| cis-prenyl transferase | <enzyme> Involved in dolichol biosynthesis Registry number: EC 2.5.1.- Synonym: cis-prenyltransferase (26 Jun 1999) |
|---|---|
| cis-toluene dihydrodiol dehydrogenase | <enzyme> Nad specific dehydrogenase; reduces ring structure Chemical name: 1,2-dihydroxy-3-methylcyclohexa-3,5-diene dehydrogenase Registry number: EC 1.3.- Synonym: ctd dehydrogenase (26 Jun 1999) |
| cis-trans-isomerases | <enzyme> Enzymes that catalyze the rearrangement of geometry about double bonds. Registry number: EC 5.2 (12 Dec 1998) |
| cis trans test | <molecular biology> The complementation test with two or more interacting genes placed in cis and in trans relationships to each other. A double mutant genome is used in the cis test made from the two single mutant genomes used in the trans test by recombination. If the wild type phenotype is restored by both cis and trans arrangements it is concluded that the two mutations are in different genes and hence that the phenotype is determined by more than one gene. If the trans test is negative and the cis positive this means that the two mutations are in the same gene. If both tests are negative then at least one of the mutations must be dominant. Thus the double test provides a means of fine mapping of genes. A lab test which is used to determine whether two mutations of different genes which affect the same phenotype are on the same functional unit (indicating a cis configuration of the mutated genes) or on different functional units (indicating a trans configuration of the mutated genes). (A functional unit can be a chromosome.) The test is done by mating an individual that has one of the mutations to an individual that has the other one, and observing whether their offspring have the mutant phenotype. If the offspring do not have the mutant phenotype, then the genes are known to be trans, because the offspring have normal copies of each mutant gene on the different functional units which are able to genetically complement each other. If the offspring do have the mutant phenotype, then the genes are known to be cis, because the offspring will always inherit at least one of the mutant genes on the one functional unit, resulting in the mutant phenotype. (09 Oct 1997) |
| 11-cis-retinal | The isomer of retinaldehyde that can combine with opsin to form rhodopsin; it is formed from 11-trans-retinal by retinal isomerase. Synonym: neoretinal b. (05 Mar 2000) |
| 11-cis-retinol | Retinol with cis configuration at the 11-position (carotenoid numbering) or 5'-position (retinol numbering) of the side chain; an intermediate in the vision cycle. Synonym: neoretinene B. (05 Mar 2000) |
| 9-cis-retinol dehydrogenase | <enzyme> Catalyses oxidation of 9-cis-retinol to 9-cis-retinaldehyde; does not catalyze oxidation of all-trans-retinol; genbank u89717 Registry number: EC 1.1.1.- Synonym: retinol dehydrogenase (9-cis) (26 Jun 1999) |
| accelerated phase of leukaemia | Refers to chronic myelogenous leukaemia that is progressing. The number of immature, abnormal white blood cells in the bone marrow and blood is higher than in the chronic phase, but not as high as in the blast phase. (12 Dec 1998) |
| acceleration phase | <cell biology, cell culture> A period of increasing growth before the log phase in a culture of microbes. After the culture is started on a medium, at first there is no growth (the lag phase) and then the microbes start to gradually grow (acceleration phase) until they reach a constant maximum rate of growth (log phase). (15 Jan 1998) |
| 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) |
| acute-phase reaction | <immunology, rheumatology> Refers to the changes in synthesis of certain proteins within the serum during an inflammatory response, which provides rapid protection for the host against microorganisms via non-specific defense mechanisms. It consists of fever, an increase in inflammatory humoral factors, and an increased synthesis by hepatocytes of a number of proteins or glycoproteins usually found in the plasma; the reaction is mediated by endogenous pyrogens, the hypothalamus, adrenal hormones, and other factors. (12 Jul 2000) |
| anal phase | In psychoanalytic personality theory, the stage of psychosexual development, occurring when a child is between 1 and 3 years, during which activities, interests, and concerns are centreed around the anal zone. (05 Mar 2000) |
| aqueous phase | The water portion of a system consisting of two liquid phase's, one mainly water, the other a liquid immiscible with water (e.g., benzene, ether). (05 Mar 2000) |
| blast phase | Refers to advanced chronic myelogenous leukaemia. In this phase, the number of immature, abnormal white blood cells in the bone marrow and blood is extremely high. Also called blast crisis. (12 Dec 1998) |
| g0 phase | Phase of the cell cycle where cells exist in a quiescent state. These cells have unduplicated DNA, degraded RNA and protein, and low enzyme activity. The ability to switch between g0 and g1 (and vice versa) determines the post-embryonic cell proliferation rate and is defectively controlled in neoplastic cells. (12 Dec 1998) |