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Biomedical subjects

V Groves

Publications and source records attributed to V Groves.

5 recordsLinked to original sources

Helicobacter pylori.

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Helicobacter Infections↗

Chronic cryptosporidiosis in Australian elapid snakes: control of an outbreak in a captive colony.

An outbreak of chronic cryptosporidiosis resulting in hypertrophic gastritis occurred in a captive colony of Australian elapid snakes. Two species of the genus Notechis were involved: Notechis ater (Black Tiger Snake) and Notechis scutatus (Eastern or Mainland Tiger Snake). The infection was eventually fatal in all 9 affected snakes. Typical histopathological findings of the stomach included mucosal thickening with cystic dilatation of gastric glands, moderate oedema and fibrosis of the lamina propria, and a mild to moderate patchy infiltration of inflammatory cells. Procedures implemented to contain the outbreak included the use of a formaldehyde-based disinfectant, prompt removal of faecal matter, uneaten and regurgitated food from enclosures, and examination of faecal specimens for Cryptosporidium oocytes and other pathogens.

Animals↗

Limited MHC polymorphism in whales.

Little is known about disease and genetic variation in aquatic mammalian species such as whales. In this paper human HLA class I and class II probes were used to study major histocompatibility complex (MHC) genes from two species of whale: Fin (Balaenoptera physalus) and Sei (B. borealis). Stronger signals were obtained on whale than on equivalent concentrations of mouse DNA. Evidence was obtained for several DRB-related genes, a DNA genes, one DQA gene, and multiple class I genes in whales. Interestingly, the whale genes, from the small panel studied, were less polymorphic than those of humans or mice. The aquatic environment of this mammalian species may be a unique factor in shaping its immune response through the MHC.

Animals↗

The human homologue of the mouse t-complex gene, TCP1, is located on chromosome 6 but is not near the HLA region.

Southern blot analysis indicates that there are four sequences in the human genome related to the mouse t-complex gene Tcp-1. All four genes were cloned and partial sequencing showed that one of them was a functional gene, and the other three were pseudogenes. The human sequences were all approximately 90% related to each other and 82-89% related to the mouse Tcp-1a sequence. Human TCP1 cDNA clones from both fibrosarcoma and B cell lines confirmed that there was a single expressed gene. mRNA transcripts of different sizes were accounted for by two different polyadenylation signals. The human TCP1 gene shared some amino acid substitutions with the mouse t-complex allele (Tcp-1a) which were not found in Tcp-1b. The functional human TCP1 gene was mapped, using a panel of somatic cell hybrids, as well as in situ analysis, to the long arm of chromosome 6 at 6q23-qter and thus is not closely linked to the HLA complex on the short arm. For this reason and others it is unlikely that there is a human equivalent of the mouse t-complex.

Amino Acid Sequence↗

Low red cell arachidonic acid in hemolytic uremic syndrome.

A defect in prostacyclin generation has been proposed in hemolytic uremic syndrome (HUS): prostacyclin is formed from arachidonic acid derived from phospholipid and low levels of some phospholipids have been described in HUS cell membranes. Therefore fatty acid content of the red blood cell membranes of 8 children with HUS was compared with 32 children with other renal disease, with 33 patients with non-renal disease and with 8 normal adults. Children with HUS consistently had lower proportions of arachidonic acid (2.7-8.4%) than all other groups (10.1-18.8%) and the mean arachidonic acid level in HUS was very significantly reduced (p less than 0.0001). These findings suggest a reduced availability of arachidonic acid for prostaglandin synthesis in HUS and are consistent with the proposition that arachidonic acid is lost through peroxidative change.

Adolescent↗