| TF | free thyroxine; tactile fremitus; tail flick [reflex]; temperature factor; testicular feminization; ... |
|---|---|
| MAF | macrophage activation factor; macrophage agglutinating factor; maximum atrial fragmentation; minimum... |
| ER | efficiency ratio; epigastric region; ejection rate; electroresection; emergency room; endoplasmic re... |
| RAR | rapidly adapting receptor; rat insulin receptor; retinoic acid receptor; right arm reclining; right ... |
| DF | decapacitation factor; decontamination factor; deferoxamine; deficiency factor; defined flora [anima... |
| platelet activation | A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable haemostatic plug. (12 Dec 1998) |
|---|---|
| neutron activation analysis | Activation analysis in which the specimen is bombarded with neutrons. Identification is made by measuring the resulting radioisotopes. (12 Dec 1998) |
| neutrophil activation | The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. The stimulatory substances, including opsonised particles, immune complexes, and chemotactic factors, bind to specific cell-surface receptors on the neutrophil. (12 Dec 1998) |
| EEG activation | The low voltage, fast pattern of attentive wakefulness. (05 Mar 2000) |
| trans-activation (genetics) | Increased rate of gene expression directed by either viral or cellular proteins. These regulatory factors (diffusible gene products) act in trans -- that is, act on homologous or heterologous molecules of DNA. (cis-acting factors act only on homologous molecules.) (12 Dec 1998) |
| energy of activation | Energy that must be added to that already possessed by a molecule or molecules in order to initiate a reaction; usually expressed in the Arrhenius equation relating a rate constant to absolute temperature. (05 Mar 2000) |
| enzyme activation | Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1) activation by ions (activators); 2) activation by cofactors (coenzymes); and 3) conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme. (12 Dec 1998) |
| juxtacrine activation | Activation of target cells by membrane anchored growth factors, also used for activation of leucocytes by PAF bound to endothelial cell surface. (18 Nov 1997) |
| feedback activation | The activation of an enzyme by an end product of a biochemical pathway in which that enzyme plays a part. For example, the activation of factors VIII and V by thrombin during blood clotting. (05 Mar 2000) |
| feed-forward activation | The activation of an enzyme by a precursor of the substrate of that enzyme. (05 Mar 2000) |
| upstream activation site | A DNA sequence that regulates transcription like an enhancer but does notwork if its located downstream from a promoter. (09 Oct 1997) |
| low-activation materials | <radiobiology> In fission reactors, one is forced to deal with the radioactive byproducts of the fission process, but in fusion reactors one generally has a choice of what materials to expose to neutrons produced by the fusion process. A major problem for fusion reactors is developing materials (such as for the reactor vacuum vessel structure) which can be exposed to high levels of neutron bombardment without becoming permanently radioactive. Candidate structural materials which have relatively low induced radiactivation (generally relative to stainless steel) are known as low-activation materials, these include titanium, vanadium, and silicon-carbide. (09 Oct 1997) |
| lymphocyte activation | <haematology> The change in morphology and behaviour of lymphocytes exposed to a mitogen or to an antigen to which they have been primed. The result is the production of lymphoblasts, cells that are actively engaged in protein synthesis and that divide to form effector populations. Should not be confused with transformation of the type associated with oncogenic viruses and activation is therefore perhaps a better term. (18 Nov 1997) |
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
| amino acid receptor | <biochemistry> Ligand gated ion channels with specific receptors for amino acid transmitters. An extended protein superfamily that also includes subunits of the nicotinic acetylcholine receptor. (18 Nov 1997) |