Low-density lipoprotein is one of the five major groups of lipoprotein which transport all fat molecules around the body in the extracellular water. These groups, from least dense, compared to surrounding water to most dense, are chylomicrons low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein and high-density lipoprotein. LDL delivers fat molecules to the cells and can drive the progression of atherosclerosis if they become oxidized within the walls of arteries, it is important to note that LDL is not "bad cholesterol". LDL is not cholesterol at all, not bad, it is an essential transport system for lipids the human body needs to survive, including cholesterol. There is both "large" and "small" particle LDL, while only small is associated with cholesterol-related issues, neither is "bad". "small" LDL is necessary to conduct nutrients to vessels that "large" LDL can't reach. Lipoproteins transfer lipids around the body in the extracellular fluid, making fats available to body cells for receptor-mediated endocytosis.
Lipoproteins are complex particles composed of multiple proteins 80–100 proteins/particle. A single LDL particle is about 220–275 angstroms in diameter transporting 3,000 to 6,000 fat molecules/particle, varying in size according to the number and mix of fat molecules contained within; the lipids carried include all fat molecules with cholesterol and triglycerides dominant. For years, it was believed that LDL particles posed a risk for cardiovascular disease when they invaded the endothelium and became oxidized, since the oxidized forms would be more retained by the proteoglycans, but there is growing evidence that this belief was supported by bad methodology, that there is no actual correlation between LDL and heart disease. A complex set of biochemical reactions regulates the oxidation of LDL particles, chiefly stimulated by presence of necrotic cell debris and free radicals in the endothelium. Increased concentrations of LDL particles is associated with the development of atherosclerosis over time.
Each native LDL particle enables emulsification, i.e. surrounding/packaging all fatty acids being carried, enabling these fats to move around the body within the water outside cells. Each particle contains a single apolipoprotein B-100 molecule, along with 80 to 100 additional ancillary proteins; each LDL has a hydrophobic core consisting of polyunsaturated fatty acid known as linoleate and hundreds to thousands esterified and unesterified cholesterol molecules. This core carries varying numbers of triglycerides and other fats and is surrounded by a shell of phospholipids and unesterified cholesterol, as well as the single copy of Apo B-100. LDL particles are 22 nm to 27.5 nm in diameter and have a mass of about 3 million daltons. Since LDL particles contain a variable and changing number of fatty acid molecules, there is a distribution of LDL particle mass and size. Determining the structure of LDL has been a tough task because of its heterogeneous structure; the structure of LDL at human body temperature in native condition, with a resolution of about 16 Angstroms using cryogenic electron microscopy, has been described.
LDL particles are formed as VLDL lose triglyceride through the action of lipoprotein lipase and they become smaller and denser, containing a higher proportion of cholesterol esters. When a cell requires additional cholesterol, it synthesizes the necessary LDL receptors as well as PCSK9, a proprotein convertase that marks the LDL receptor for degradation. LDL receptors are inserted into the plasma membrane and diffuse until they associate with clathrin-coated pits; when LDL receptors bind LDL particles in the bloodstream, the clathrin-coated pits are endocytosed into the cell. Vesicles containing LDL receptors bound to LDL are delivered to the endosome. In the presence of low pH, such as that found in the endosome, LDL receptors undergo a conformation change, releasing LDL. LDL is shipped to the lysosome, where cholesterol esters in the LDL are hydrolysed. LDL receptors are returned to the plasma membrane, where they repeat this cycle. If LDL receptors bind to PCSK9, transport of LDL receptors is redirected to the lysosome, where they are degraded.
