Oxidized low density lipoprotein (ox-LDL), a risk factor of atherosclerosis, facilitates the formation and vulnerability of atherosclerotic plaque, thus contributing to several clinical complications. Stem cells participate in vascular repair after damage and atherosclerosis is a process of inflammation accompanied with vascular injury.
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The oxidative modification hypothesis of atherosclerosis, which assigns to oxidized low-density lipoproteins (LDLs) a crucial role in atherosclerosis initiation and progression, is still debated.
1 Department of Medicine (DIMED), Internal Medicine 4, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. The oxidative modification hypothesis of atherosclerosis, which assigns to oxidized low-density lipoproteins (LDLs) a crucial role in atherosclerosis initiation and progression, is still debated.
Atherosclerosis begins with an injury to the endothelial cells that line the arterial walls. Possible causes of endothelial injury include the common risk factors for atherosclerosis, such as smoking, hypertension, diabetes, increased levels of low-density lipoprotein, decreased levels of high-density lipoprotein, and autoimmunity.
Moreover, oxidized LDL, lysophosphatidyl-choline, and oxidized fatty acids induce the expression not only of these adhesion molecules but also of scavenger receptors, such as CD-36, SR-A, and LOX-1. Recently, we isolated and characterized the novel receptors for oxidized LDL, namely, LOX-1 and SR-PSOX.
A critical event in the early stages of atherosclerosis is the focal accumulation of lipid-laden foam cells derived from macrophages. In various cholesterol-fed animal models of atherosclerosis , localized attachment of circulating monocytes to arterial endothelial cells appeared to precede the formation of foam cells.
In vivo and in vitro experiments have identified molecules, such as ICAM-1, VCAM-1, and P-selectin, that can support the adhesion of monocytes and lymphocytes.
By stimulating the sympathetic nervous system. Angiotensin II is released during myocardial ischemia and contributes to the pathogenesis of a myocardial infarction ( MI) in several ways. First, it results in the systemic effects of peripheral vasoconstriction and fluid retention .
Infective endocarditis is a general term used to describe infection and inflammation of the endocardiumGespecially the cardiac valves. Bacteria are the most common cause of infective endocarditis, especially streptococci, staphylococci, or enterococci.
During the recovery period (10 to 14 days after infarction), individuals feel more capable of increasing activities and thus may stress the newly formed scar tissue. After 6 weeks, the necrotic area is completely replaced by scar tissue, which is strong but unable to contract and relax like healthy myocardial tissue.
Highly sensitive CRP (hs-CRP) is an acute phase reactant or protein mostly synthesized in the liver and, of the available options, is an indirect measure of atherosclerotic plaque-related inflammation.
Because mitral valve prolapse often is associated with other inherited connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta), it is thought to result from a genetic or environmental disruption of valvular development during the fifth or sixth week of gestation.
Inflammation' thrombus formation, and vasospasm can eventually occlude and obliterate portions of small and medium-size arteries. The digital, tibial, and plantar arteries of the feet and the digital, palmar, and ulnar arteries of the hands are typically affected.
Possible causes of endothelial injury include the common risk factors for atherosclerosis, such as smoking, hypertension, diabetes, increased levels of low-density lipoprotein, decreased levels of high-density lipoprotein, and autoimmunity. The remaining options occur only after the endothelial cells are injured.
Neoplastic disorder of the lining of the arteries and veins of the upper extremitie. ANS: A. Buerger disease is an inflammatory disease of the peripheral arteries. Inflammation, thrombus formation, and vasospasm can eventually occlude and obliterate portions of small- and medium-size arteries.
By stimulating the sympathetic nervous system. Angiotensin II is released during myocardial ischemia and contributes to the pathogenesis of a myocardial infarction ( MI) in several ways. First, it results in the systemic effects of peripheral vasoconstriction and fluid retention .
Angiotensin II is also locally released, where it is a growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts; promotes catecholamine release; and causes coronary artery spasm. This selection is the only option that accurately describes how angiotensin II increases workload after a MI.
Of the options available, only amniotic fluid displaces blood, thereby reducing oxygen, nutrients, and waste exchange; however, it also introduces antigens, cells, and protein aggregates that trigger inflammation, coagulation, and the immune response in the bloodstream.
d. Most cholesterol produced by the cells is converted to the low-density form. Although cholesterol can easily be obtained from dietary fat intake, most body cells can also manufacture cholesterol. This selection is the only option that accurately describes the cellular role in cholesterol synthesis.