." In Concise Cardiology, 36–88. Heidelberg: Steinkopff, 1991. http://dx.doi.org/10.1007/978-3-642-85407-1_4.

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Conference papers on the topic "Atherosclerosis"

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Brown, Thomas. "Atherosclerosis." In ACM SIGGRAPH 2009 Computer Animation Fesitval. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1596685.1596697.

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Cruz, Mariana Portella Lopes, João Gustavo dos Anjos Morais Oliveira, Gabriela Sarno Brandão, Ana Flávia Paiva Bandeira Assis, Isaac Rêgo Purificação, Leonardo Mattos Santos, Matheus Almeida Ribeiro da Cunha, Isabella Trindade Lopes Alves, and Raimundo Nonato Ribeiro Fernandes. "Influence of atherosclerosis on intracranial aneurysm rupture: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.391.

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Background: Aneurysms have their wall more susceptible to rupture. It is postulated whether the presence of atherosclerotic plaque can influence this, protecting or not. Objective: This review aims to investigate atherosclerosis (AT) as a potential risk factor for rupture of intracranial aneurysms. Design and Setting: this is a literature review, produced in Bahiana School of Medicine and Public Health. Methods: The evaluated studies were obtained in published between 2011 and 2021, using the MeSH terms with following search: ((“atherosclerosis” OR “atherogenesis” OR “atheroscleroses” OR “Vascular Disease”)) AND ((“intracranial aneurysm” OR “brain aneurysm” OR “brain aneurysms” OR “cerebral aneurysm” OR “cerebral aneurysms”)) AND ((“ruptured” OR “rupture” OR “subarachnoid hemorrhage”)). Those that did not correspond the purpose of this review were excluded. Results: 13 of the 103 articles found, were selected. In 03 retrospective cohorts, AT was not a risk factor associated with aneurysm rupture, but a protective factor. In the control case, AT did not obtain statistical significance, but hypercholesterolemia was considered a protective factor. In the postmortem, atheromatous plaque was found only in a one patient who had subarachnoid hemorrhage. The other studies were inconclusive on the subject. Conclusions: Atherosclerosis cannot yet be said as a risk factor for aneurysm rupture due to literary insufficiency. In this way, new research is needed to ensure the evidence.
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Van Doormaal, Mark A., and C. Ross Ethier. "Design Optimization of an In Vitro Shear Stress and Mass Transfer Modifier for Endothelial Cell Culture." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205439.

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Atherosclerosis, a disease of the large and medium arteries, is the leading cause of death in Western countries. Fluid dynamic and mass transfer phenomena are thought to play a role in the initiation and progression of atherosclerosis [1–3]. Atherosclerotic lesions are known to localize to areas such as bifurcations and curved arterial segments where shear stress and mass transfer patterns differ from those in straight arteries. However, the precise roles of wall shear stress and mass transfer in the localization of atherosclerotic lesions are not known, and this remains an active area of research. Determining the separate roles of wall shear stress and mass transfer in atherosclerosis is made more difficult because areas of abnormal wall shear stress often co-localize with areas of abnormal mass transfer.
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Szekanecz, Z. "SP0131 Autoimmune atherosclerosis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7194.

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Teng, Zhongzhao, Allen H. Hoffman, Jie Zheng, Pamela K. Woodard, and Dalin Tang. "Ultimate Strength of the Adventitia and Media of Human Atherosclerotic Carotid Arteries in the Axial and Circumferential Directions." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204715.

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The abrupt closure of an artery by an occlusive thrombus is the main cause of myocardial infarcts and other thrombotic sequelae of atherosclerosis. This thrombosis is often associated with rupture of an atherosclerotic plaque [1,2]. Histology has shown that most rupture sites are also sites of increased mechanical stress [2]. It has been widely accepted that atherosclerosis leads to locally increased stresses in the region of lesions. However, validation of this hypothesis has been impeded by a lack of experimental data on the material strength of atherosclerotic tissues. Knowledge of mechanical properties of human atherosclerotic tissues is essential for understanding the rupture mechanism and also for creating more accurate computational models for predicting fatal cardiovascular events [3]. Moreover, an increased understanding of the mechanical properties of atherosclerotic tissue is important for developing greater insight into the pathophysiology of the cardiovascular system and as well as for predicting the outcome of interventional treatments such as balloon angioplasty.
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Campbell, Ian C., Daiana Weiss, John N. Oshinski, and W. Robert Taylor. "Histological Determination of Murine Plaque Mechanics and Implications for Plaque Rupture." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19295.