LDL interfere with the quorum sensing system that upregulates genes required for invasive Staphylococcus aureus infection. The mechanism of antagonism entails binding Apolipoprotein B to a S. aureus autoinducer pheromone, preventing signaling through its receptor. Mice deficient in apolipoprotein B are more susceptible to invasive bacterial infection. LDL can be grouped based on its size: large low density LDL particles are described as pattern A, small high density LDL particles are pattern B. Pattern B has been associated by some with a higher risk for coronary heart disease; this is thought to be because the smaller particles are more able to penetrate the endothelium of arterial walls. Pattern I, for intermediate, indicates that most LDL particles are close in size to the normal gaps in the endothelium. According to one study, sizes 19.0–20.5 nm were designated as pattern B and LDL sizes 20.6–22 nm were designated as pattern A. Other studies have shown no such correlation at all; some evidence suggests the correlation between Pat
A dressing is a sterile pad or compress applied to a wound to promote healing and protect the wound from further harm. A dressing is designed to be in direct contact with the wound, as distinguished from a bandage, most used to hold a dressing in place. Many modern dressings are self-adhesive. A dressing can have a number of purposes, depending on the type and position of the wound, although all purposes are focused towards promoting recovery and protecting from further harm. Key purposes of a dressing are: Stem bleeding – to help to seal the wound to expedite the clotting process; the aim of a dressing is to promote healing of the wound by providing a sterile and moist environment that facilitates granulation and epithelialization. This will reduce the risk of infection, help the wound heal more and reduce scarring. Dressings were made of a piece of material a cloth, but the use of cobwebs, dung and honey have been described. However, modern dressings include dry or impregnated gauze, plastic films, foams, alginates and polysaccharide pastes and beads.
They all provide different physical environments suited to different wounds: Absorption of exudate, to regulate the moisture level surrounding the wound- for example, dry gauzes absorb exudate drying the wound, hydrocolloids maintain a moist environment and film dressings do not absorb exudate. Pressure dressings are used to treat burns and after skin grafts, they prevent fluids from collecting in the tissue. Dressings can regulate the chemical environment of a wound with the aim of preventing infection by the impregnation of topical antiseptic chemicals. Used antiseptics include povidone-iodine, boracic lint dressings or castor oil. Antibiotics are often used with dressings to prevent bacterial infection. Medical grade honey is another antiseptic option, there is moderate evidence that honey dressings are more effective than common antiseptic and gauze for healing infected post-operative wounds. Bioelectric dressings can be effective in attacking certain antibiotic-resistant bacteria and speeding up the healing process.
Dressings are often impregnated with analgesics to reduce pain. The physical features of a dressing can impact the efficacy of such topical medications. Occlusive dressings, made from substances impervious to moisture such as plastic or latex, can be used to increase their rate of absorption into the skin. Dressings are secured with adhesive tape and/or a bandage. Many dressings today are produced as an "island" surrounded by an adhesive backing, ready for immediate application – these are known as island dressings; these products are indicated for only superifical and dry wounds with minimal exudates. They can be used as secondary dressings. Examples are: Gauze, adhesive bandage, cotton wool; the main aim is to protect the wound from bacterial contamination. They are used for secondary dressing. Gauze dressing is made up of woven or non-woven fibres of cotton and polyester. Gauze dressing requires frequent changing. Excessive wound discharge would cause the gauze to adhere to the wound, thus causes pain when trying to remove the gauze from the wound.
Bandages are made up of cellulose, or polyamide materials. Cotton bandages can act as a secondary dressing while compression bandages provides good compressions for venous ulcers. On the other hand, tulle gras dressing, impregnated with paraffin oil is indicated for superficial clean wound. Several types of interactive products are: semi-permeable film dressings, semi-permeable foam dressings, hydrogel dressings, hydrocolloid dressings, alginate dressings. Apart from preventing bacteria contamination of the wound, they keep the wound environment moist in order to promote healing. Semi-permeable film dressing - This dressing is a transparent film made up of polyurethane, it allows the movement of water vapor and carbon dioxide into and out of the dressing. It plays an additional role in autolytic debridement, less painful when compared to manual wound debridement inside the operating theater, it is elastic and flexible, thus is adhered to the skin. As the dressing is transparent, wound inspection is possible without removing the dressing.
