Acids and bases are two types of corrosive substances. Any substance with a pH value between 0 up to 7 is considered acidic, whereas a pH value of 7 to 14 is a base. Ionic compounds are a compound with a positive or negative charge. Bases, on the other hand are ionic compounds that break apart to form a negatively charged hydroxide ion OH- in water.
Morphology change[ edit ] Mitochondrial hyperpolarization is a key event in initiating changes in morphology. The continuous changes in shape from the unactivated to the fully activated platelet is best seen on scanning electron microscopy. Three steps along this path are named early dendritic, early spread and spread.
The surface of the unactivated platelet looks very similar to the surface of the brain, with a wrinkled appearance from numerous shallow folds to increase the surface area; early dendritic, an octopus with multiple arms and legs; early spread, an uncooked frying egg in a pan, the "yolk" being the central body; and the spread, a cooked fried egg with a denser central body.
This complex runs just beneath these membranes, and is the chemical motor which literally pulls the invaginated OCS out of the interior of the platelet, like turning pants pockets inside out, creating the dendrites. This process is similar to the mechanism of contraction in a muscle cell.
The entire OCS thus becomes indistinguishable from the initial platelet membrane as it forms the "fried egg". This dramatic increase in surface area comes about with neither stretching nor adding phospholipids to the platelet membrane.
One of the signaling pathways turns on scramblasewhich moves negatively charged phospholipids from the inner to the outer platelet membrane surface. These phospholipids then bind the tenase Solutions hmwk prothrombinase complexes, two of the sites of interplay between platelets and the coagulation cascade.
Calcium ions are essential for the binding of these coagulation factors. Classically it was thought that this was the only mechanism involved in aggregation, but three new mechanisms have been identified which can initiate aggregation, depending on the velocity of blood flow i.
Wound repair The blood clot is only a temporary solution to stop bleeding; tissue repair is needed. Small interruptions in the endothelium are handled by physiological mechanisms; large interruptions by the trauma surgeon.
This support clinical data which show that many with serious bacterial or viral infections have thrombocytopenia, thus reducing their contribution to inflammation. Also platelet-leukocyte aggregates PLAs found in circulation are typical in sepsis or inflammatory bowel diseaseshowing the connection between thrombocytes and immune cells sensu stricto.
Thus, hemostasis and host defense were intertwined in evolution. For example, in the Atlantic horseshoe crab living fossil estimated to be over million years oldthe only blood cell type, the amebocytefacilitates both the hemostatic function and the encapsulation and phagocytosis of pathogens by means of exocytosis of intracellular granules containing bactericidal defense molecules.
Blood clotting supports the immune function by trapping the pathogenic bacteria within. The thrombosis is directed in concordance of platelets, neutrophils and monocytes. The process is initiated either by immune cells sensu stricto by activating their pattern recognition receptors PRRsor by platelet-bacterial binding.
Platelets can bind to bacteria either directly through thrombocytic PRRs  and bacterial surface proteins, or via plasma proteins that bind both to platelets and bacteria.
Neutrophils facilitate the blood coagulation by NETosis. In turn, the platelets facilitate neutrophils' NETosis.
NETs bind tissue factor, binding the coagulation centres to the location of infection. They also activate the intrinsic coagulation pathway by providing its negatively charged surface to the factor XII. Other neutrophil secretions, such as proteolytic enzymes, which cleave coagulation inhibitors, also bolster the process.
Regulatory defects in immunothrombosis are suspected to be major factor in causing pathological thrombosis in many forms, such as disseminated intravascular coagulation DIC or deep vein thrombosis. DIC in sepsis is a prime example of both dysregulated coagulation process as well as undue systemic inflammatory response resulting in multitude of microthrombi of similar composition to that in physiological immunothrombosis - fibrin, platelets, neutrophils and NETs.
Platelets modulate neutrophils by forming platelet-leukocyte aggregates PLAs. Interaction with PLAs also induce degranulation and increased phagocytosis in neutrophils. They are able to recognize and adhere to many surfaces, including bacteria. They are even able to fully envelop them in their open canalicular system OCPleading to proposed name of the process being "covercytosis", rather than phagocytosis, as OCS is merely an invagination of outer plasma membrane.
These platelet-bacteria bundles are then used as an interation platform for neutrophilsm which destroy the bacteria using the NETosis and phagocytosis. Platelets also participate in chronic inflammatory diseases, such as synovitis or rheumatoid arthritis.
Proinflammatory platelet microvesicles trigger constant cytokine secretion from neighboring fibroblast-like synoviocytesmost prominently Il-6 and IlProQuest powers research in academic, corporate, government, public and school libraries around the world with unique content, including rich academic databases, and technologies that connect people with information, simply and precisely.
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