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Biomedical subjects

R F Carter

Publications and source records attributed to R F Carter.

At least 73 records · Page 4Linked to original sources

Familial pericentric inversion of chromosome 19, inv(19) (p13q13) with a note on genetic counseling of pericentric inversion carriers.

An inmate of a hospital for the mentally retarded was found during a cytogenetic screening programme to have karyotype 46,XY,inv(19)(p13q13)mat. Clinical, cytogenetic and family findings are presented and it is concluded that the chromosomes abnormality was probably not the cause of the patient's retardation. The problem of genetic counseling of inversion carriers is examined in some detail and estimates of risk are given.

Adolescent↗

Sudden infant death syndrome in South Australia. Measurement of serum IgE antibodies to three common allergens.

Radioallergosorbent test (RAST) studies showed that IgE antibodies to Dermatophagoides pteronyssinus (house dust mite), Aspergillus fumigatus and bovine beta-lactoglobulin were significantly elevated in the sera of infants who died as a result of the sudden death in infancy syndrome (SDIS). No significant differences were found in the levels of total IgE, IgA, IgG or IgM in the sera of SDIS victims or controls. The possible role of hypersensitivity in the aetiology of SDIS is discussed.

Allergens↗

A case of hartmannellid amebic meningoencephalitis in Zambia.

A case of amebic meningoencephalitis recognized in an adult Zambian is described. This is the first authenticated case from Africa. The morphologic features of the organism, its ability to form cysts in tissue, and the granulomatous tissue response denote that the ameba is an hartmannellid rather than a Naegleria. Free-living amebas of the family Hartmannellidae have not been incriminated before as a cause of primary amebic meningoencephalitis in man. To our knowledge this is the only case where such an ameba was responsible for fulminating meningoencephalitis. The presence of the amebas in a cellulocutaneous abdominal lesion suggests hematogenous dissemination.

Amebiasis↗

Comparative measurements of the shortterm lung clearance and translocation of PuO2 and mixed Na2O + PuO2 aerosols in mice.

Mice were exposed to aerosols of either plutonium dioxide alone, or mixed oxides of plutonium and sodium with atomic ratios (Na/Pu) in the range 1.5 to 16. In the case of the mixed oxides, the lung clearance of the plutonium was represented by the sum of two exponentials, of which the short-term component accounted for 27 +/- 8% of the initial lung content with a clearance half-time of 6.0 +/- 2.7 h. These measurements were made over a period of up to 35 days after exposure, and similar measurements for a plutonium dioxide fume indicated that any early clearance phase was obscured by data variability, but was small and probably accounted for less than 10% of the initial lung deposit. The translocation of plutonium to the liver and skeleton by 1 day after exposure represented about 0.05% of the initial lung content in the case of the plutonium dioxide fume, and 7% of the initial lung content for the mixed oxide particulate where the atomic ratio was 16. The results of the animal exposures are discussed briefly with respect to the physical characterization of the particulate by electron microscopy, and in vitro filtration methods.

Aerosols↗

Sensitivity to amphotericin B of a Naegleria sp. isolated from a case of primary amoebic meningoencephalitis.

An amoeba of the genus Naegleria causing fatal meningoencephalitis in a human subject has been investigated for its sensitivity to several drugs. Penicillin, sulphadiazine, chloramphenicol, oxytetracycline hydrochloride, streptomycin, methotrexate, emetine, quinine, and metronidazole had no effect on the organism in vitro at levels in excess of those likely to be attained therapeutically in the brain. Amphotericin B was highly amoebicidal in vitro and protected mice from infection with the organism. Used in high dosage by the intraventricular as well as the intravenous route, this drug might be successful in the treatment of further cases of primary amoebic meningoencephalitis.

Amebiasis↗