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Among the most common models in atherosclerosis research is the atherosclerosis-prone mouse. Genetically manipulated mouse strains such as the ApoE−/− mouse will reliably form plaques under certain conditions, and these lesions have been noted to exhibit morphological and biochemical similarities with human atherosclerotic plaques. Unlike plaques in humans, however, murine plaques are not observed to rupture and form occlusive thrombi [1]. As atherosclerosis and its complications are the leading cause of death in the modern world, a comprehensive understanding of the mechanisms of plaque disruption is essential to develop diagnostic and interventional techniques. Although the mouse model is frequently employed to study plaque formation, its validity for studying plaque disruption events such as rupture or erosion has been questioned.
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Van der Heiden, K., H. C. Groen, P. C. Evans, L. Speelman, F. Gijsen, M. de Jong, A. F. W. van der Steen, and J. J. Wentzel. "Non-Invasive Molecular Imaging of Shear Stress-Induced Endothelial Activation and Atherosclerotic Plaque Vulnerability." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80515.

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Atherosclerosis is a lipid- and inflammation driven disease of the larger arteries and is found at specific locations in the arterial tree, i.e. at branches and bends where endothelial cells are exposed to low and low, oscillatory shear stress. Shear stress, the frictional force acting on the endothelial cells as a result of the blood flow, affects endothelial physiology. It determines the location of atherosclerotic lesion development as low and low, oscillatory shear stress induce pro-inflammatory transcription factors but reduce expression and/or activity of anti-inflammatory transcription factors in endothelial cells, rendering the vascular wall vulnerable for inflammation. Consequently, in the presence of atherosclerotic risk factors, such as hypercholesterolemia and diabetes, atherosclerotic lesion development can occur. Although the relationship between low and low, oscillatory shear stress and the prevalence of atherosclerosis has been recognized for several decades, insight into the mechanisms underlying this relationship is still incomplete. The correlation between shear stress and endothelial inflammation was demonstrated by in vitro experiments, in which cultured endothelial cells were exposed to specific flow profiles, and confirmed in vivo by gene expression pattern studies at atherosclerosis-susceptible sites. However, the relationship was not substantiated by direct causal in vivo evidence. Therefore, we developed a method to change the local shear stress field in mice in vivo and studied its effect on the endothelial molecular pathways and resulting atherosclerotic plaque formation. Moreover it allowed us to develop non-invasive molecular imaging strategies to detect vulnerable plaques.
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Liu, Biyue, and Dalin Tang. "Computer Simulations of the Blood Flows and the Growth of Stenosis in Arteries With Bends and Bifurcations." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203654.

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Heart attack and stroke are the chief and the 3rd largest causes of death in the United States, respectively. A heart attack occurs when the blood supply to an area of heart muscle is blocked, usually by a clot in a coronary artery; a stroke occurs when the blood supply to a region of the brain is lost. The most frequent cause of loss of blood supply to brain tissue or to heart muscle is atherosclerosis, which involves complex interactions between the artery wall and the blood flow. Caro et al first suggested that the distribution of fatty streaking in human aorta may be coincident with regions in which the shear rate at the arterial wall is locally reduced [1]. After that, intensive research has been conducted to statistically study the role of shear stress in atherosclerosis and to quantitatively determine the correlation between the low shear stress and the development of atherosclerotic plaques [2–8]. It is widely believed that fluid shear stress acting on the artery wall plays an important role in the pathogenesis of atherosclerosis. The objectives of this project are to investigate how the geometrical adaptation of atherosclerotic plaques is related to the wall shear stress (WSS) and to study the influences of the flow parameters on the growth of the atherosclerotic plaque using computational models.
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Hoffman, Allen H., Zhongzhao Teng, Calvin Mui, Jie Zheng, Pamela K. Woodard, and Dalin Tang. "Stiffness Comparisons Between Adventitia, Media and Full Thickness Specimens From Human Atherosclerotic Carotid Arteries." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206401.

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Arteries display highly nonlinear, anisotropic material behavior and can be considered to be a layered composite of fiber oriented materials composed of three layers: intima, media and adventitia. The intima does not affect the material properties of the artery. Thus, the mechanical properties of an artery result from the combined interaction of the media and adventitia with each layer displaying different material properties. It has been widely accepted that atherosclerosis changes the material properties of the arterial wall. However, little experimental data exists relating the properties of the media and adventitia of atherosclerotic vessels to the overall properties of the artery. Knowledge of the properties of human atherosclerotic tissues is essential for an improved understanding the effects of atherosclerosis and also for creating more accurate computational models for predicting the effects of the disease [1]. A prior study of bovine carotid arteries determined the properties of the adventitia and media using a deductive method [2]. This paper focuses on directly measuring and comparing the stiffness of paired samples of adventitia, media and full thickness specimens from human atherosclerotic carotid arteries.
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Booth, R. F. G., J. F. Martin, S. Moncada, and A. C. Honey. "IS ATHEROSCLEROSIS A DISEASE OF THE OUTSIDE OF ARTERIES?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643083.