Due to the limited absorption capacity, such dressing is only used in superficial wounds with low amount of discharge. Semi-permeable foam dressing- This dressing is made up of foam with hydrophilic properties and outer layer of hydrophobic properties with adhesive borders; the hydrophobic layer protects the wound from the outside fluid contamination. Meanwhile, the inner hydrophilic layer is able to absorb moderate amount of discharge from the wound. Therefore
A capillary is a small blood vessel from 5 to 10 micrometres in diameter, having a wall one endothelial cell thick. They are the smallest blood vessels in the body: they convey blood between the arterioles and venules; these microvessels are the site of exchange of many substances with the interstitial fluid surrounding them. Substances which exit include water and glucose. Lymph capillaries connect with larger lymph vessels to drain lymphatic fluid collected in the microcirculation. During early embryonic development new capillaries are formed through vasculogenesis, the process of blood vessel formation that occurs through a de novo production of endothelial cells which form vascular tubes; the term angiogenesis denotes the formation of new capillaries from pre-existing blood vessels and present endothelium which divides. Blood flows from the heart through arteries, which branch and narrow into arterioles, branch further into capillaries where nutrients and wastes are exchanged; the capillaries join and widen to become venules, which in turn widen and converge to become veins, which return blood back to the heart through the venae cavae.
Individual capillaries are part of the capillary bed, an interweaving network of capillaries supplying tissues and organs. The more metabolically active a tissue is, the more capillaries are required to supply nutrients and carry away waste products. There are two types of capillaries: true capillaries, which branch from arterioles and provide exchange between tissue and the capillary blood, metarterioles, found only in the mesenteric circulation, they are short vessels that directly connect the arterioles and venules at opposite ends of the beds. Metarterioles are found in the mesenteric microcirculation; the physiological mechanisms underlying precapillary resistance is no longer considered to be a result of precapillary sphincters outside of the mesentery organ. Lymphatic capillaries are larger in diameter than blood capillaries, have closed ends; this structure permits interstitial fluid to flow into them but not out. Lymph capillaries have a greater internal oncotic pressure than blood capillaries, due to the greater concentration of plasma proteins in the lymph.
There are three types of blood capillaries: Continuous capillaries are continuous in the sense that the endothelial cells provide an uninterrupted lining, they only allow smaller molecules, such as water and ions to pass through their intercellular clefts. Lipid-soluble molecules can passively diffuse through the endothelial cell membranes along concentration gradients. Continuous capillaries can be further divided into two subtypes: Those with numerous transport vesicles, which are found in skeletal muscles, fingers and skin; those with few vesicles, which are found in the central nervous system. These capillaries are a constituent of the blood–brain barrier. Fenestrated capillaries have pores in the endothelial cells that are spanned by a diaphragm of radially oriented fibrils and allow small molecules and limited amounts of protein to diffuse. In the renal glomerulus there are cells with no diaphragms, called podocyte foot processes or pedicels, which have slit pores with a function analogous to the diaphragm of the capillaries.
Both of these types of blood vessels have continuous basal laminae and are located in the endocrine glands, intestines and the glomeruli of the kidney. Sinusoid capillaries are a special type of open-pore capillary, that have larger openings in the endothelium; these types of blood vessels allow red and white blood cells and various serum proteins to pass, aided by a discontinuous basal lamina. These capillaries lack pinocytotic vesicles, therefore utilize gaps present in cell junctions to permit transfer between endothelial cells, hence across the membrane. Sinusoid blood vessels are located in the bone marrow, lymph nodes, adrenal glands; some sinusoids are distinctive in. They are called discontinuous sinusoidal capillaries, are present in the liver and spleen, where greater movement of cells and materials is necessary. A capillary wall is simple squamous epithelium; the capillary wall performs an important function by allowing nutrients and waste substances to pass across it. Molecules larger than 3 nm such as albumin and other large proteins pass through transcellular transport carried inside vesicles, a process which requires them to go through the cells that form the wall.
Molecules smaller than 3 nm such as water and gases cross the capillary wall through the space between cells in a process known as paracellular transport. These transport mechanisms allow bidirectional exchange of substances depending on osmotic gradients and can be further quantified by the Starling equation. Capillaries that form part of the blood–brain barrier however only allow for transcellular transport as tight junctions between endothelial cells seal the paracellular space. Capillary beds may control their blood flow via autoregulation; this allows an organ to maintain constant flow despite a change in central blood pressure. This is achieved by myogenic response, in the kidney by tubuloglomerular feedback; when blood pressure increases, arterioles are stretched and subsequently constrict to counteract the
Cholesterol is an organic molecule. It is a type of lipid. Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell membranes. Cholesterol serves as a precursor for the biosynthesis of steroid hormones, bile acid and vitamin D. Cholesterol is the principal sterol synthesized by all animals. In vertebrates, hepatic cells produce the greatest amounts, it is absent among prokaryotes, although there are some exceptions, such as Mycoplasma, which require cholesterol for growth. François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. However, it was not until 1815 that chemist Michel Eugène Chevreul named the compound "cholesterine". There is only one kind of cholesterol. There is no "good cholesterol" or "bad cholesterol"; the system that transports cholesterol where it is needed in the human body uses LDL and HDL to do so. Those are proteins, not lipids like cholesterol, neither of them are "bad", both are necessary to human health.
