Sir James Paget, 1st Baronet FRS HFRSE was an English surgeon and pathologist, best remembered for naming Paget's disease and, considered, together with Rudolf Virchow, as one of the founders of scientific medical pathology. His famous works included Lectures on Lectures on Surgical Pathology. There are several medical conditions which were described and named after Paget: Paget's disease of bone Paget's disease of the nipple Extramammary Paget's disease refers to a group of similar, more rare skin lesions discovered by Radcliffe Crocker in 1889 which affect the male and female genitalia. Paget–Schroetter disease Paget's abscess, an abscess that recurs at the site of a former abscess which had resolved. Paget was born in Great Yarmouth, England, on 11 January 1814, the son of Samuel Paget, a brewer and shipowner, his wife, Sarah Elizabeth Tolver, he was one of a large family, his brother Sir George Edward Paget, who became Regius Professor of Physic at the University of Cambridge in 1872 had a distinguished career in medicine and was made a K.
C. B.. James attended a day-school in Yarmouth, afterwards was destined for the navy. At the end of his apprenticeship, he published with one of his brothers a careful Sketch of the Natural History of Yarmouth and its Neighbourhood. In October 1834, he entered as a student in London. Here he is noted to have described the first journal club. Medical students in those days were left much to themselves, he swept the board of prizes in 1835, again in 1836. In May 1836, he passed his examination at the Royal College of Surgeons, became qualified to practice; the next seven years were spent in London lodgings, were a time of poverty, for he made only 15 pounds a year by practice, his father, having failed in business, could not give him any help. He managed to keep himself by writing for the medical journals, preparing the catalogues of the hospital museum and of the pathological museum of the Royal College of Surgeons. In 1836, he had been made curator of the hospital museum, in 1838, demonstrator of morbid anatomy at the hospital, but his advancement there was hindered by the privileges of the hospital apprentices, because he had been too poor to afford a house-surgeoncy, or a dressership.
In 1841, he was made surgeon to the Finsbury Dispensary, but this appointment did not give him any experience in the graver operations of surgery. He was appointed lecturer on general anatomy and physiology at the hospital in 1843, warden of the hospital college founded. For the next eight years, he lived within the walls of the hospital, in charge of about 30 students resident in the little college. Besides his lectures and his superintendence of the resident students, he had to enter all new students, to advise them how to work, to manage the finances and the general affairs of the school. Thus, he was occupied with the business of the school, passed a week, or more, without going outside the hospital gates. In 1844, he married youngest daughter of the Rev. Henry North. In 1847, he was appointed an assistant-surgeon to the hospital, Arris and Gale professor at the Royal College of Surgeons, he held this professorship for each year gave six lectures in surgical pathology. The first edition of these lectures, which were the chief scientific work of his life, was published in 1853 as Lectures on Surgical Pathology.
He was elected a Fellow of the Royal Society in 1851. In October 1851, he resigned the wardenship of the hospital, he had now become known as a great physiologist and pathologist. Paget was the father of Sir John Paget. Paget was friends with Thomas Henry Huxley, he maintained there was no conflict between religion and science. No famous surgeon, not John Hunter, was to have founded his practice deeper in science than Paget did, or waited longer for his work to come back to him. In physiology, he had mastered the chief English, German and Italian literature of the subject, by incessant study and microscope work had put himself level with the most advanced knowledge of his time, so that it was said of him by Robert Owen, in 1851, that he had his choice, either to be the first physiologist in Europe, or to have the first surgical practice in London, with a baronetcy, his physiological lectures at St Bartholomew's Hospital were the chief cause of the rise in the fortunes of its school, which in 1843 had gone down to a
Veins are blood vessels that carry blood toward the heart. Most veins carry deoxygenated blood from the tissues back to the heart. In contrast to veins, arteries carry blood away from the heart. Veins are less muscular than arteries and are closer to the skin. There are valves in most veins to prevent backflow. Veins are present throughout the body as tubes. Veins are classified in a number of ways, including superficial vs. deep, pulmonary vs. systemic, large vs. small. Superficial veins are those closer to the surface of the body, have no corresponding arteries. Deep veins have corresponding arteries. Perforator veins drain from the superficial to the deep veins; these are referred to in the lower limbs and feet. Communicating veins are veins. Pulmonary veins are a set of veins. Systemic veins deliver deoxygenated blood to the heart. Most veins are equipped with valves to prevent blood flowing in the reverse direction. Veins are translucent, so the color a vein appears from an organism's exterior is determined in large part by the color of venous blood, dark red as a result of its low oxygen content.
