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Biomedical subjects

J Slack

Publications and source records attributed to J Slack.

At least 91 records · Page 5Linked to original sources
PubMed1977

Restriction in the immune response to flagellar proteins in inbred mice.

Anti-idiotypic sera prepared in both AL/N mice and rabbits identify specificities common to the IgA MOPC 467 myeloma protein and day-7 affinity-absorbed antibodies to Salmonella milwaukee polymerized flagellin (S. mil-POL) raised in BALB/c and C57BL/Ka mice. Isoelectric focusing (IEF) of reduced and alkylated BALB/c anti-S. mil-POL gave a banding pattern of L and H-chains identical to MOPC 467. C57BL/Ka anti-S. mil-POL had a similar L-chain pattern but a different H-chain pattern. Both BALB/c and C57BL/Ka contain predominantly IgA. The IEF patterns in the two strains are consistent with a monoclonal response at day 7.

Animals↗
PubMed1975

Influence of heredity and environment in determination of skinfold thickness in children.

Triceps and subscapular skinfold thicknesses were measured in 222 pairs of like-sex twins (78 monozygotic and 144 dizygotic) aged 3-15 years. Log transformations of the measurements were standardized for age and sex and the results used to estimate heritability--that is, the proportion of total variation determined by genetic factors. The overall contribution of non-genetic familial effects was small. There were appreciable differences in heritability between limb and trunk fat and between the sexes and at different ages. Over the age of 10 heritability was high for both sites in boys and girls. In younger children environmental factors contributed more to the variation.

Adolescent↗
PubMed1975

The genetic contribution to coronary heart disease through lipoprotein concentrations.

Many factors both genetic and environmental contribute to the liability to coronary heart disease and one of the genetically determined risk factors is the concentration of lipoproteins in the blood. The evidence so far is that serum cholesterol level is polygenically determined, but that in a minority of the population it is determined by a single mutant gene of large effect. There is evidence that the risk of coronary death for affected individuals is very high and that the condition warrants a maximum effort at identification and treatment. For the remainder of the population whose hyperlipidaemia is polygenically determined, the liability to coronary heart disease might be substantially reduced by simple and appropriate environmental measures aimed at reducing the total liability. The measures if correctly applied should effectively improve the population risks of early coronary death.

Cholesterol↗
PubMed1972

Do fats matter?

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Adult↗