Last edited by Telkis
Saturday, May 9, 2020 | History

6 edition of Immune Mechanisms in Atherogenesis found in the catalog.

Immune Mechanisms in Atherogenesis

K. M. Heng

Immune Mechanisms in Atherogenesis

by K. M. Heng

  • 94 Want to read
  • 2 Currently reading

Published by R. G. Landes .
Written in English

    Subjects:
  • Biochemistry,
  • Immunology,
  • Cardiology,
  • Arteriosclerosis,
  • Medical / Nursing,
  • Medical

  • Edition Notes

    Medical Intelligence Unit Series

    The Physical Object
    FormatHardcover
    Number of Pages250
    ID Numbers
    Open LibraryOL9835595M
    ISBN 100412130319
    ISBN 109780412130311
    OCLC/WorldCa230952826

    Current knowledge links lipid-induced activation of the innate and adaptive immunity in the chronic inflammation that explains many mechanisms of atherogenesis, including the role of immune cells such as macrophages, dendritic cells, and a variety of effector molecules, including cytokines. The host–parasite relationship evolved so that rather than provoking needless damaging aggressive immune responses, these organisms cause a pattern of maturation of dendritic cells such that these drive Treg cells rather than Th1 or Th2 effector cells. 36, 37 This in turn leads to two mechanisms that help to control inappropriate inflammation Cited by:

    Journal of Leukocyte Biology considers manuscripts of original investigations focusing on the origins, developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes, and other cells involved in host defense. These include full-length papers on original research, rapid communications of new discoveries, letters, commentaries, and invited reviews. Low-grade chronic inflammation is a common denominator in atherogenesis and related diseases. Solid evidence supports the occurrence of an impairment in the innate and adaptive immune system with senescence, favoring the development of acute and chronic age-related diseases. Cardiovascular (CV) diseases (CVD), in particular, are a leading cause of death even at older greggdev.com by: 6.

    User Review - Flag as inappropriate After readig this book I asked myself the following: Need to lose weight? How to lose weight fast? How to lose weight in a week? 3/5(1). The importance of blood pressure as a risk factor for atherosclerosis and cardiovascular events has long been recognized. More recent clinical information has highlighted the importance of pulse pressure—the difference between the systolic pressure and minimum diastolic arterial pressure—as a prognostic indicator of cardiovascular risk.


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Immune Mechanisms in Atherogenesis by K. M. Heng Download PDF EPUB FB2

Atherogenesis is the process of forming plaques in the intima layer of arteries. Atherosclerosis is developed progressively with inflammation and lipid accumulation varying significantly among individuals.

The accumulation of LDL and the inflammation of the arterial wall is the first stage of atherosclerosis. Atherosclerosis is a disease of chronic inflammation, characterized by a dysfunctional interplay between the immune apparatus Immune Mechanisms in Atherogenesis book lipids.

Immune cells, as well as nonimmune cells, drive plaque inflammation through a complex crosstalk of inflammatory mediators. The cells are activated by risk factor–induced triggers, which are present in the circulation and in the vessel wall, such as shear Author: Ida Gregersen, Bente Halvorsen.

Atherosclerosis, the principal cause of heart attack, stroke, and peripheral vascular disease, remains a major contributor to morbidity and mortality in the Western World. Disease progression is slow, beginning in childhood and usually becoming clinically manifest in middle age or later.

Although the aetiology of atherosclerosis is not fully understood, it is generally accepted that. Available data from both animal experiments and human studies indicate that atherosclerosis is an inflammatory disease, and that the immune system may modulate the disease and both promote and decrease atherogenesis.

The outcome of specific immune reactions may depend on which antigen is used, type of immune reaction and cytokine profile in the. Yet, although macrophages constitute the largest cell population, other immune cell subsets, namely dendritic cells (DCs) and T cells, can also be found within atherosclerotic plaques and seem to participate in immune responses during atherogenesis.

DCs are the pacemakers of the immune greggdev.com by: 2. A large body of evidence implicates the immune system in the pathogenesis and modulation of atherosclerosis. Dendritic cells and lymphocytes are among the many components of the i. Immune-mediated mechanisms of atherosclerosis and implications for the clinic Article in Expert Review of Clinical Immunology 12(11) · June with 50 Reads How we measure 'reads'.

May 01,  · Atherosclerosis, the major cause of cardiovascular disease (CVD), is a chronic inflammatory condition with immune competent cells in lesions producing mainly pro-inflammatory cytokines. Dead cells and oxidized forms of low density lipoproteins (oxLDL) are greggdev.com by: In the past decade an upsurge of interest in the role of immune mechanisms in the development of arteriosclerosis has emerged.

In the present review we will analyzed data suggesting that immunological factors may contribute, directly or indirectly, to the sequence of pathological events leading to the development of greggdev.com by: 9.

Subcutaneous immunization of animals with HSP65 induced atheroma formation in the arterial wall. Furthermore, circulating immunoglobulin (Ig) G and IgM oxidized low-density lipoprotein (oxLDL) antibodies are present in the plasma of animals and humans and form immune complexes with oxLDL in atherosclerotic greggdev.com by: Atherosclerosis is a disease in which the inside of an artery narrows due to the build up 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 greggdev.comcations: Coronary artery disease.

Vessel wall biology, and pathobiology of the blood vessels leading to atherogenesis. Immune mechanisms in vascular inflammation and atherosclerosis.

Lipoprotein interactions with vascular cells and matrix components. Endothelial and smooth muscle cell biology, reactive oxygen/nitrogen species and oxidized lipoproteins on vascular cells.

Keywords:Atherosclerosis, calcium, cardiovascular disease, immune system, inflammation, osteoblasts, vascular endothelium. Abstract:In the beginning, atherosclerosis was considered to be the result of passive lipid accumulation in the vascular walls. After tremendous technological advancements in research, we are now able to almost admire the.

Jan 07,  · With atherosclerosis being the number one cause of death in the western world, this handbook and ready reference provides a comprehensive account of the different stages and factors in the development of the atherosclerotic plaque. Each chapter is written by experts in the field and highlights the role of specific mediators of atherosclerotic plaque development, as well as potential.

Describe and discuss the basic molecular mechanisms that integrate cellular metabolism and the immune response in the context of obesity, metabolic syndrome and atherosclerosis; Describe and discuss novel research on the various forms of cell death, and their pathophysiologic and therapeutic implications.

NIH Center for Scientific Review (CSR) The Atherosclerosis and Inflammation of the Cardiovascular System (AICS) Study Section reviews applications involving inflammation of the vascular system with a focus on the pathobiology of the blood vessels leading to atherogenesis, its reversal and prevention.

Immunology Research Scope. Research in immunology seeks to elucidate the form and function of organismal defense mechanisms. Immunity, defined as a physiological response to foreign agents aimed at maintaining homeostasis, is mediated by a complex array of humoral (e.g., secreted antibodies and complement) and cellular mechanisms which have been traditionally classified under innate or.

38) “Statins seem to act as immune suppressive agents and may have beneficial effects on those who have excessive and/or life threatening immune-inflammatory reactions, such as in transplantations. However, immune suppression may be harmful in those who have no immune/inflammatory disease.”.

This finding is important because it shows that arteriogenesis is the result of a combination of signaling cascades and growth factors as opposed to being tied to a single chemical.

CCL2. MCP1 (now called CCL2) is especially important in arteriogenesis. Since MCP-1 attracts monocytes it can produce an immune cascade to aid inflammation. In this review, we aim to summarize the existing evidence on statins as an anti-inflammatory agent in atherogenesis. We describe the molecular mechanisms responsible for the antiinflammatory effects of statins, as well as clinical data on the non lipid-lowering, anti-inflammatory effects of statins on cardiovascular greggdev.com by:.

Quick access to statistics from the NIH Data Book and annual reports produced by the NIH OER’s Division of Information Services. Effect of antioxidant enzymes on BaP-induced atherogenesis GUO, ZHONGMAO MEHARRY MEDICAL COLLEGE Innate Immune Mechanisms in Chlamydia Pneumoniae Induced Acceleration of Atherosc.Immune theranostics holds promise for realizing technologies that harness the full potential of immunotherapy in the treatment of a wide range of inflammatory disorders.

BACKGROUND. The immune system is a dynamic and highly responsive network of bioactive molecules, cells, and tissues.Inflammation furnishes a series of pathogenic pathways that couple the risk factors for atherosclerosis with altered behavior of the intrinsic cells of the arterial wall, endothelium, and smooth muscle and promote the disease and its complications.

Myeloid cells participate critically in all phases of atherosclerosis from initiation through progression, and ultimately the thrombotic Cited by: