| C2 | second cervical nerve; second cervical vertebra; second component of complement |
|---|---|
| C2a | activated second component of complement |
| C3 | third cervical nerve; third cervical vertebra; third component of complement |
| C3a | activated third component of complement |
| C4 | fourth cervical nerve; fourth cervical vertebra; fourth component of complement |
| complement membrane attack complex | The assembly of complement plasma glycoproteins c5b, c6, c7, c8, and polymeric c9 as a group on biological membranes. The complex forms transmembrane channels which displace lipid molecules and other constituents, thus disrupting the phospholipid bilayer of target cells leading to cell lysis by osmotic leakage. The formation of the membrane attack complex is the terminal step in the complement cascade. (12 Dec 1998) |
|---|---|
| complement pathway, alternative | The complement activation sequence initiated by the activation of complement factor c3, which is triggered by the interaction of microbial polysaccharides and properdin without participation of an antigen-antibody reaction. (12 Dec 1998) |
| complement pathway, classical | The sequential activation of complement, initiated by antigen-antibody complex and the binding of complement factor c1q to the fc region of the antibody. (12 Dec 1998) |
| complement system | A group of more than 20 serum proteins, some of which can be serially activated and participate in a cascade resulting in cell lysis. (05 Mar 2000) |
| complement unit | The smallest amount (highest dilution) of complement that will cause haemolysis of a unit of red blood cells in the presence of a haemolysin unit. Synonym: alexin unit. (05 Mar 2000) |
| component of complement | Any one of the nine distinct protein units (designated C1 through C9 and distributed in the a, b, and g electrophoretic partitions of normal serum) that effect the immunological activities long associated with complement. C1 is a complex of three subunits: C1q, C1r, and C1s. C1q (overbar indicates "active form") activates proenzyme C1r to C1r which activates C1s to C1s (also known as C1 esterase), which converts proenzyme C2 to C2b and produces C4b from C4. C2b combines with C4b to form "classical-complement-pathway C3/C5 convertase" (also known as C3 convertase, C5 convertase, and C42). This enzyme cleaves C3 to C3a and C3b, and C5 to yield C5a and C5b, as does "alternative-complement-pathway C3/C5 convertase" (also known as proenzyme factor B, properdin factor B, C3 proactivator, and heat-labile factor). Complement factor I (also known as C3b or C3b/C4b inactivator) inactivates C3b and C4b by a different proteolytic cleavage. Several autosomal recessive disorders have been identified in which one or more of the complement components have been deficient or completely absent. (05 Mar 2000) |
| heparin complement | The protein component of heparin in blood. (05 Mar 2000) |
| thyrotoxic complement-fixation factor | A form of thyrotoxin; an antigen found most readily in thyroid tissue from thyrotoxic individuals; known to be chemically and immunologically distinct from thyroglobulin, and fixes complement when combined with antibody related to the gamma-globulin fraction of serum. With the exception of extremely small concentrations, the antigen is rarely found in normal glands or in diseased glands that are not associated with thyrotoxicosis; it is probably an intracellular substance (possibly a constituent of the "microsomal fraction"), and does not contain iodine in significant quantity. Not related to the complement-fixation reaction occurring with serum in Hashimoto's disease, in which the antigen is thyroglobulin. (05 Mar 2000) |
| abdominal muscle deficiency syndrome | <syndrome> Congenital absence (partial or complete) of abdominal muscles, in which the outline of the intestines is visible through the protruding abdominal wall; in males, genitourinary anomalies (urinary tract dilation and cryptorchidism) are also found; genetics unclear. (05 Mar 2000) |
| adult lactase deficiency | Onset of lactase deficiency, with resulting milk intolerance and malabsorption, in adulthood. Inherited forms may not be manifested until adulthood; any process that damages the intestinal lining cells can cause lactase deficiency in adults. (05 Mar 2000) |
| alpha-1 antitrypsin deficiency | <chest medicine> Deficiency of the protease inhibitor alpha-1 antitrypsin, leads primarily to degradation of elastin of the alveolar walls, as well as other structural proteins of a variety of tissues. The lack of this protein leads to damage of various organs, but mainly to the lung and liver. symptoms may become apparent at a very early age or in adulthood, manifesting either as shortness of breath or liver related symptoms (jaundice, fatigue, fluid in the abdomen, mental changes, or gastrointestinal bleeding). There are several options for treatment of the lung disease, including replacement of the missing protein. Treatment of the liver disease is a well-timed liver transplant (12 Dec 1998) |
| alpha-1-proteinase deficiency | Absence of a serum proteinase inhibitor that may cause nodular non-suppurative panniculitis. (05 Mar 2000) |
| alpha-antitrypsin deficiency | <enzyme> A specific enzyme (alpha 1 antitrypsinase) that when absent genetically can result in panacinar emphysema (lung disease) and liver disease. There is no specific treatment for this condition other than supportive care for the liver and lung complications. Medications such as alpha-1proteinase inhibitor is given regularly to these patients. Incidence: approximately 1 in 10,000. (02 Jan 1998) |
| anaemia, iron deficiency | Deficiency of iron results in anaemia because iron is necessary to make haemoglobin, the key molecule in red blood cells responsible for the transport of oxygen. In iron deficiency anaemia, the red cells are unusally small (microcytic) and pale (hypochromic). Characteristic features of iron deficiency anaemia in children include failure to thrive (grow) and increased infections. The treatment of iron deficiency anaemia, whether it be in children or adults, is with iron and iron-containing foods. Food sources of iron include meat, poultry, eggs, vegetables and cereals (especially those fortified with iron). According to the National Academy of Sciences, the Recommended Dietary Allowances of iron are 15 milligrams per day for women and 10 milligrams per day for men. Anaemia characterised by low or absent iron stores, low serum iron concentration, elevated free erythrocyte porphorin, low transferrin saturation, elevated transferrin, low serum ferritin, low haemoglobin concentration or haematocrit, and hypochromic microcytic red blood cells. Symptoms may include pallor, angular stomatitis and other oral lesions, gastrointestinal complaints, retinal haemorrhages and exudates, and thinning and brittleness of the nails. Among the causes of iron-deficiency anaemia are inadequate iron intake, impaired iron absorption, increased blood loss and increased requirements such as infancy, pregnancy, and lactation. (12 Dec 1998) |
| antibody deficiency disease | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |