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Biomedical subjects

J D Mathews

Publications and source records attributed to J D Mathews.

At least 127 records · Page 7Linked to original sources
PubMed1970

Australia antigen in chronic hepatitis in Australia.

Of 53 cases of active chronic liver disease two were found to be carriers of Australia antigen Au (1)-an elderly woman with typical lupoid hepatitis and an elderly mortuary attendant with serologically atypical active chronic hepatitis. Au (1) was detected also in the serum of 7 out of 20 patients with clinically atypical acute hepatitis-one was an elderly Italian woman, one had hepatitis in the puerperium, and five had a history of transfusion or inoculation. The antigen was not found in 20 typical cases of infectious hepatitis in young people in 86 patients with other diseases. Antibody to Au (1) was present in only 2 out of 102 patients who had received numerous transfusions.We conclude, firstly, that Au (1) antigen is rare in white Australians (in keeping with the low incidence of serum hepatitis in Australia), and, secondly, that Au (1) positivity in hepatitis patients is associated with transfusions and with older age. We suggest that active chronic hepatitis and lupoid hepatitis may follow infection of susceptible individuals with Au (1)-positive hepatitis virus, but persistence of the virus in high titre does not appear to be necessary for chronicity of the disease.

Acute Disease↗
PubMedDate not supplied

Genetic analysis of systolic blood pressure in Melbourne families.

1. Circumstantial evidence suggests that immunological mechanisms might contribute to hypertension in man. If so, it would be expected that those genetic loci which influence the human immune response would also influence the risk of hypertension. 2. To test this hypothesis, the distribution of systolic blood pressure (SBP) was studied in seventy-eight families comprising 437 adults ascertained through fifty-eight probands with hypertension and twenty probands with low to normal levels of blood pressure. After allowing for the method of ascertainment of the families, and adjusting for the effects of age and sex, about 55% of the phenotypic variance of SBP could be attributed to genetic factors including 23% (42% of the additive genetic variance) attributable to the effects of immunogenetic loci (HLA and Gm). 3. This suggests that relatives with a greater number of HLA and Gm haplotypes in common had more similar SBP levels than similar relatives with fewer HLA and Gm haplotypes in common. This finding supports the hypothesis that immunological mechanisms contribute to hypertension in man.

Adult↗