Published January 1982 by Raven Press .
Written in EnglishRead online
|Contributions||Antonio M., Jr. Gotto (Other Contributor)|
|The Physical Object|
|Number of Pages||164|
Download Atherosclerosis REV
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. Introduction Atherosclerosis. Med Clin Rev.Atherosclerosis has been derived from a Greek word, Athero meaning gruel . Marchand introduced the term “atherosclerosis” describing the assosciation of fatty degeneration and vessel stiffening .
It’s the patchy intramural thickening of Cited by: 5. 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 approaches to arterial and vascular biology and disease, as well as their risk factors including: disturbances of lipid and lipoprotein metabolism, diabetes and.
Rev Port Car diol 19 Law M, Tang JL Atherosclerosis is the leading cause of the cardiovascular disease (CVD). “popular press” books Atherosclerosis REV book peer-reviewed, research articles. Buono C, Binder CJ, Stavrakis G, Witztum JL, Glimcher LH, Lichtman AH.
T-bet deficiency reduces atherosclerosis and alters plaque antigen-specific immune responses. Proc Natl Acad Sci U S A. ;(5)– PubMed PubMedCentral CrossRef Google Scholar.
Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. In westernized societies, it is the underlying cause of about 50% of all deaths.
Epidemiological. [For an excellent review, see Russell Ross: Cell biology of atherosclerosis. Annu. Rev. Physiol. Atherosclerosis is a disease process which is triggered by sometimes subtle physical or chemical insults to the endothelial cell layer of arteries.
The "Response to Injury Theory" now has widespread acceptance among scientific and. Dean Ornish, MD, founder and president of the Preventive Medicine Research Institute, has written six best-selling books, including Dr. Dean Ornish's Program for Reversing Heart Disease. The book was so accessible, I found myself finishing it in a couple of days-then going back to research further some of the intriguing scientific studies it cited.
What an anomaly: a book both readable and scholarly. Now I was persuaded enough to recommend SAM-e to my patients-and even try it myself for arthritis (a very bad thing for an aging.
Atherosclerosis is a word you probably hear a lot more than you care refers to the hardening of your arteries due to a buildup of plaque, which is essentially a combination of “cholesterol, fatty substances, cellular waste products, calcium and fibrin (a clotting material in the blood).” ().
REV-ERBs have been demonstrated to play important roles in regulation of metabolism and immune function [11,18,20–22]. We were particularly intrigued by a recent study demonstrating that hematopoetic knock down of REV-ERBα increases atherosclerosis in LDLR null mice providing clear evidence that REV-ERB plays a role in atherosclerosis.
Carolyn Dean is a medical doctor and naturopath. She’s the author of over 35 books including best seller The Magnesium Miracle along with IBS for Dummies, Hormone Balance, Death by Modern Medicine, and Kindleshe launched RnA ReSet and brought her 50 years of experience into her proprietary, unique formulations that give every individual at any stage of wellness.
Given the results from a recent study demonstrating that genetic REV-ERB deficiency in macrophages exacerbates atherosclerosis, the effect of pharmacologic activation of REV-ERB activity on atherosclerosis was examined in LDL receptor deficient mice were fed a western diet throughout the experiment and were treated with the REV-ERB agonist, SR ( mg/kg, q.d.), or.
A previously characterized synthetic REV-ERB agonist, SR, was used to determine if activation of REV-ERB activity would affect atherosclerosis in LDL receptor deficient mice. Atherosclerotic plaque size was significantly reduced (p.
ﬁeld of atherosclerosis in recent years, under-standing of pathophysiology of atherosclerosis made more and more accessible at lipoprotein metabolic level as well as at inﬂammatory mole-cular level .
Recent understanding of pathogenesis of atherosclerosis (Figure 2) explained it as imbal-anced lipid metabolism integrated with Figure 1.