Cholesterol is essential for all animal life, with each cell capable of synthesizing it by way of a complex 37-step process. This begins with the mevalonate or HMG-CoA reductase pathway, the target of statin drugs, which encompasses the first 18 steps; this is followed by 19 additional steps to convert the resulting lanosterol into cholesterol. A human male weighing 68 kg synthesizes about 1 gram of cholesterol per day, his body contains about 35 g contained within the cell membranes. Typical daily cholesterol dietary intake for a man in the United States is 307 mg. Most ingested cholesterol is esterified; the body compensates for absorption of ingested cholesterol by reducing its own cholesterol synthesis. For these reasons, cholesterol in food, seven to ten hours after ingestion, has little, if any effect on concentrations of cholesterol in the blood. However, during the first seven hours after ingestion of cholesterol, as absorbed fats are being distributed around the body within extracellular water by the various lipoproteins, the concentrations increase.
Cholesterol is recycled in the body. The liver excretes it in a non-esterified form into the digestive tract. About 50% of the excreted cholesterol is reabsorbed by the small intestine back into the bloodstream. Plants make cholesterol in small amounts. Plants manufacture phytosterols, which can compete with cholesterol for reabsorption in the intestinal tract, thus reducing cholesterol reabsorption; when intestinal lining cells absorb phytosterols, in place of cholesterol, they excrete the phytosterol molecules back into the GI tract, an important protective mechanism. The intake of occurring phytosterols, which encompass plant sterols and stanols, ranges between ~200–300 mg/day depending on eating habits. Specially designed vegetarian experimental diets have been produced yielding upwards of 700 mg/day. Cholesterol, given that it composes about 30% of all animal cell membranes, is required to build and maintain membranes and modulates membrane fluidity over the range of physiological temperatures.
The hydroxyl group of each cholesterol molecule interacts with the water molecules surrounding the membrane as do the polar heads of the membrane phospholipids and sphingolipids, while the bulky steroid and the hydrocarbon chain are embedded in the membrane, alongside the nonpolar fatty-acid chain of the other lipids. Through the interaction with the phospholipid fatty-acid chains, cholesterol increases membrane packing, which both alters membrane fluidity and maintains membrane integrity so that animal cells do not need to build cell walls; the membrane remains stable and durable without being rigid, allowing animal cells to change shape and animals to move. The structure of the tetracyclic ring of cholesterol contributes to the fluidity of the cell membrane, as the molecule is in a trans conformation making all but the side chain of cholesterol rigid and planar. In this structural role, cholesterol reduces the permeability of the plasma membrane to neutral solutes, hydrogen ions, sodium ions.
Within the cell membrane, cholesterol functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits, including caveola-dependent and clathrin-dependent endocytosis; the role of cholesterol in endocytosis of these types can be investigated by using methyl beta cyclodextrin to remove cholesterol from the plasma membrane. Recent studies show that cholesterol is implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane, which brings receptor proteins in close proximity with high concentrations of second messenger molecules. In multiple layers and phospholipids, both electrical insulators, can facilitate speed of transmission of electrical impulses along nerve tissue. For many neuron fibers, a myelin sheath, rich in cholesterol since it is derived from compacted layers of Schwann cell membrane, provides insulation for more efficient conduction of impulses.
