Steroid isolation , depending on context, is the isolation of chemical matter required for chemical structure elucidation, derivitzation or degradation chemistry, biological testing, and other research needs (generally milligrams to grams, but often more  or the isolation of "analytical quantities" of the substance of interest (where the focus is on identifying and quantifying the substance (for example, in biological tissue or fluid). The amount isolated depends on the analytical method, but is generally less than one microgram.  [ page needed ] The methods of isolation to achieve the two scales of product are distinct, but include extraction , precipitation, adsorption , chromatography , and crystallization . In both cases, the isolated substance is purified to chemical homogeneity; combined separation and analytical methods, such as LC-MS , are chosen to be "orthogonal"—achieving their separations based on distinct modes of interaction between substance and isolating matrix—to detect a single species in the pure sample. Structure determination refers to the methods to determine the chemical structure of an isolated pure steroid, using an evolving array of chemical and physical methods which have included NMR and small-molecule crystallography .  : 10–19 Methods of analysis overlap both of the above areas, emphasizing analytical methods to determining if a steroid is present in a mixture and determining its quantity. 
Aspirin is the common name for acetyl salicylic acid. This is hydrolysed to an active form, salicylate, which irreversibly binds COX by an acetylation reaction and has a high affinity for COX in platelets. Because of this affinity, the drug has an anti-thrombotic effect which is more pronounced at low doses where platelet production of TXA2 (aggregatory) is inhibited but that of PGI2 (disaggregatory) is not. At higher doses, PGI2 formation is also affected, reducing the dis-aggregatory influence it provides and therefore the anti-thrombotic effects of aspirin. Once COX is bound by salicylate, TXA2 production is inhibited for the life of that platelet, and so new platelets are required to raise body TXA2 levels again. At the low doses required for anti-thrombosis, aspirin has no analgesic or anti-inflammatory properties.