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The early stages of atherosclerosis are characterised by: (i) Intimal infiltration by macrophages, (ii) Intimal smooth muscle cell (SMC) proliferation and (iii) Accumulation of cholesterol within the vessel wall. Many studies have suggested that these changes occur subsequent to endothelial cell (EC) damage and platelet deposition. We now describe a new animal model with characteristics of early human atherosclerosis but without observable EC damage or platelet deposition. 12 rabbits were separated into 2 groups; each was fed normal laboratory chow and one group was supplemented with lg/day cholesterol. At day 0, under anaesthesia, a silastic collar (internal volume 0.3ml) was placed around the left carotid artery. The collar was filled with whole blood and sealed without causing Constriction of the vessel. The right carotid arteries were sham operated. The vessels were replaced and the animals allowed to recover. After 14 days both carotids were perfuse-fixed in situ. The left carotid arteries were separated into:(A)A mid-region from within the collar,(B)A region proximal to the collar and (C)A distal region. These regions were subdivided for histology and scanning E.M. Medial/Intimal ratios of transverse sections of each region were analysed by computerised image analysis and shown below.Histology demonstrated an intense proliferation within 14 days which resembled early atherosclerosis. There was intimal monocyte infiltration and SMC proliferation and loss of SMC from the medial layer. Scanning E.M. revealed no observable EC damage or platelet adhesion. The lesion was highly focal and generally restricted to the collar region. Dietary cholesterol did not enhance proliferation but did cause foam cell formation. Sham operated vessels showed no significant atherosclerotic changes. Thus, early atherosclerotic lesions may be the result of damage to the outer layers of blood vessels.
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Reports on the topic "Atherosclerosis"

1

Ugusman, Azizah, Nur Syahidah Nor Hisam, Nur Syakirah Othman, Nur Najmi Mohamad Anuar, Adila A. Hamid, Jaya Kumar, and Amilia Aminuddin. PHARMACOLOGICAL INTERVENTIONS FOR INTRAPLAQUE NEOVASCULARIZATION IN ATHEROSCLEROSIS. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2024. http://dx.doi.org/10.37766/inplasy2024.3.0005.

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Atherosclerosis Biomarkers by Computed Tomography Angiography (CTA). Chair Andrew Buckler, Luca Saba, and Uwe Joseph Schoepf. Radiological Society of North America (RSNA) / Quantitative Imaging Biomarkers Alliance (QIBA), March 2023. http://dx.doi.org/10.1148/qiba/20230328.

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The clinical application of Computed Tomography Angiography (CTA) is widely available as a technique to optimize the therapeutic approach to treating vascular disease. Evaluation of atherosclerotic arterial plaque characteristics is currently based on qualitative biomarkers. However, the reproducibility of such findings has historically been limited even among experts (1). Quantitative imaging biomarkers have been shown to have additive value above traditional qualitative imaging metrics and clinical risk scores regarding patient outcomes (2). However, many definitions and cut-offs are present in the current literature; therefore, standardization of quantitative evaluation of CTA datasets is needed before becoming a valuable tool in daily clinical practice. To establish these biomarkers in clinical practice, techniques are required to standardize quantitative imaging across different manufacturers with cross-calibration. Moreover, the post-processing of atherosclerotic plaque segmentation needs to be optimized and standardized. The goal of a Quantitative Imaging Biomarker Alliance (QIBA) Profile is to provide an implementation guide to generate a biomarker with an effective level of performance, mostly by reducing variability and bias in the measurement. The performance claims represent expert consensus and will be empirically demonstrated at a subsequent stage. Users of this Profile are encouraged to refer to the following site to understand the document’s context: http://qibawiki.rsna.org/index.php/QIBA_Profile_Stages. All statistical performance assessments are stated in carefully considered metrics and according to strict definitions as given in (3-8), which also includes detailed, peer-reviewed rationale on the importance of adhering to such standards. The expected performance is expressed as Claims (Section 1.2). To achieve those claims, Actors (Scanners, Reconstruction Software, Image Analysis Tools, Imaging Physicians, Physicists, and Technologists) must meet the Checklist Requirements (Section 3) covering Subject Handling, Image Data Acquisition, Image Data Reconstruction, Image QA, and Image Analysis. This Profile is at the Clinically Feasible stage (qibawiki.rsna.org/index.php/QIBA_Profile_Stages) which indicate that multiple sites have performed the Profile and found it to be practical and expect it to achieve the claimed performance. QIBA Profiles for other CT, MRI, PET, and Ultrasound biomarkers can be found at qibawiki.rsna.org
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3