Demyelination is believed to be part of the basis for multiple sclerosis. Within cells, cholesterol is a precursor molecule for several biochemical pathways. For example, it is the precursor molecule for the synthesis of vitamin D and all steroid hormones, including the adrenal gland ho
Compression stockings are a specialized hosiery designed to help prevent the occurrence of, guard against further progression of, venous disorders such as edema and thrombosis. Compression stockings are elastic garments worn around the leg; this reduces the diameter of distended veins and increases venous blood flow velocity and valve effectiveness. Compression therapy helps decrease venous pressure, prevents venous stasis and impairments of venous walls, relieves heavy and aching legs. Knee-high compression stockings are used not only to help increase circulation, but to help prevent the formation of blood clots in the lower legs, they aid in the treatment of ulcers of the lower legs. Unlike traditional dress or athletic stockings and socks, compression stockings use stronger elastics to create significant pressure on the legs and feet. Compression stockings are tightest at the ankles and become less constrictive toward the knees and thighs. By compressing the surface veins and muscles, they force circulating blood through narrower channels.
As a result, the arterial pressure is increased, which causes more blood to return to the heart and less blood to pool in the feet. There are two types of compression stockings and anti-embolism. Treatment is prescribed by a physician to relieve all manifestations of chronic venous disease and prevent venous troubles. Compression stockings are recommended under the following conditions: Edema is a condition where the opposing forces that occur in the small blood vessels and capillaries cause a net ultrafiltration of plasma water into the soft tissues. Chronic peripheral venous insufficiency is when the veins cannot pump deoxygenated blood back to the heart. Varicose veins are saccular and distended veins which can expand and may cause painful venous inflammation. Once developed, they will not disappear on their own; the formation of varicose veins is an externally visible sign of venous weakness. Deep vein thrombosis occurs when blood flow decreases, causing blood to pool in the legs and leading to blood clot formation.
Evidence does not suggest a benefit in post thrombotic syndrome rates following DVT. Compression stockings are beneficial in reducing symptomless deep vein thrombosis among airline passengers flying for 7 hours or more. Pharmacological and mechanical measures are used to prevent venous thromboembolism in clinical practice. For cases in which the bleeding risk is high and pharmacologic measures are contraindicated, the use of mechanical prophylaxis is recommended. Graduated compression stockings can prevent VTE in hospitalized patients by applying different pressure to the leg; the meta-analysis of general surgical patients revealed that graduated compression stockings decreased their risk of developing VTE by 68% compared to placebo. Nineteen randomized controlled trials analyzed the effectiveness of graduated compression stockings alone or with other additional prophylaxis in prevention of deep vein thrombosis; these trials included 1681 patients after general surgery, orthopedic surgery, medical patients.
They concluded that graduated compression stockings are effective in deep vein thrombosis prophylaxis in post-surgical patients. Combining graduated compression stockings with other mechanical and pharmacological measures can increase the effectiveness of VTE prophylaxis by 60%. However, another study performed in France involved 407 ICU patients and showed no difference in the effectiveness of the VTE prevention for patients who used compression stockings alone or in combination with intermittent pneumatic devices. Lymphedema occurs when a body part swells due to an abnormal accumulation of lymph fluid, occurring when there is interference with the normal drainage of lymph fluid back into the blood swelling the arm, neck or abdomen. Phlebitis is the term used when inflammation and clotting occurs in a vein, most a leg vein, due to infection, inflammation, or trauma. People with varicose veins are more affected. Inflammation occurs causing the thrombus to adhere to the vein wall and risking clogging a superficial vein.
Lipodermatosclerosis is the term used to refer to the inflammation of subcutaneous fat, a form of panniculitis. Hormones released during pregnancy and the expanding uterus can affect leg veins; the use of elastic compression stockings can reduce volumetric variations during standing hours. The use of stockings for the entire day is more effective than just half the day or not using compression stockings at all. Many physicians and vein specialists recommend wearing compression stockings after varicose vein stripping, but studies show that wearing an elastic compression stocking has no additional benefit after the application of elastic bandaging for three days in post-operative care following the stripping of the great saphenous vein as assessed by control of limb, pain and return to work. Caution should be used in those with advanced peripheral obstructive arterial disease, heart failure, septic phlebitis, oozing dermatitis and advanced peripheral neuropathy in regard to wearing compression stockings.