Veins appear blue because the subcutaneous fat absorbs low-frequency light, permitting only the energetic blue wavelengths to penetrate through to the dark vein and reflect back to the viewer. The colour of a vein can be affected by the characteristics of a person's skin, how much oxygen is being carried in the blood, how big and deep the vessels are; when a vein is drained of blood and removed from an organism, it appears grey-white. The largest veins in the human body are the venae cavae; these are two large veins which enter the right atrium of the heart from below. The superior vena cava carries blood from the arms and head to the right atrium of the heart, while the inferior vena cava carries blood from the legs and abdomen to the heart; the inferior vena cava is retroperitoneal and runs to the right and parallel to the abdominal aorta along the spine. Large veins feed into these two veins, smaller veins into these. Together this forms the venous system. Whilst the main veins hold a constant position, the position of veins person to person can display quite a lot of variation.
The pulmonary veins carry oxygenated blood from the lungs to the heart. The superior and inferior venae cavae carry deoxygenated blood from the upper and lower systemic circulations, respectively; the portal venous system is a series of venules that directly connect two capillary beds. Examples of such systems include hypophyseal portal system; the peripheral veins carry blood from feet. Microscopically, veins have a thick outer layer made of connective tissue, called the tunica externa or tunica adventitia. During procedures requiring venous access such as venipuncture, one may notice a subtle "pop" as the needle penetrates this layer; the middle layer of bands of smooth muscle are called tunica media and are, in general, much thinner than those of arteries, as veins do not function in a contractile manner and are not subject to the high pressures of systole, as arteries are. The interior is lined with endothelial cells called tunica intima; the precise location of veins varies much more from person to person than that of arteries.
Veins serve to return blood from organs to the heart. Veins are called "capacitance vessels" because most of the blood volume is contained within veins. In systemic circulation oxygenated blood is pumped by the left ventricle through the arteries to the muscles and organs of the body, where its nutrients and gases are exchanged at capillaries. After taking up cellular waste and carbon dioxide in capillaries, blood is channeled through vessels that converge with one another to form venules, which continue to converge and form the larger veins; the de-oxygenated blood is taken by veins to the right atrium of the heart, which transfers the blood to the right ventricle, where it is pumped through the pulmonary arteries to the lungs. In pulmonary circulation the pulmonary veins return oxygenated blood from the lungs to the left atrium, which empties into the left ventricle, completing the cycle of blood circulation; the return of blood to the heart is assisted by the action of the muscle pump, by the thoracic pump action of breathing during respiration.
Standing or sitting for a prolonged period of time can cause low venous return from venous pooling shock. Fainting can occur but baroreceptors within the aortic sinuses initiate a baroreflex such that angiotensin II and norepinephrine stimulate vasoconstriction and heart rate increases to return blood flow. Neurogenic and hypovolaemic shock can cause fainting. In these cases, the smooth muscles surrounding the veins become slack and the veins fill with the majority of the blood in the body, keeping blood away from the brain and causing unconsciousness. Jet pilots wear pressurized suits to help maintain their venous blood pressure; the arteries are perceived as carrying oxygenated blood to the tissues, while veins carry deoxygenated blood back to the heart. This is true of the systemic circulation, by far the larger of the two circuits of blood in the body, which transports oxygen from the heart to the tissues of the body. However, in pulmonary circulation, the arteries carry deoxygenated blood from the heart to the lungs, veins return blood from the lungs to the heart.
The difference between veins a
An arteriole is a small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries. Arterioles are the primary site of vascular resistance; the greatest change in blood pressure and velocity of blood flow occurs at the transition of arterioles to capillaries. In a healthy vascular system the endothelium lines all blood-contacting surfaces, including arteries, veins, venules and heart chambers; this healthy condition is promoted by the ample production of nitric oxide by the endothelium, which requires a biochemical reaction regulated by a complex balance of polyphenols, various nitric oxide synthase enzymes and L-arginine. In addition there is direct electrical and chemical communication via gap junctions between the endothelial cells and the vascular smooth muscle. Blood pressure in the arteries supplying the body is a result of the work needed to pump the cardiac output through the vascular resistance termed total peripheral resistance by physicians and researchers.
