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Biomedical subjects

R T Johnson

Publications and source records attributed to R T Johnson.

At least 289 records · Page 16Linked to original sources
PubMed1971

Viral infections and malformations of the nervous system.

Experimental viral infections are described which cause malformations of the developing nervous system. These include influenza virus infection of chick embryos causing defects in neural tube closure and flexion, parvovirus infections of rodents and cats resulting in a granuloprival cerebellar malformation, and myxovirus infections of rodents inducing stenosis of the aqueduct of Sylvius. In each experimental model the pathogenesis of the malformation is different, but in each the resultant noninflammatory malformation bears resemblances to malformations in man considered to have a genetic basis.

Animals↗
PubMed1971

Slow viral infections of the nervous system and genetic disease.

Slow viral infections are characterized by a long incubation period, protracted clinical course, and limited host range. Scrapie of sheep and kuru and Creutzfeldt-Jakob disease of man are slow infections which have been regarded at one time or another as being of genetic etiology. The initial assumption that these represented hereodofamilial degenerative diseases came from their occurrence in families or in population aggregates, their chronic afebrile clinical courses and their histopathologic changes of noninflammatory degeneration. The role of genetics in these diseases is uncertain although in scrapie genetic susceptibility appears important in the natural infection. A more intimate virus-gene interrelationship in the form of a temperate infection has been postulated; however, little evidence exists at this time to support this hypothesis.

Adult↗
PubMed1969

Complementation analysis on virus-fused Chinese hamster cells with nutritional markers.

Cell fusion experiments have been carried out with Chinese hamster cell mutants with different nutritional growth requirements. Conditions have been devised in which approximately 1 to 2 percent of the cell population remaining after fusion are fused, hybrid cells. The all-or-none nature of the genetic markers employed and the extremely low reversion rates insure that no contamination of the hybrid population with parental forms occurs. Hybrids between glycine- and hypoxanthine-requiring mutants are prototrophic, which indicates that both mutations are recessive. Hybrids between a glycine-deficient mutant and a singlestep mutant which requires glycine, hypoxanthine, and thymidine are relieved of the glycine dependency, an indication that the two loci associated with glycine dependence are different. This mutation to the triple-supplement requirement as well as a proline deficiency were also shown to be recessive mutations. The system appears applicable to a variety of genetic problems.

Animals↗