In the clinical setting the applying of the antiembolism stockings is performed by physicians and other trained personnel. First the proper size stocking is determined by measuring the legs. Aseptic technique is not necessary; the person is placed in the supine position in bed for fifteen minutes prior
Foam cells are the fat-laden M2 macrophages that serve as the hallmark of early stage atherosclerotic lesion formation. As these plaques mature, they become more inflamed. Foam cell formation is triggered by a number of factors including the uncontrolled uptake of modified low density lipoproteins, the upregulation of cholesterol esterification and the impairment of mechanisms associated with cholesterol release. Foam cells are formed when circulating monocyte-derived cells are recruited to the atherosclerotic lesion site or fat deposits in the blood vessel walls. Recruitment is facilitated by the molecules P-selectin and E-selectin, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1. Monocytes are able to penetrate the arterial wall as a result of impaired endothelial integrity which increases permeability. Once in the sub endothelium space, inflammation processes induce the differentiation of monocytes into mature macrophages. Macrophages are able to internalize modified lipoproteins like βVLDL, AcLDL and OxLDL through their binding to the scavenger receptors such as CD36 and SR-A on the macrophage surface.
These scavenger receptors act as "Pattern recognition receptors" on macrophages and are responsible for recognizing and binding to oxLDL, which in turn promotes the formation of foam cells through internalization of these lipoproteins. Coated-pit endocytosis and pinocytosis are responsible for lipoprotein internalization. Once internalized, scavenged lipoproteins are transported to endosomes or lysosomes for degradation, whereby the cholesteryl esters are hydrolyzed to unesterified free cholesterol by lysosomal acid lipase. Free cholesterol is transported to the endoplasmic reticulum where it is re-esterified by ACAT1 and subsequently stored as cytoplasmic liquid droplets; these droplets are responsible for the foamy appearance of the macrophage and thus the name of foam cells. At this point, foam cells can either be degraded though the de-esterification and secretion of cholesterol, or can further promote foam cell development and plaque formation – a process, dependent on the balance of free cholesterol and esterified cholesterol.
Low-density lipoprotein cholesterol and modified forms of LDL cholesterol such as oxidized, glycated, or acetylated LDL, is contained by a foam cell - a marker of atherosclerosis. The uptake of LDL-C alone does not cause foam cell formation. Modified LDL affects the intracellular trafficking and metabolism of native LDL, such that not all LDL need to be modified for foam cell formation when LDL levels are high. Foam cell degradation or more the breakdown of esterified cholesterols, is facilitated by a number of efflux receptors and pathways. Esterified cholesterol from cytoplasmic liquid droplets are once again hydrolyzed to free cholesterol by acid cholesterol esterase. Free cholesterol can be secreted from the macrophage by the efflux to ApoA1 and ApoE discs via the ABCA1 receptor; this pathway is used by modified or pathological lipoproteins like AcLDL, OxLDL and βVLDL. FC can be transported to a recycling compartment through the efflux to ApoA1 containing HDLs via aqueous diffusion or transport through the SR-B1 or ABCG1 receptors.
While this pathway can be used by modified lipoproteins, LDL derived cholesterol can only use this pathway to excrete FC. The differences in excretory pathways between types of lipoproteins is a result of the cholesterol being segregated into different areas; the maintenance of foam cells and the subsequent progression of plaque build-up is caused by the secretion of chemokines and cytokines from macrophages and foam cells. Foam cells secrete pro-inflammatory cytokines such as interleukins: IL-1, IL-6. Macrophages within the atherosclerotic legion area have a decreased ability to migrate, which further promotes plaque formation as they are able to secrete cytokines, reactive oxygen species and growth factors that stimulate modified lipoprotein uptake and vascular smooth muscle cell proliferation. VSMC can accumulate cholesteryl esters. To summarize, in chronic hyperlipidemia, lipoproteins aggregate within the intima of blood vessels and become oxidized by the action of oxygen free radicals generated either by macrophages or endothelial cells.
