| CCH | C-cell hyperplasia; chronic chloride hemagglutination; chronic cholestatic hepatitis |
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| CH | case history; Chediak-Higashi [syndrome]; chiasma; Chinese hamster; chloral hydrate; cholesterol; Ch... |
| CHB | chronic hepatitis B; complete heart block; congenital heart block |
| CLH | chronic lobular hepatitis; cleft limb-heart [syndrome]; corpus luteum hormone; cutaneous lymphoid hy... |
| CPH | Certificate in Public Health; chronic paroxysmal hemicrania; chronic persistent hepatitis; chronic p... |
| buffalo type | Term used to describe the distribution of a fat deposit seen posteriorly over the upper thoracic vertebrae; seen in hyperadrenocorticalism (Cushing's syndrome). Synonym: buffalo hump. (05 Mar 2000) |
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| vaccination, haemophilus influenzae type b | See vaccination, hib. (12 Dec 1998) |
| gastroenteritis virus type A | A RNA virus, about 27 nm in diameter, which has not been cultured in vitro; it is the cause of epidemic nonbacterial gastroenteritis; at least five antigenically distinct serotypes have been recognised, including the Norwalk agent. These viruses are probably classified with the Caliciviruses in the family Caliciviridae. Synonym: gastroenteritis virus type A. (05 Mar 2000) |
| gastroenteritis virus type B | <virology> Genus of the Reoviridae having a double layered capsid and 11 double stranded RNA molecules in the genome. They have a wheel like appearance in the electron microscope and cause acute diarrhoeal disease in their mammalian and avian hosts. Probably the most important cause of severe dehydrating diarrhoea in children under three years of age worldwide. Symptoms include nausea, vomiting, low-grade fever and diarrhoea. Aggressive fluid replacement is generally required. (27 Sep 1997) |
| gaucher's disease, type 1 | A progressive genetic disease caused by a defect in an enzyme. The enzyme, called glucocerebrosidase, is needed to break down the chemical glucocerebroside. The enzyme defect in persons with Gaucher's disease (GD) leads to the accumulation of glucocerebroside in the spleen, liver, and lymph nodes. The most common early sign is enlargement of the spleen (located in the upper left abdomen). Other signs include low red blood cell counts (anaemia), a decrease in blood clotting cells (platelets), increased pigmentation of the skin, and a yellow fatty spot on the white of the eye (a pinguecula). Severe bone involvement can lead to pain and collapse of the bone of the hips, shoulders, and spine. The GD gene is on chromosome 1. The disease is a recessive trait. Both parents carry a GD gene and transmit it for their child with the disease. The parents' risk of a child with the disease is 1 in 4 with each pregnancy. This type of Gaucher's disease (noncerebral juvenile Gaucher's disease) is most common in Ashkenazi Jews (of European origin) and is the most common genetic disease among Jews in the United States. (12 Dec 1998) |
| Recklinghausen's disease type I | type 2 neurofibromatosis |
| mating type gene | Genes that, in Saccharomyces cerevisiae specify into which of the two mating types (a and _) a particular cell falls. Only unlike mating type haploids will fuse. The interest derives from the way in which mating type is switched, the existing gene is removed and a new gene, derived from a (silent) master copy elsewhere in the genome is spliced in. Later this gene will in its turn be replaced by a new copy of the old gene, also derived from a silent master. The a and _ genes code for pheromones that affect cells of the opposite mating type. Similar mating type genes are known from other yeasts and the switching mechanism (cassette mechanism) may be used more generally. (18 Nov 1997) |
| central Recklinghausen's disease type II | type 1 neurofibromatosis |
| central type neurofibromatosis | Type I neurofibromatosis. Incomplete neurofibromatosis, multiple neurofibromas with minimal manifestations, perhaps limited to cafe-au-lait spots; individuals with minimal lesions may have offspring with severe involvement. Synonym: abortive neurofibromatosis. (05 Mar 2000) |
| glycogen storage disease type I | <disease> An autosomal recessive disease in which gene expression of glucose-6-phosphatase is absent, resulting in hypoglycaemia due to lack of glucose production. Accumulation of glycogen in liver and kidney leads to organomegaly, particularly massive hepatomegaly. Increased concentrations of lactic acid and hyperlipidemia appear in the plasma. Clinical gout often appears in early childhood. Inheritance: autosomal recessive. (12 Dec 1998) |
| glycogen storage disease type II | <disease> Glycogenosis due to alpha-1,4-glucosidase (acid maltase) deficiency. It affects muscle, heart, and other organs. (12 Dec 1998) |
| glycogen storage disease type III | <disease> An autosomal recessive metabolic disorder due to deficient expression of amylo-1,6-glucosidase (one part of the glycogen debranching enzyme system). The clinical course of the disease is similar to that of glycogen storage disease type I, but milder. Massive hepatomegaly, which is present in young children, diminishes and occasionally disappears with age. Levels of glycogen with short outer branches are elevated in muscle, liver, and erythrocytes. Six subgroups have been identified, with subgroups type IIIa and type IIIb being the most prevalent. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type IV | <disease> An autosomal recessive metabolic disorder due to a deficiency in expression of branching enzyme (alpha-1,4-glucan-6-alpha-glucosyltransferase), resulting in an accumulation of abnormal glycogen with long outer branches. Clinical features are muscle hypotonia and cirrhosis. Death from liver disease usually occurs before age 2. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type V | <disease> Glycogenosis due to muscle phosphorylase deficiency. Characterised by painful cramps following sustained exercise. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type VI | <disease> A hepatic glycogen storage disease in which there is an apparent deficiency of hepatic phosphorylase activity. However, studies have not been able to distinguish between phosphorylase deficiency and phosphorylase kinase deficiency in patients with hepatic glycogenosis. (12 Dec 1998) |