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Monday, August 3, 2020 | History

4 edition of Pathobiology of the human atherosclerotic plaque found in the catalog.

Pathobiology of the human atherosclerotic plaque

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  • 30 Currently reading

Published by Springer-Verlag in New York .
Written in English

    Subjects:
  • Atherosclerosis -- Pathophysiology -- Congresses.,
  • Atherosclerosis -- Etiology -- Congresses.,
  • Arteriosclerosis -- pathology -- congresses.,
  • Ultrasonic Diagnosis -- congresses.

  • Edition Notes

    StatementSeymour Glagov, William P. Newman III, Sheldon A. Schaffer, editors.
    ContributionsGlagov, Seymour., Newman, William P., Schaffer, Sheldon A.
    Classifications
    LC ClassificationsRC692 .P353 1990
    The Physical Object
    Paginationxxx, 923 p. :
    Number of Pages923
    ID Numbers
    Open LibraryOL2200098M
    ISBN 100387971300
    LC Control Number89021674

    In this respect, the pathobiology of rabbit and human atherosclerosis has marked differences. Atherosclerotic lesions in rabbits are induced in weeks following an acute injury response, whereas patients develop atherosclerotic plaques over the course of many decades. Applications that emphasize blood-brain barrier and vascular functions in development and treatment of neural injury will be reviewed in BINP, for animal studies, or ANIE, for human subjects. Applications that emphasize the role of hemodynamics in atherosclerotic plaque formation and rupture in aneurysm formation will be reviewed in AVI.

    Atherosclerosis is a disease in which the inside of an artery narrows due to the buildup of plaque. Initially, there are generally no symptoms. When severe, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney problems, depending on which arteries are affected. Symptoms, if they occur, generally do not begin until middle age. Methods and Results. DNA methylation profiles of AHRR in monocytes ( CpG sites ± kb of AHRR, using Illumina K array) were integrated with smoking habits and ultrasound-measured carotid plaque scores from 1, participants of the Multi-Ethnic Study of Atherosclerosis (MESA).Methylation of cg significantly associated (p = ×10 −) with smoking status (current vs. never).

    These observations demonstrate that significant sources of tissue ACE in human atherosclerotic plaques are regions of inflammatory cells, especially areas of clustered macrophages as well as microvessel endothelial cells. These results suggest that ACE accumulation within the plaque . This review is intended to explore the pathophysiology underlying atherosclerotic plaque development and the clinical sequellae of plaque rupture in the coronary arteries. With a more detailed understanding of the biology of the atherosclerotic plaque, it is hoped that treatment strategies for the acute coronary syndromes will continue to develop.


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Pathobiology of the human atherosclerotic plaque Download PDF EPUB FB2

The proceedings were published subsequently in a volume entitled "Evolution of the Atherosclerotic Plaque", edited by Richard J. Jones (1). Both experimental and human lesions were considered and several provocative new approaches to the disorder were discussed. Seymour Glagov The last meeting, devoted exclusively to an examination of the atherosclerotic plaque, took place in Chicago 25 years ago under the joint auspices of the Council on Arteriosclerosis of the American Heart Association and the Chicago Heart Association.

The proceedings were published. Phenotypic Changes in Smooth Muscle Cells of Human Atherosclerotic Plaques.- 6.

Changes in the Cells of Atherosclerotic Lesions as Advanced Lesions Evolve in Coronary Arteries of Children and Young Adults.- 7. Inflammatory Components of the Human Atherosclerotic Plaque.- 8. The Role of Macrophages in Human Atherosclerosis.- 9. Pris: kr. Häftad, Skickas inom vardagar. Köp Pathobiology of the Human Atherosclerotic Plaque av Seymour Glagov, William P Newman, Sheldon A Schaffer på Pris: kr.

E-bok, Laddas ned direkt. Köp Pathobiology of the Human Atherosclerotic Plaque av Seymour Glagov, Iii Newman William P, Sheldon A Schaffer på   The results showed that atherosclerotic regression restored endothelium-dependent relaxation.

29 VolumeNumber 6, Part 2 American Heart Journal Dzau Human studies have also shown that it is possible to induce regression of atherosclerotic lesions30 and restore endothelium-dependent relaxation, 32 Atherosclerotic regression is a. At the initial meeting on “Evolution of the Atherosclerotic Plaque” inthe importance of specific glycosaminoglycans (GAG) (acid mucopolysaccharides) in atherosclerosis was shown (1).