An increase in the media to lumenal diameter ratio has been observed in hypertensive arterioles as the vascular wall thickens and/or lumenal diameter decreases. The up and down fluctuation of the arterial blood pressure is due to the pulsatile nature of the cardiac output and determined by the interaction of the stroke volume versus the volume and elasticity of the major arteries; the decreased velocity of flow in the capillaries increases the blood pressure, due to Bernoulli's principle. This induces gas and nutrients to move from the blood to the cells, due to the lower osmotic pressure outside the capillary; the opposite process occurs when the blood leaves the capillaries and enters the venules, where the blood pressure drops due to an increase in flow rate. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation. Further local responses to stretch, carbon dioxide, pH, oxygen influence arteriolar tone.
Norepinephrine and epinephrine are vasoconstrictive acting on alpha 1-adrenergic receptors. However, the arterioles of skeletal muscle, cardiac muscle, pulmonary circulation vasodilate in response to these hormones when they act on beta-adrenergic receptors. Stretch and high oxygen tension increase tone, carbon dioxide and low pH promote vasodilation. Pulmonary arterioles are a noteworthy exception. Brain arterioles are sensitive to pH with reduced pH promoting vasodilation. A number of hormones influence arteriole tone such as angiotensin II, bradykinin, atrial natruretic peptide, prostacyclin. Arteriole diameters decrease with exposure to air pollution. Any pathology which constricts blood flow, such as stenosis, will increase total peripheral resistance and lead to hypertension. Arteriolosclerosis is the term used for the hardening of arteriole walls; this can be due to decreased elastic production from fibrinogen, associated with ageing, or hypertension or pathological conditions such as atherosclerosis.
The muscular contraction of arterioles is targeted by drugs that lower blood pressure, for example the dihydropyridines, which block the calcium conductance in the muscular layer of the arterioles, causing relaxation. This decreases the resistance to flow into peripheral vascular beds, lowering overall systemic pressure. A "metarteriole" is an arteriole. Surface chemistry of microvasculature Venule
Leopold von Schrötter
Leopold Schrötter Ritter von Kristelli, was an Austrian internist and laryngologist born in Graz. He was the son of chemist Anton Schrötter von Kristelli, father to physician Hermann Schroetter-Kristelli. Leopold Schrötter Ritter von Kristelli studied at the Akademisches Gymnasium in Austria. In 1861 he received his medical doctorate from the University of Vienna, following graduation remained in Vienna as an apprentice-surgeon to Franz Schuh. From 1863 to 1869, he was an assistant to Josef Škoda, receiving his habilitation in 1867. Following the death of Ludwig Türck, he attained the first chair of laryngology at Vienna, three years became director of the world's first laryngological clinic at Vienna General Hospital. In 1875, he became an associate professor of laryngology, from 1875 to 1881, he was head of the department of internal medicine. In 1881 he was appointed Primararzt at the General Hospital, in 1890 was named professor and director of the third medical clinic in Vienna. In addition to his expertise in the field of laryngology, Schrötter is remembered for his work involving diseases of the heart and lungs.
He was a driving force in construction of the Alland Lungenheilanstalt, an institution that began attending to patients in 1898. With British surgeon James Paget, the eponymous Paget-Schrötter disease is named; this disorder involves primary thrombosis of the axillary subclavian vein. Among his written works is a treatise on heart diseases, included in Hugo Wilhelm von Ziemssen's Handbuch der speciellen Pathologie und Therapie. Other noted works by Schrötter include: Beitrag zur Behandlung der Larynx-Stenosen, 1876. Beitrag zur localen Anaesthesie des Larynx, 1881. Über die Lungentuberkulose und die Mittel zu ihrer Heilung, 1891. Hygiene der Lunge im gesunden und kranken Zustand, 1903. Über Hotelbau vom hygienischen Standpunkte, 1906. Leopold von Schrötter @ Who Named It "Parts of this article are based on a translation of an equivalent article at the German Wikipedia"
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
International Standard Serial Number
An International Standard Serial Number is an eight-digit serial number used to uniquely identify a serial publication, such as a magazine. The ISSN is helpful in distinguishing between serials with the same title. ISSN are used in ordering, interlibrary loans, other practices in connection with serial literature; the ISSN system was first drafted as an International Organization for Standardization international standard in 1971 and published as ISO 3297 in 1975. ISO subcommittee TC 46/SC 9 is responsible for maintaining the standard; when a serial with the same content is published in more than one media type, a different ISSN is assigned to each media type. For example, many serials are published both in electronic media; the ISSN system refers to these types as electronic ISSN, respectively. Conversely, as defined in ISO 3297:2007, every serial in the ISSN system is assigned a linking ISSN the same as the ISSN assigned to the serial in its first published medium, which links together all ISSNs assigned to the serial in every medium.
