| DDS | damaged disc syndrome; dendrodendritic synaptosome; dental distress syndrome; depressed DNA synthesi... |
|---|---|
| G1 | presynthetic gap [phase of cells prior to DNA synthesis] |
| G2 | postsynthetic gap [phase of cells following DNA synthesis] |
| IDS | iduronate sulfatase; immune deficiency state; inhibitor of DNA synthesis; integrated delivery system... |
| LS | lateral suspensor; left sacrum; left septum; left side; legally separated; leiomyosarcoma; length of... |
| serine proteinase inhibitors | Exogenous or endogenous compounds which inhibit serine proteinases. (12 Dec 1998) |
|---|---|
| serotonin uptake inhibitors | Compounds that specifically inhibit the reuptake of serotonin in the brain. This increases the serotonin concentration in the synaptic cleft which then activates serotonin receptors to a greater extent. These agents have been used in treatment of depression, panic disorder, obsessive-compulsive behaviour, and alcoholism, as analgesics, and to treat obesity and bulimia. Many of the adrenergic uptake inhibitors also inhibit serotonin uptake; they are not included here. (12 Dec 1998) |
| hydroxymethylglutaryl-CoA reductase inhibitors | Compounds that inhibit hmg-CoA reductases. They have been shown to directly lower cholesterol synthesis. (12 Dec 1998) |
| neurotransmitter uptake inhibitors | Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects. (12 Dec 1998) |
| dopamine uptake inhibitors | Drugs that block the transport of dopamine into axon terminals or into storage vesicles within terminals. most of the adrenergic uptake inhibitors also inhibit dopamine uptake. (12 Dec 1998) |
| integrase inhibitors | Compounds which inhibit or antagonise biosynthesis or actions of integrase. (12 Dec 1998) |
| tissue inhibitors of metalloproteinase | <cell biology> Family of proteins of around 200 residues that can inhibit metalloproteinases, for example collagenase, by binding to them. (18 Nov 1997) |
| enzyme inhibitors | Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (12 Dec 1998) |
| enzymes, coenzymes, and enzyme inhibitors | Proteins or RNA that act as biological catalysts, their cofactors, and inhibitors. (12 Dec 1998) |
| trypsin inhibitors | Serine proteinase inhibitors which inhibit trypsin. They may be endogenous or exogenous compounds. (12 Dec 1998) |
| lipoxygenase inhibitors | Compounds or agents that combine with lipoxygenase and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of the eicosanoid products hydroxyeicosatetraenoic acid and various leukotrienes. (12 Dec 1998) |
| acetoacetyl-acyl carrier protein synthase | <enzyme> E coli enzyme, that catalyses condensation of malonyl-acyl carrier protein plus acetyl-acyl carrier protein; not inhibited by cerulenin Registry number: EC 2.3.1.- Synonym: acetoacetyl-acp synthase (26 Jun 1999) |
| acid soluble spore protein | <molecular biology> A DNA binding protein in the spores of some bacteria, thought to stabilise the DNA in an A configuration, so protecting it from cleavage by enzymes or UV light. (18 Nov 1997) |
| acute-phase protein | <haematology> These plasma proteins (in addition to fibrinogen) increase 25% or more in response to inflammation and injury are under direct control of interleukin-6 (IL-6) (hepatocyte-stimulating factor). Other proteins which increase are ceruloplasmin, C3 and C4 which increase 50% or more; alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin and fibrinogen (the major determinant of viscosity 1 ) which increase two- to fourfold; C-reactive protein (CRP) and serum amyloid A which increase several hundred-fold. Despite long-held clinical opinion to the contrary, available data indicate that neither ESR nor measurement of specific acute-phase reactants are useful in excluding underlying infection or inflammation regardless of the pretest probability. These proteins are secreted into the blood in increased or decreased quantities by hepatocytes in response to trauma, inflammation, or disease. They can serve as inhibitors or mediators of the inflammatory processes. Certain acute-phase proteins have been used to diagnose and follow the course of diseases or as tumour markers. See also: amyloid, c-reactive protein, erythrocyte sedimentation rate, viscosity. (25 Jun 1999) |
| acyl-(acyl-carrier-protein)-phospholipid acyltransferase | <enzyme> Catalyses the formation of phosphatidylethanolamine from acyl-acyl carrier protein and 2-acyl-sn-glycero-3-phosphoethanolamine Registry number: EC 2.3.1.40 Synonym: 2-acyl-gpe acyltransferase, 2-acylglycerophosphoethanolamine acyltransferase (26 Jun 1999) |