Saba, Luca, and Uwe Joseph Schoepf. Atherosclerosis Biomarkers by Computed Tomography Angiography (CTA) - Maintenance version June 2024. Chair Andrew Buckler. Radiological Society of North America (RSNA) / Quantitative Imaging Biomarkers Alliance (QIBA), June 2024. http://dx.doi.org/10.1148/qiba/202406.

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The clinical application of Computed Tomography Angiography (CTA) is widely available as a technique to optimize the therapeutic approach to treating vascular disease. Evaluation of atherosclerotic arterial plaque characteristics is currently based on qualitative biomarkers. However, the reproducibility of such findings has historically been limited even among experts. Quantitative imaging biomarkers have been shown to have additive value above traditional qualitative imaging metrics and clinical risk scores regarding patient outcomes. However, many definitions and cut-offs are present in the current literature; therefore, standardization of quantitative evaluation of CTA datasets is needed before becoming a valuable tool in daily clinical practice. To establish these biomarkers in clinical practice, techniques are required to standardize quantitative imaging across different manufacturers with cross-calibration. Moreover, the post-processing of atherosclerotic plaque segmentation needs to be optimized and standardized. The goal of a Quantitative Imaging Biomarker Alliance (QIBA) Profile is to provide an implementation guide to generate a biomarker with an effective level of performance, mostly by reducing variability and bias in the measurement. The performance claims represent expert consensus and will be empirically demonstrated at a subsequent stage. Users of this Profile are encouraged to refer to the following site to understand the document’s context: http://qibawiki.rsna.org/index.php/QIBA_Profile_Stages. All statistical performance assessments are stated in carefully considered metrics and according to strict definitions as given in (3-8), which also includes detailed, peer-reviewed rationale on the importance of adhering to such standards. The expected performance is expressed as Claims (Section 1.2). To achieve those claims, Actors (Scanners, Reconstruction Software, Image Analysis Tools, Imaging Physicians, Physicists, and Technologists) must meet the Checklist Requirements (Section 3) covering Subject Handling, Image Data Acquisition, Image Data Reconstruction, Image QA, and Image Analysis. This Profile is at the Clinically Feasible stage (qibawiki.rsna.org/index.php/QIBA_Profile_Stages) which indicate that multiple sites have performed the Profile and found it to be practical and expect it to achieve the claimed performance. QIBA Profiles for other CT, MRI, PET, and Ultrasound biomarkers can be found at qibawiki.rsna.org.
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4

Wang, Jun, Congcong Wang, Hongjuan Fu, Zezhong Liu, Yimin Zhang, and Tong Zhang. TNF alpha antagonists improve oxidative stress and atherosclerosis induced by rheumatoid arthritis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0033.

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wang, chen, peizheng zhang, and yuting yang. Effect of traditional Chinese exercise on abnormal lipid metabolism in patients with atherosclerosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0093.

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Men, Jie, Wenjuan Wang, Jian Zhao, Jie Wen, Qingqing Hao, and Shufeng Li. Effectiveness of exercise in atherosclerosis in ischemic strokes: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0078.

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Aminuddin, Amilia, Ubashini Vijakumaran, Nazirah Samah, Faridah Mohd Nor, Wan Mohd Hafiz Wan Razali, Shawal Faizal Mohamad, Faizal Amri Hamzah, Adila A. Hamid, and Azizah Ugusman. Unveiling TIMPs: A Systematic Review of Their Role as Biomarkers in Atherosclerosis and Coronary Artery Disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2024. http://dx.doi.org/10.37766/inplasy2024.7.0070.

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Ni, Zhichao, Qinwen Xiao, Zhongyuan Huang, Zihao Xia, and Dezhong Peng. Efficacy and safety of Acupuncture for carotid atherosclerosis: A protocol for systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0005.

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Sun, Huiqing, Wei Qu, Guangjia Chen, Xiaonan Sun, and Shichuan Shao. Efficacy and safety of Traditional Chinese patent medicine on carotid artery atherosclerosis in adults:a network meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0036.

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Niu, Xiaowei, and Shuwen Hu. Efficacy and safety of PCSK9 inhibitors and statin lipid-lowering therapy in coronary atherosclerosis: A meta-analysis of randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0019.

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