Atherosclerosis is a chronic inflammatory disease in which an initial endothelial damage leads to deposition and denaturation of lipids in the vessel walls for several years, as shown in Fig. The vascular endothelial cell dysfunction can be caused by various vascular risk factors, such as hypertension, diabetes, and smoking, resulting in increased permeability among the endothelial cells.
Rev. 68(4), – (). Crossref, Medline, Google Scholar 95 Brown AL, Zhu X, Rong S et al. Omega-3 fatty acids ameliorate atherosclerosis by favorably altering monocyte subsets and limiting monocyte recruitment to aortic lesions. Atherosclerosis, characterized by the formation of fat-laden plaques, is a chronic inflammatory disease.
ABCA1 promotes cholesterol efflux, reduces cellular cholesterol accumulation, and regulates. Inthe lead author of this article wrote a book titled: Prevention of Coronary Heart Disease: From the Cholesterol Hypothesis to Omega-6/Omega-3 Balance This book concludes that: • “High blood cholesterol level is not a major causative factor for atherosclerosis”.
A second edition was published in The concept of GAPS has become a global phenomenon and the book has been translated into 20 languages. She is also the author of Put Your Heart in Your Mouth (rev ed. ), and Vegetarianism Explained published in She is also a Member of The Society of Authors, The British Society for Environmental Reviews: Atherosclerotic vascular disease is the underlying cause of myocardial infarction (heart attack), stroke, unstable angina (ischemic heart pain), and sudden cardiac death (Lusis, ).Collectively, these diseases account for the leading cause of death in the world, and the incidence is continuing to rise as a result of the international epidemic of obesity and type 2 diabetes, which are potent.
Atherosclerosis development is a multifactorial process, which is characterized by degenerative changes in the wail of large arteries with subsequent blood vessel occlusion and ischemia of organs and tissues.
Subclinical (asymptomatic) atherosclerosis is a. 50 year old woman with multifocal severe coronary artery vasospasm mistaken for diffuse atherosclerosis (Case Rep Med ;) 70 year old man with congenital coronary fistulae with coronary atherosclerosis (Rev Invest Clin ;) Large atherosclerotic left main coronary aneurysm (Int J Cardiol ;).
Objective The aim of this systematic review and meta-analysis was to provide evidence that biomarkers of large artery atherosclerosis, including arterial stenosis and greater carotid intima-media thickness (cIMT), may serve as clinical markers of subclinical haemorrhage-prone cerebral small vessel disease, reflected by cerebral microbleeds (CMBs).
Methods We searched PubMed, MEDLINE, Web of. Atherosclerosis is the buildup of plaque on the inside walls of arteries. Plaque is made up of low density lipoprotein (LDL), macrophages, smooth muscle cells, platelets, and other substances.
Pathogenic and Regulatory Pathways - Physiol. Rev., Immune function in atherogenesis - J. Lipid Research, Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms Harumi Okuyama Nagoya City University and Institute for Consumer Science and Human Life, Kinjo Gakuin University, Omori, Moriyama, NagoyaJapan Correspondence [email protected] Introduction.
It was a great honor to have been selected by my peers in the ATVB Council to deliver the George Lyman Duff Memorial Lecture at the Scientific Sessions of the American Heart Association in Dallas. Because this award is meant not only to commemorate the many important contributions of Dr Duff to the field of atherosclerosis but also to recognize the career achievements of the.
Atherosclerosis is a biologically active process where vascular risk factors promote vascular endothelial dysfunction, expression of cellular adhesion molecules, and binding of circulating inflammatory cells to the vessel wall.
2 Monocytes transmigrate into the vessel intima, differentiate into pro-inflammatory macrophages and later engulf. Cardiovascular disease is one of the leading causes of death and disability in the world.
Atherosclerosis, characterized by lipid accumulation and chronic inflammation in the vessel wall, is the main feature of cardiovascular disease.
Although the amounts of fruits and vegetables present in the diets vary by country, diets, worldwide, contain large amounts of spices; this may have positive or. Cytokines in atherosclerosis: key players in all stages of disease and promising therapeutic targets.
Cytokine Growth Factor Rev. 26(6), – (). • Describes in detail implication of cytokines in ef, Medline, CAS, Google Scholar; 5.
Buckley ML, Ramji DP. NIH Data Book. Provides basic summary statistics on extramural grants and contract awards. Atherosclerosis NIGMS 1P20GM Identification of Rev-Erb alpha/beta nuclear receptor modulators.
OBJECTIVE —Glycemic control (HbA1c [A1C]) is strongly associated with microvascular disease in individuals with diabetes, but its relation to macrovascular disease and atherosclerosis is less clear.
This study examines the relationship between A1C, carotid intima-media thickness (IMT), and traditional cardiovascular risk factors in individuals with diabetes.
Mean flow predictions obtained from a host of turbulence models were found to be in poor agreement with recent direct numerical simulation results for turbulent flow distal to an idealized eccentric stenosis.
The Lifestyle Heart Trial found that 82% of patients diagnosed with heart disease who followed this plant-based diet program had some level of regression of atherosclerosis and 91% had a reduction in the frequency of angina episodes, whereas 53% of the control group, fed the American Heart Association diet, had progression of atherosclerosis.
The Atherosclerosis Risk in Communities (ARIC) study has been selected for this analysis because (a) these data have already been collected for a large population-based sample with extensive information on dietary intake, (b) the geographic area from which the ARIC population was sampled is diverse with respect to the wealth and racial makeup.
Although inflammation is an important component of atherosclerosis, it is unknown whether inhaled corticosteroids (ICS) as anti-inflammatory drugs prevent atherosclerosis.
In the present study, carotid atherosclerosis was evaluated by ultrasonography in asthmatic patients who had been regularly treated with ICS, and in matched nonasthmatic controls, with an assessment of.
Getting at the root cause of CAD requires a different approach. CAD begins with progressive endothelial injury, 8 inflammatory oxidative stress, diminution of nitric oxide production, foam cell formation, and development of plaques that may rupture to cause a myocardial infarction (MI) or stroke.
9 This cascade is set in motion in part by, and is exacerbated by, the western diet of added oils. The book’s three appendices are focused on two supposedly definitive proofs of the Cholesterol Theory—the Lipid Research Clinics Trial and the Helsinki Heart Study—along with an informative section on how to read a medical journal report.
Curtis’ dismantling of these two studies is masterful, and easily understood by lay readers. Atherosclerosis is a major contributor to many cardiovascular events, including myocardial infarction, ischemic stroke, and peripheral arterial disease, making it the leading cause of death worldwide.
High-density lipoproteins (HDL), also known as “good cholesterol”, have been shown to demonstrate anti-atherosclerotic efficacy through the removal of cholesterol from foam cells in.
The IGF system has repeatedly been suggested to be involved in the pathology of atherosclerosis, and both PAPP-A and IGF-1 are proposed biomarkers and therapeutic targets for this disease. Several experimental approaches based on atherosclerosis mouse models have been undertaken to obtain causative and mechanistic insight to the role of these.
In atherosclerosis, the nature of the antigen(s) responsible for the activation of T cells is still not well understood.
19, 20 For atherosclerosis immunotherapy, DCs obtained from the peripheral blood can be pulsed ex vivo by cultivating them in a medium containing a total extract or. Gofman JW, Glazier F, Tamplin A, et al. Lipoproteins, coronary heart disease and atherosclerosis. Physiol Rev 34(): Gofman JW, Tamplin A, Strisower B.
Relation of fat intake to atherosclerosis. J Am Diet Assoc 30(): Lyon TP, Yankley A, Gofman GW, et al. Lipoproteins and diet in coronary heart disease. A five-year study.Unfortunately, this book can't be printed from the OpenBook.
If you need to print pages from this book, we recommend downloading it as a PDF. Visit to get more information about this book, to buy it in print, or to download it as a free PDF.