Advances in lipoprotein and atherosclerosis researh, diagnostic and treatment

proceedings of the 9th International Dresden Lipid Symposium, held at Dresden, June 27-29, 1997
  • 282 Pages
  • 0.77 MB
  • English
G. Fischer , Jena
Atherosclerosis -- Pathogenesis -- Congresses, Blood lipoproteins -- Congresses, Lipoproteins -- Metabolism -- Congresses, Lipoproteins -- Pathophysiology -- Congr
Statementeditors Markolf Hanefeld ... [et al.]
ContributionsHanefeld, Markolf
LC ClassificationsRC692 .I474 1997
The Physical Object
Pagination282 p. :
ID Numbers
Open LibraryOL18355257M
ISBN 103437310984

Lp(a) is a low-density lipoprotein (LDL)-like particle formed directly in the liver in which apoB is bound to apolipoprotein (a) [apo (a)], which has a homology with plasminogen and thus the potential for explaining the prothrombotic and antifibrinolytic activity.

Like LDL particles, Lp(a) increases atherosclerosis by inflammation and pro. Atherosclerosis is a chronic immune inflammatory disease. Atherosclerosis and relevant disease are threatening human life and health.

Oxygenized low density lipoprotein (oxLDL) is a molecular basis in the pathogenesis of atherosclerosis and able to induce inflammation, stimulate immune system and interfere with lipid metabolism in the occurrence and development of by: 8.

Cholesterol and Lipoprotein Metabolism and Atherosclerosis: Recent Advances In reverse Cholesterol Transport. Wang HH(1), Garruti G(2), Liu M(3), Portincasa P(4), Wang DQ(5). Author information: (1)Department of Medicine, Division of Gastroenterology and Liver Diseases, Marion Bessin Liver Research Center, Albert Einstein College of Medicine Cited by: Elevated serum lipoprotein (a), also referred to as Lp (a), is a risk factor for CVD.

There is a causal relationship between Lp (a) excess and risk for myocardial infarction (MI), stroke, and aortic valve stenosis. (See 'Risk factor versus cause' below.) This topic will review the genetics, structure, and function of Lp (a), as well as its. Role of LPL in lipoprotein bridging and selective CE uptake.

An important facet of potential proatherogenic activity of LPL is linked to its capacity to enhance binding of lipoproteins to cellular receptors, such as LRP, and to heparan sulfate on cell surfaces and extracellular matrix.This subject was dealt with extensively in a recent review ; we shall discuss the aspect of LPL Cited by:   The European Atherosclerosis Society (EAS) was founded in with the aim of “advancing and exchanging knowledge concerning the causes, natural history, treatment.

Lipoprotein(a) is a low-density lipoprotein variant containing a protein called apolipoprotein(a).Genetic and epidemiological studies have identified lipoprotein(a) as a risk factor for atherosclerosis and related diseases, such as coronary heart disease and stroke.

Lipoprotein(a) was discovered Advances in lipoprotein and atherosclerosis researh by Kåre Berg. The human gene encoding apolipoprotein(a) was successfully cloned in Aliases: LPA, AK38, APOA, LP, Lipoprotein(a), Lp(a).

Advances in Experimental Dyslipidemia and Atherosclerosis Article Literature Review (PDF Available) in Laboratory Investigation 81(9) October with Reads How we measure 'reads'. High cholesterol levels lead to clogged arteries, which can ultimately lead to heart disease.

WebMD explains how cholesterol levels - both good and bad - raise the risk of heart attacks and strokes. Elevated plasma levels of the lipoprotein Lp(a) are associated with increased risk for atherosclerosis and its manifestations, myocardial infarction, stroke and restenosis (for reviews, see refs ).

The Lipoprotein and Coronary Atherosclerosis Study (LCAS) was conducted to determine whether lipid-lowering therapy with fluvastatin would reduce the progression or induce the regression of coronary atherosclerotic lesions and/or reduce new lesion formation in patients with CAD and mildly to moderately elevated LDL by: Lipoprotein(a) as a cardiovascular risk factor: current status or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both.

We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a. Atherosclerosis has an open access mirror journal Atherosclerosis: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review.

Atherosclerosis brings together, from all sources, papers concerned with investigation on atherosclerosis, its risk factors and clinical sclerosis covers basic and translational, clinical and population research.

Recent studies confirm and extend previous evidence that lipoprotein[a] (Lp[a]) plays a significant role in atherosclerosis and is one of the top five or six risk factors for cardiovascular disease.

In Japanese patients, Lp[a] levels and apo[a] phenotypes are significant predictors for myocardial infarction. Lp[a] levels are significantly higher in ischemic stroke patients than in by: Atherosclerosis is the underlying cause of most acute coronary syndromes (ACS) such as myocardial infarction and unstable angina, which are major causes of mortality in the Western world.

Histological studies have demonstrated that ACS are triggered by disruption of vulnerable atherosclerotic plaques which results in luminal thrombosis, but. Researchers have identified a new culprit that leads to atherosclerosis, the accumulation of fat and cholesterol that hardens into plaque and narrows arteries.

