| deoxyribonucleases, type III site-specific | <enzyme> Enzyme systems composed of two subunits and requiring ATP and magnesium for endonucleolytic activity; they do not function as atpases. They exist as complexes with modification methylases of similar specificity. The systems recognise specific short DNA sequences and cleave a short distance, about 24 to 27 bases, away from the recognition sequence to give specific double-stranded fragments with terminal 5'-phosphates. Enzymes from different microorganisms with the same specificity are called isoschizomers. Registry number: EC 3.1.21.5 (12 Dec 1998) |
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| type III acrocephalosyndactyly | An autosomal dominant syndrome with variable expression of brachycephaly, maxillary hypoplasia, prominent ear crus, syndactyly, facial asymmetry, shallow orbits, telecanthus, and nasal septal deviation; may show mental retardation. Synonym: Saethre-Chotzen syndrome. (05 Mar 2000) |
| type III collagen | Collagen characteristic of reticular fibres. (05 Mar 2000) |
| type III familial hyperlipoproteinaemia | Hyperlipoproteinaemia characterised by increased plasma levels of LDL, beta-lipoproteins, pre-beta-lipoproteins, cholesterol, phospholipids, and triglycerides; hypertriglyceridemia induced by a high carbohydrate diet, and glucose tolerance is abnormal; frequent eruptive xanthomas and atheromatosis, particularly coronary artery disease; biochemical defect lies in apolipoproteins; there are many varieties. Synonym: carbohydrate-induced hyperlipaemia, dysbetalipoproteinaemia, familial hyperbetalipoproteinaemia and hyperprebetalipoproteinaemia, familial hypercholesterolaemia with hyperlipaemia. (05 Mar 2000) |
| type III hyperlipoproteinaemia | <biochemistry> An inherited disorder (gene defect) where both cholesterol and triglycerides are elevated in the same patient. This condition accelerates the effects of atherosclerosis and thus increases the risk of cardiovascular disease. Conditions such as hypothyroidism, obesity and diabetes enhances this risk. Origin: Gr. Haima = blood (27 Sep 1997) |
| type III hypersensitivity reaction | An immunologic category of diseases evoked by the deposition of antigen-antibody or antigen-antibody-complement complexes on cell surfaces, with subsequent involvement of breakdown products of complement, platelets, and polymorphonuclear leukocytes, and development of vasculitis; nephritis is common. Arthus phenomenon and serum sickness are classic examples, but many other disorders, including most of the connective tissue disease's, may belong in this immunologic category; immune complex disease's can also occur during a variety of disease's of known aetiology, such as subacute bacterial endocarditis. See: autoimmune disease. Synonym: immune complex disorder, type III hypersensitivity reaction. (05 Mar 2000) |
| mucopolysaccharidosis | Any of a group of lysosomal storage diseases that have in common a disorder in metabolism of mucopolysaccharides, as evidenced by excretion of various mucopolysaccharides in urine and infiltration of these substances into connective tissue, with resulting various defects of bone, cartilage, and connective tissue. (05 Mar 2000) |
| mucopolysaccharidosis I | Systemic lysosomal storage disease caused by a deficiency of alpha-l-iduronidase and characterised by progressive physical deterioration with urinary excretion of dermatan sulfate and heparan sulfate. There are three recognised phenotypes representing a spectrum of clinical severity from severe to mild: hurler's syndrome, hurler-scheie syndrome and scheie's syndrome (formerly mucopolysaccharidosis v). Symptoms may include dwarfism, hepatosplenomegaly, gargoyle-like facies, corneal clouding, cardiac complications, and noisy breathing. (12 Dec 1998) |
| mucopolysaccharidosis II | Systemic lysosomal storage disease marked by progressive physical deterioration and caused by a deficiency of l-sulfoiduronate sulfatase. This disease differs from mucopolysaccharidosis I by slower progression, lack of corneal clouding, and x-linked rather than autosomal recessive inheritance. The mild form produces near-normal intelligence and life span. The severe form usually causes death by age 15. (12 Dec 1998) |
| mucopolysaccharidosis IV | Genetic disorder of mucopolysaccharide metabolism characterised by skeletal abnormalities, joint instability, development of cervical myelopathy, and excessive urinary keratan sulfate. There are two biochemically distinct forms, each due to a deficiency of a different enzyme. (12 Dec 1998) |
| mucopolysaccharidosis vi | Mucopolysaccharidosis with excessive chondroitin sulfate b in urine, characterised by dwarfism and deafness. It is caused by a deficiency of n-acetylgalactosamine-4-sulfatase (arylsulfatase b). (12 Dec 1998) |
| mucopolysaccharidosis vii | Mucopolysaccharidosis characterised by excessive dermatan and heparan sulfates in the urine and hurler-like features. It is caused by a deficiency of beta-glucuronidase. (12 Dec 1998) |
| angiotensin III | <chemical> A heptapeptide formed by the enzymatic hydrolysis of angiotensin II. It has greater activity than angiotensin II for stimulating aldosterone synthesis and in the release of prostaglandins but only 20% of the pressor activity. Chemical name: Angiotensin II, 1-de-L-aspartic acid- (12 Dec 1998) |
| annexin III | <enzyme> A protein of the annexin family that catalyses the conversion of 1-d-inositol 1,2-cyclic phosphate and water to 1-d-myo-inositol 1-phosphate. Chemical name: 1-D-myo-Inositol-1,2-cyclic-phosphate 2-inositolphosphohydrolase Registry number: EC 3.1.4.36 (12 Dec 1998) |
| antithrombin III | <haematology> Antithrombin III is a protein which stimulates the removal of blood clots in the bloodstream. Small blood clots form normally within the bloodstream, but are normally dissolved via the bodys antithrombin III. Conditions that may have an associated low value of antithrombin III include: liver disease and DIC. Normal values are: 0.20 to 0.45 mg/ml or more than 50% of the laboratory control value. Conditions where there is a deficiency of this important protease inhibitor can result in a condition of hypercoagulation, resulting in an increased risk for blood clot formation. Inheritance: autosomal dominant. (13 Jan 1998) |