Atherosclerosis in the context of "Cholesteryl ester"

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Atherosclerosis in the context of Inflammation

Inflammation (from Latin: inflammatio) is part of the biological defence response of body tissues. Inflammatory immunovascular responses can be triggered by a broad range of stimuli, including physical trauma, "dead, damaged, malfunctioning or stressed tissues", pathogens, irritants, toxins, overuse, autoimmunity, allergens, and foreign bodies (e.g. silica and asbestos). The five cardinal signs are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa).

Inflammation is a generic response, and therefore is considered a mechanism of innate immunity, not adaptive immunity. It involves immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out damaged cells and tissues, and initiate tissue repair. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. However, inflammation can also have negative effects. For instance, too much inflammation, in the form of chronic inflammation, is associated with various diseases, such as hay fever, periodontal disease, atherosclerosis, and osteoarthritis.

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Atherosclerosis in the context of Cardiovascular disease

Cardiovascular disease (CVD) is any disease involving the heart or blood vessels. CVDs constitute a class of diseases that includes: coronary artery diseases (e.g. angina, heart attack), heart failure, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, arrhythmia, congenital heart disease, valvular heart disease, carditis, aortic aneurysms, peripheral artery disease, thromboembolic disease, and venous thrombosis.

The underlying mechanisms vary depending on the disease. It is estimated that dietary risk factors are associated with 53% of CVD deaths. Coronary artery disease, stroke, and peripheral artery disease involve atherosclerosis. This may be caused by high blood pressure, smoking, diabetes mellitus, lack of exercise, obesity, high blood cholesterol, poor diet, excessive alcohol consumption, and poor sleep, among other things. High blood pressure is estimated to account for approximately 13% of CVD deaths, while tobacco accounts for 9%, diabetes 6%, lack of exercise 6%, and obesity 5%. Rheumatic heart disease may follow untreated strep throat.

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Atherosclerosis in the context of Lifestyle disease

Lifestyle diseases can be defined as the diseases linked to the manner in which a person lives their life. These diseases are non-communicable, and can be caused by lack of physical activity, unhealthy eating, alcohol, substance use disorders and smoking tobacco, which can lead to heart disease, stroke, obesity, type II diabetes and lung cancer. The diseases that appear to increase in frequency as countries become more industrialized and people live longer include Alzheimer's disease, arthritis, atherosclerosis, asthma, cancer, chronic liver disease or cirrhosis, chronic obstructive pulmonary disease, colitis, irritable bowel syndrome, type 2 diabetes, heart disease, hypertension, metabolic syndrome, chronic kidney failure, osteoporosis, PCOD, stroke, depression, obesity and vascular dementia.

Concerns were raised in 2011 that lifestyle diseases could soon have an impact on the workforce and the cost of health care. Treating these non-communicable diseases can be expensive. It can be critical for the patient's health to receive primary prevention and identify early symptoms of these non-communicable diseases. These lifestyle diseases are expected to increase throughout the years if people do not improve their lifestyle choices.

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Atherosclerosis in the context of Drug class

A drug class is a group of medications and other compounds that share similar chemical structures, act through the same mechanism of action (i.e., binding to the same biological target), have similar modes of action, and/or are used to treat similar diseases. The FDA has long worked to classify and license new medications. Its Drug Evaluation and Research Center categorizes these medications based on both their chemical and therapeutic classes.

In several major drug classification systems, these four types of classifications are organized into a hierarchy. For example, fibrates are a chemical class of drugs (amphipathic carboxylic acids) that share the same mechanism of action (PPAR agonist), the same mode of action (reducing blood triglyceride levels), and are used to prevent and treat the same disease (atherosclerosis). However, not all PPAR agonists are fibrates, not all triglyceride-lowering agents are PPAR agonists, and not all drugs used to treat atherosclerosis lower triglycerides.A drug class is typically defined by a prototype drug, the most important, and typically the first developed drug within the class, used as a reference for comparison.

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Atherosclerosis in the context of Visceral fat

Adipose tissue (also known as body fat or simply fat) is a loose connective tissue composed mostly of adipocytes. It also contains the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body.

Previously treated as being hormonally inert, in recent years adipose tissue has been recognized as a major endocrine organ, as it produces hormones such as leptin, estrogen, resistin, and cytokines (especially TNFα). In obesity, adipose tissue is implicated in the chronic release of pro-inflammatory markers known as adipokines, which are responsible for the development of metabolic syndrome—a constellation of diseases including type 2 diabetes, cardiovascular disease and atherosclerosis.

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Atherosclerosis in the context of Small vessel disease

Microangiopathy (also known as microvascular disease, small vessel disease (SVD) or microvascular dysfunction) is a disease of the microvessels, small blood vessels in the microcirculation. It can be contrasted to macroangiopathies such as atherosclerosis, where large and medium-sized arteries (e.g., aorta, carotid and coronary arteries) are primarily affected.

Small vessel diseases (SVDs) affect primarily organs that receive significant portions of cardiac output such as the brain, the kidney, and the retina. Thus, SVDs are a major etiologic cause in debilitating conditions such as renal failure, blindness, lacunar infarcts, and dementia.

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Atherosclerosis in the context of Oxidative stress

Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by the reactive oxygen species generated, e.g., O
2
(superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide). Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling.

In humans, oxidative stress is thought to be involved in the development of cancer, Parkinson's disease, Lafora disease, Alzheimer's disease, atherosclerosis, heart failure, myocardial infarction, fragile X syndrome, sickle-cell disease, lichen planus, vitiligo, infection, chronic fatigue syndrome, and depression; however, reactive oxygen species can be beneficial, as they are used by the immune system as a way to attack and kill pathogens. Oxidative stress due to noise was estimated at cell level using model of growing lymphocytes. Exposure of sound with frequency 1 KHz and intensity 110 dBA for 4 hours and eight hours per day may induce oxidative stress in growing lymphocytes causing the difference in viable cell count. However the catalase activity depends on duration of exposure. In case of noise exposure of 8 hours per day, it declines significantly as compared to noise exposure of 4 hours per day.

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