The research explains why. Lipoprotein(a) Oxidation, Autoimmune and Atherosclerosis, Coronary Artery Disease - New Insights and Novel Approaches, Angelo Squeri, IntechOpen, DOI: / Available from: Jun-Jun Wang (March 16th ).Author: Jun-Jun Wang. Start studying CVP - atherosclerosis, lipid disorders & treatments.

Learn vocabulary, terms, and more with flashcards, games, and other study tools. The lipoprotein that is the major carrier of dietary triglycerides and is not normally visible in a fasting specimen chylomicrons The lipoprotein class involved in the transport of dietary triglycerides,from the small intestine through the circulation to various tissues is.

Lipoprotein(a) [Lp(a)] consists of a low-density lipoprotein (LDL)-like core and apo(a), a large molecular weight glycoprotein.

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Apo(a) is highly homologous to plasminogen, yet in contrast exhibits a unique size polymorphism that is characterized by an increasing number of kringle-IV (K-IV) repeats. The number of K-IV repeats ranges from n = 2 to n = 40 or even : Indumathi Chennamsetty, Gert M. Kostner. The treatment of atherosclerosis using lipid-lowering drugs has evolved markedly over the past decade.

It has been driven by the results and implications of major clinical trials. There has been a paradigm shift in the last decade from stable coronary lesions of high Cited by: 8.

Details Advances in lipoprotein and atherosclerosis researh, diagnostic and treatment FB2

Introduction. Dyslipidemia is a well-established risk factor for the development of coronary artery disease (CAD), and this has been demonstrated in several clinical and epidemiological studies High plasma low-density lipoprotein (LDL-C) concentrations are directly correlated with the development of coronary artery disease 8, and low high-density lipoprotein (HDL-C) concentrations have.

Animal models of atherosclerosis have proven to be an invaluable asset in understanding the pathogenesis of the disease. However, large animal models may be needed in order to assess novel therapeutic approaches to the treatment of atherosclerosis. Porcine models of coronary and peripheral atherosclerosis offer several advantages over rodent models, including similar anatomical size to Cited by: Evidence that elevated lipoprotein(a) (Lp[a]) levels contribute to cardiovascular disease (CVD) and calcific aortic valve stenosis (CAVS) is substantial.

Development of isoform-independent assays, in concert with genetic, epidemiological, translational, and pathophysiological insights, have established Lp(a) as an independent, genetic, and likely causal risk factor for CVD and CAVS. Predict Adult Atherosclerosis?* Stephen R.

Daniels, MD, PHD, FACC Denver, Colorado Since the initial publication of the recommendations of the National Cholesterol Education Program (NCEP) Pediat-ric Panel inthere has been intense interest in and concern about the identification and treatment of lipid and lipoprotein abnormalities in Cited by: 3.

The Lipoproteins and Atherosclerosis laboratory is investigating the body's natural protective mechanism process which removes excess cholesterol from the vessel wall. This mechanism is dependent on two functions, the cells ability to transfer excess cholesterol to the plasma, and the plasma's capacity to receive excess cholesterol from the cells.

saturated fat (Harlan Teklab). Atherosclerosis was studied in off-spring from the same mating at ages indicated in text.

The study protocol was approved by the Institutional Animal Care and Use Committee and all animals received humane treatment according to the criteria stated by the National Academy of Sciences National. Atherosclerosis and the genetic basis of lipoprotein disease Atherosclerosis and the genetic basis of lipoprotein disease Rother, Anne L.; Collard, Charles D.

Atherosclerosis has a multifactorial aetiology, resulting from a complex interaction of genetic and environmental factors.

Description Advances in lipoprotein and atherosclerosis researh, diagnostic and treatment EPUB

Plasma lipoproteins play a central role in atherogenesis. Lipoprotein(a) [Lp(a)] has been considered a cardiovascular risk factor for many years.1 Owing to incomplete scientific evidence, screening for and treatment of high Lp(a) levels have to date been performed principally by lipid specialists.

However, during the last few years, major advances have been achieved in under. Background/Purpose: Patients with various inflammatory rheumatic diseases (IRD) have increased cardiovascular morbidity caused by atherosclerosis.

The aetiology of the accelerated atherosclerosis in IRD is still unclear, but both traditional cardiovascular risk factors and inflammation seem to play a role.

There has been increasing attention to Lipoprotein (a) (LP(a)) as a risk factor for. Lipoprotein(a), a unique and relatively pervasive lipoprotein abnormality, is an independent risk factor for, and causal agent in, cardiovascular disease. It is estimated that 1 in 5 patients, or 63 million Americans, are affected by this atherogenic lipoprotein.

Treatment includes clinically based therapies aimed at managing known risk factors and dramatically lowering LDL cholesterol.The uptake of lipoprotein-bound cholesterol in macrophages occurs through the process of receptor-mediated endocytosis (). The initial event is the binding of the lipoprotein to a cell surface receptor.

Although macrophages express few receptors for normal plasma lipoproteins, they. A new study by researchers in Sweden shows that the immune defense's T cells can attack the "bad" LDL cholesterol and thereby cause an inflammation that .