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platelet : ウィキペディア英語版
platelet

Platelets, also called thrombocytes, are a component of blood whose function (along with the coagulation factors) is to stop bleeding by clumping and clotting blood vessel injuries. Platelets have no cell nucleus: they are fragments of cytoplasm that are derived from the megakaryocytes of the bone marrow, and then enter the circulation. These unactivated platelets are biconvex discoid (lens-shaped) structures,〔Michelson, Platelets, 2013, p. 117-118〕 2–3 µm in greatest diameter. Platelets are found only in mammals, whereas in other animals (e.g. birds, amphibians) thrombocytes circulate as intact mononuclear cells.〔Michelson, Platelets, 2013, p. 3〕
On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood cells. The smear is used to examine platelets for size, shape, qualitative number, and clumping. The ratio of platelets to red blood cells in a healthy adult is 1:10 to 1:20.
The main function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted endothelium. They gather at the site and unless the interruption is physically too large, they plug the hole. First, platelets attach to substances outside the interrupted endothelium: ''adhesion''. Second, they change shape, turn on receptors and secrete chemical messengers: ''activation''. Third, they connect to each other through receptor bridges: ''aggregation''. Formation of this platelet plug (primary hemostasis) is associated with activation of the coagulation cascade with resultant fibrin deposition and linking (secondary hemostasis). These processes may overlap: the spectrum is from a predominantly platelet plug, or "white clot" to a predominantly fibrin clot, or "red clot" or the more typical mixture. The final result is the ''clot''. Some would add the subsequent ''clot retraction'' and ''platelet inhibition'' as fourth and fifth steps to the completion of the process〔Berridge, M.J. (2012) Cell Signalling Biology; 〕 and still others a sixth step ''wound repair''.
Low platelet concentration is thrombocytopenia and is due to either ''decreased production'' or ''increased destruction''. Elevated platelet concentration is thrombocytosis and is either ''congenital'', ''reactive'' (to cytokines), or due to ''unregulated production'': one of the ''myeloprolerative neoplasms'' or certain other myeloid neoplasms. A disorder of platelet function is a thrombocytopathy.
Normal platelets can respond to an ''abnormality on the vessel wall'' rather than to hemorrhage, resulting in inappropriate platelet adhesion/activation and thrombosis: the formation of a clot within an intact vessel. These arise by different mechanisms than a normal clot. Examples are: extending the fibrin clot of venous thrombosis; extending an unstable or ruptured arterial plaque, causing arterial thrombosis; and microcirculatory thrombosis. An arterial thrombus may partially obstruct blood flow, causing downstream ischemia; or completely obstruct it, causing downstream tissue death.
==Discovery, early observations, and naming==
George Gulliver in 1841 drew pictures of platelets〔Lancet, 1882, ii. 916; Notes of Gulliver's Researches in Anatomy, Physiology, Pathology, and Botany, 1880; Carpenter's Physiology, ed. Power, 9th ed., see Index under 'Gulliver.'〕 using the twin lens (compound) microscope invented in 1830 by Joseph Jackson Lister.〔

This microscope improved resolution sufficiently to make it possible to see platelets for the first time. William Addison in 1842 drew pictures of a platelet-fibrin clot.〔"Why the Platelets were Discovered", British Journal of Haematology, 12 Mar 2008, Volume 13 Issue s1, Pages 618 – 637〕 Lionel Beale in 1864 was the first to publish a drawing showing platelets. Max Schultze in 1865 described what he called "spherules", which he noted were much smaller than red blood cells, occasionally clumped, and were sometimes found in collections of fibrin material. Queen's College, Birmingham (a predecessor college of Birmingham University) physician Dr Richard Hill Norris was the first to describe the action of platelets in 1880.〔http://www.birmingham.ac.uk/Documents/university/our-impact.pdf〕 Giulio Bizzozero in 1882 studied the blood of amphibians microscopically ''in vivo''. He named Schultz's spherules (It.) ''piastrine'': little plates. William Osler observed them and, in published lectures in 1886, called them a ''third corpuscle'' and a blood ''plaque'' and described them as a colorless protoplasmic disc. James Wright examined blood smears using the stain named for him, and used the term ''plates'' in his 1906 publication but changed to ''platelets'' in his 1910 publication which has become the universally accepted term.
The term ''thrombocyte'' (clot cell) came into use in the early 1900s and is sometimes used as a synonym for platelet; but not generally in the scientific literature, except as a root word for other terms related to platelets (e.g. '' thrombocytopenia'' meaning low platelets).〔 Thrombocytes are cells found in the blood of non-mammalian vertebrates. They are the functional equivalents of platelets, but circulate as intact mononuclear cells, and are not simply cytoplasmic fragments of bone marrow megakaryocytes.〔
In some contexts, the word ''thrombus'' is used interchangeably with the word ''clot'', regardless of its composition (white, red, or mixed). In other contexts it is used to contrast a normal from an abnormal clot: ''thrombus'' arises from physiologic hemostasis, ''thrombosis'' arises from a pathologic and excessive quantity of clot. In a third context it is used to contrast the result from the process: ''thrombus'' is the result, ''thrombosis'' is the process.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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