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Biomedical subjects

R Mohamed

Publications and source records attributed to R Mohamed.

24 records · Page 2Linked to original sources
PubMed1986

Ionizing radiation and DNA-chain elongation in ataxia telangiectasia lymphoblastoid cells.

DNA-chain elongation rates, determined by sedimentation analysis, were found to be similar in control and ataxia-telangiectasia lymphoblastoid cells. A gamma-radiation dose of 6 Gray, which had previously been shown to have a marked inhibitory effect on initiation of DNA replication, had no appreciable effect on elongation rates in either cell type. Elongation rates were also determined at 20 Gray of gamma-rays by pulsing cells with [3H]thymidine prior to irradiation to avoid anomalous sedimentation behaviour. At this radiation dose elongation was almost completely inhibited in control cells while little or no inhibition was observed in ataxia-telangiectasia cells. Deoxyribonucleoside triphosphate pool equilibration times were not altered at either dose.

Ataxia Telangiectasia↗
PubMed1983

DNA replication and repair in ataxia telangiectasia cells exposed to bleomycin.

A marked increase in sensitivity to bleomycin was observed in two ataxia telangiectasia (AT) lymphoblastoid cell lines compared to that in cell lines from two normal individuals. This sensitivity was obtained at two different concentrations of bleomycin. While normal cells showed a rapid recovery of ability to divide, there was no indication of such a recovery in AT cells up to 120 h after bleomycin treatment. A similar level of breakage of DNA occurred in both cell types after incubation with bleomycin. The rate of repair of these breaks was also the same. DNA synthesis was found to be more resistant to bleomycin in AT cells than in control cells. The latter data are in keeping with results previously obtained using ionizing radiation.

Ataxia Telangiectasia↗
PubMed1981

Outbreak of aplastic crises in sickle cell anaemia associated with parvovirus-like agent.

Since 1952, 112 children with sickle cell anaemia (SCA) in Jamaica have had an aplastic crisis. Outbreaks occurred in 1956, 1960, 1065-67, 1971-73, and 1979-80. Most cases occurred in children under 10 years of age, and an aplastic crisis in a patient over the age of 15 years is rare. There were 38 cases in 1979-80 and stored serum specimens from 28 of these were available for virus studies. Evidence for infection with a parvovirus-like agent was found in 24 of these 28 cases. Viral antigen was detected in 2 patients, both of whom demonstrated seroconversion. Seroconversion during 1980 was detected in a further 7, increasing amounts of antibody during the convalescent period were found in 5, antibody was found in 2 of 4 patients from whom only an acute phase specimen was available and the remaining 10 were antibody positive in the only convalescent phase sample available for testing. Antibody was found in 4 of 94 controls with the SS genotype (in retrospect 2 of these may have had an aplastic crisis) and in 17% of 48 controls with a normal haemoglobin (AA) genotype. The results accord with the possibility that the parvovirus-like agent is the principal cause of aplastic crisis in SCA.

Adolescent↗