The format of the ISSN is an eight digit code, divided by a hyphen into two four-digit numbers. As an integer number, it can be represented by the first seven digits; the last code digit, which may be 0-9 or an X, is a check digit. Formally, the general form of the ISSN code can be expressed as follows: NNNN-NNNC where N is in the set, a digit character, C is in; the ISSN of the journal Hearing Research, for example, is 0378-5955, where the final 5 is the check digit, C=5. To calculate the check digit, the following algorithm may be used: Calculate the sum of the first seven digits of the ISSN multiplied by its position in the number, counting from the right—that is, 8, 7, 6, 5, 4, 3, 2, respectively: 0 ⋅ 8 + 3 ⋅ 7 + 7 ⋅ 6 + 8 ⋅ 5 + 5 ⋅ 4 + 9 ⋅ 3 + 5 ⋅ 2 = 0 + 21 + 42 + 40 + 20 + 27 + 10 = 160 The modulus 11 of this sum is calculated. For calculations, an upper case X in the check digit position indicates a check digit of 10. To confirm the check digit, calculate the sum of all eight digits of the ISSN multiplied by its position in the number, counting from the right.
The modulus 11 of the sum must be 0. There is an online ISSN checker. ISSN codes are assigned by a network of ISSN National Centres located at national libraries and coordinated by the ISSN International Centre based in Paris; the International Centre is an intergovernmental organization created in 1974 through an agreement between UNESCO and the French government. The International Centre maintains a database of all ISSNs assigned worldwide, the ISDS Register otherwise known as the ISSN Register. At the end of 2016, the ISSN Register contained records for 1,943,572 items. ISSN and ISBN codes are similar in concept. An ISBN might be assigned for particular issues of a serial, in addition to the ISSN code for the serial as a whole. An ISSN, unlike the ISBN code, is an anonymous identifier associated with a serial title, containing no information as to the publisher or its location. For this reason a new ISSN is assigned to a serial each time it undergoes a major title change. Since the ISSN applies to an entire serial a new identifier, the Serial Item and Contribution Identifier, was built on top of it to allow references to specific volumes, articles, or other identifiable components.
Separate ISSNs are needed for serials in different media. Thus, the print and electronic media versions of a serial need separate ISSNs. A CD-ROM version and a web version of a serial require different ISSNs since two different media are involved. However, the same ISSN can be used for different file formats of the same online serial; this "media-oriented identification" of serials made sense in the 1970s. In the 1990s and onward, with personal computers, better screens, the Web, it makes sense to consider only content, independent of media; this "content-oriented identification" of serials was a repressed demand during a decade, but no ISSN update or initiative occurred. A natural extension for ISSN, the unique-identification of the articles in the serials, was the main demand application. An alternative serials' contents model arrived with the indecs Content Model and its application, the digital object identifier, as ISSN-independent initiative, consolidated in the 2000s. Only in 2007, ISSN-L was defined in the
In human anatomy, the axillary vein is a large blood vessel that conveys blood from the lateral aspect of the thorax and upper limb toward the heart. There is one axillary vein on each side of the body, its origin is at a continuation of the brachial vein. This large vein is formed by the basilic vein. At its terminal part, it is joined by the cephalic vein. Other tributaries include the subscapular vein, circumflex humeral vein, lateral thoracic vein and thoraco-acromial vein, it terminates at the lateral margin of the first rib. It is accompanied along its course by a named artery, the axillary artery. Gray's s149 lesson3axillaryart&vein at The Anatomy Lesson by Wesley Norman