These complex sugars were noted to be an integral part of the arterial wall connective tissue matrix that changes with the type of atherosclerotic lesion.

Falk E () Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis: Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi.

Brit. The frequent granulomatous foci of advanced human plaques, together with the lymphocytic infiltration (1–3) are but two overt histologic manifestations of the inflammatory nature of human atherosclerosis.

The collagen-rich fibromuscular cap is the hallmark of the advanced human atherosclerotic plaque. Collagen is the major extracellular product representing one-third of the dry weight and up to 60% of the total protein content of the plaque (1–3). In the normal human. Pathobiology of the Human Atherosclerotic Plaque [Glagov, Seymour, Newman, William P.

III, Schaffer, Sheldon A.] on *FREE* shipping on qualifying offers. Pathobiology of the Human Atherosclerotic Plaque. Luk, A.I. Gotlieb, in Pathobiology of Human Disease, Abstract. Atherosclerosis is a chronic inflammatory vascular disease characterized by the formation of an atherosclerotic plaque (atheroma or fibroinflammatory lipid plaque) in the vessel wall of medium- or large-sized elastic or muscular arteries, thereby impairing arterial function.

Lesions develop at sites of endothelial injury. Get this from a library. Pathobiology of the Human Atherosclerotic Plaque. [Seymour Glagov; William P Newman; Sheldon A Schaffer] -- With sixty-three contributions from leading experts around the world, this volume is the most comprehensive presentation of the human atherosclerotic plaque up to now.

Based on the papers presented. Atherosclerosis and its related clinical complications, such as myocardial infarction or stroke, represent the leading cause of death in the Western world. Accumulating experimental evidence has revealed a key role for microRNAs in regulating cellular and molecular processes related to atherosclerosis development, ranging from risk factors, to.

Overall Comparison of the Human Oral, Gut, and Atherosclerotic Plaque Microbiotas. We surveyed the atherosclerotic plaque, oral cavity (swab from periodontium area), and gut (feces) bacterial communities of 15 patients with clinical atherosclerosis and 15 age- and sex-matched healthy controls (Table 1).The 5′ variable regions (V1–V2) of the bacterial 16S ribosomal RNA (rRNA) gene.

An intriguing aspect of the pathobiology of atherosclerosis is the observation that the earliest lesions, in both humans and various experimental animal models, characteristically develop in a distinctive, nonrandom pattern, the geometry of which correlates with arterial branch points and other regions of altered hemodynamics.

– Atherosclerosis is associated with inflammation in the arteries, which is a major cause of heart attacks and strokes. Reducing the extent of local inflammation at atherosclerotic plaques can be an attractive strategy to combat atherosclerosis.

While statins can exhibit direct anti-inflammatory activities, th. Results. To investigate microbiome diversity within human atherosclerotic tissue samples, we employed high-throughput metagenomic analysis on: (1) atherosclerotic plaques obtained from a group of patients who underwent endarterectomy due to recent transient cerebral ischemia or stroke.

Luk, A.I. Gotlieb, in Pathobiology of Human Disease, Plaque rupture. The atherosclerotic plaque remains stable provided the fibrous cap remains intact. Structural changes such as erosion and fissuring of fibrous caps extending from the luminal surface act as a site of cap weakness and may promote rupture.

The established stable plaque. In this cross section of a human coronary artery there is an established fibrolipid plaque with a core of lipid. The lipid core is separated from the lumen by the plaque cap. The plaque only occupies part of the circumference. Atherosclerosis, chronic disease caused by the deposition of fats, cholesterol, calcium, and other substances in the innermost layer of endothelium of the large and medium-sized arteries.

Atherosclerosis is the most common arterial abnormality characterized as arteriosclerosis, which is defined by the loss of arterial elasticity due to vessel thickening and stiffening.Book design: Santiago Carballal-Pose, Maria Garcia-Cameselle, Miguel Gonzalez­ muscle cells cultured from human coronary atherosclerotic and restenotic lesions.

CbapterIV: providing a unique opportuniry for the study of the pathobiology of the atheromatous plaque in each of these conditions. In the work presented in.Principles Of Pathobiology Download book Principles Of book with title Principles Of Pathobiology by Mariano F.

La Via suitable to read on your Kindle device, PC, phones or tablets. Available in PDF, EPUB, and Mobi Format. Principles Of Pathobiology.