The macrophages engulf oxidized low-density lipoproteins by endocytosis via scavenger receptors, which are distinct from LDL receptors. The oxidized LDL accumulates in the macrophages and other phagocytes, which are known as foam cells. Foam cells form the fatty streaks of the plaques of atheroma in the tunica intima of arteries. Foam cells are not dangerous as such, but can become a problem when they accumulate at particular foci thus creating a necrotic centre of atherosclerosis. If the fibrous cap that prevents the necrotic centre from spilling into the lumen of a vessel ruptures, a thrombus can form which can lead to emboli occluding smaller vessels; the occlusion of small vessels results in ischemia, contributes to stroke and myocardial infarction, two of the leading causes of cardiovascular-related death. Foam cells are small in size and can only be detected by examining a fatty
John Hunter (surgeon)
John Hunter was a Scottish surgeon, one of the most distinguished scientists and surgeons of his day. He was scientific method in medicine, he was a teacher of, collaborator with, Edward Jenner, pioneer of the smallpox vaccine. He is alleged to have paid for the stolen body of Charles Byrne, proceeded to study and exhibit it against the deceased's explicit wishes, his wife, Anne Hunter, was some of whose poems were set to music by Joseph Haydn. He learned anatomy by assisting his elder brother William with dissections in William's anatomy school in Central London, starting in 1748, became an expert in anatomy, he spent some years as an Army surgeon, worked with the dentist James Spence conducting tooth transplants, in 1764 set up his own anatomy school in London. He built up a collection of living animals whose skeletons and other organs he prepared as anatomical specimens amassing nearly 14,000 preparations demonstrating the anatomy of humans and other vertebrates, included 3,000+ animals. Hunter became a Fellow of the Royal Society in 1767.
The Hunterian Society of London was named in his honour, the Hunterian Museum at the Royal College of Surgeons preserves his name and his collection of anatomical specimens. It still contains the illegally procured body of Charles Byrne, despite ongoing protests. Hunter was born at the youngest of ten children; the exact date of his birth is uncertain. Family papers cite his birthday as being variously on 9 February. Three of Hunter's siblings died of illness. An elder brother was the anatomist; as a youth, John showed little talent, helped his brother-in-law as a cabinet-maker. When nearly 21 he visited William in London, where his brother had become an admired teacher of anatomy. John started as his assistant in dissections, was soon running the practical classes on his own, it has been alleged that Hunter's brother William, his brother's former tutor William Smellie, were responsible for the deaths of many women whose corpses were used for their studies on pregnancy. John is alleged to have been connected to these deaths, since at the time he was acting as William's assistant.
However, persons who have studied life in Georgian London agree that the number of gravid women who died in London during the years of Hunter's and Smellie's work was not high for that locality and time. In The Anatomy of the Gravid Uterus Exhibited in Figures, published in 1774, Hunter provides case histories for at least four of the subjects illustrated. Hunter researched blood while bloodletting patients with various diseases; this helped him develop his theory that inflammation was a bodily response to disease, was not itself pathological. Hunter studied under William Cheselden at Chelsea Hospital and Percival Pott at St. Bartholomew's Hospital. Hunter studied with Marie Marguerite Bihéron, a famous anatomist and wax modeler teaching in London. After qualifying, he became assistant surgeon at St George's surgeon. Hunter was commissioned as an Army surgeon in 1760 and was staff surgeon on expedition to the French island of Belle Île in 1761 served in 1762 with the British Army. Contrary to prevailing medical opinion at the time, Hunter was against the practice of'dilation' of gunshot wounds.
This practice involved the surgeon deliberately expanding a wound with the aim of making the gunpowder easier to remove. Although sound in theory, in the unsanitary conditions of the time it increased the chance of infection, Hunter's practice was not to perform dilation'except when preparatory to something else' such as the removal of bone fragments. Hunter left the Army in 1763, spent at least five years working in partnership with James Spence, a well-known London dentist. Although not the first person to conduct tooth transplants between living people, he did advance the state of knowledge in this area by realising that the chances of a successful tooth transplant would be improved if the donor tooth was as fresh as possible and was matched for size with the recipient; these principles are still used in the transplanation of internal organs. Although donated teeth never properly bonded with the recipients' gums, one of Hunter's patients stated that he had three which lasted for six years, a remarkable period at the time.
Hunter started in private surgical practice. In 1765, Hunter bought a house near the Earl's Court district in London; the house had large grounds which were used to house a collection of animals including'zebra, Asiatic buffaloes and mountain goats', as well as jackals. In the house itself, Hunter boiled down the skeletons of some of these animals as part of research on animal anatomy. A newspaper article reported that many animals there were'supposed to be hostile to each other but... in this new paradise, the greatest friendship prevails', this image may have been the inspiration for the Doctor Dolittle literary character. Hunter was elected as Fellow of the Royal Society in 1