Biomedical subjects

J H Barrett

Publications and source records attributed to J H Barrett.

46 records · Page 3Linked to original sources

PubMed1996

High risk of lymphomas in children of Asian origin: ethnicity or confounding by socioeconomic status?

To examine the role of ethnic origin as a risk factor for paediatric lymphoma, a cancer registry-based analysis was undertaken in Yorkshire, UK. Children of Asian ethnic origin were found to have an odds ratio for lymphomas of 1.60 (CI 0.98-2.62), after adjusting for age and sex. After adjusting also for 'super profile group' as an indicator of socioeconomic status, the estimate became 1.99 (CI 1.08-3.68). Hodgkin's disease and non-Hodgkin's lymphomas were analysed separately with similar results. Super profile group is an area-based measure and may not reflect the individual variation in living standards, especially among the Asian immigrants. Our results indicate that socioeconomic status does not confound the relationship between lymphomas and ethnic origin. However, there is a need for studies of ethnicity that include indicators of individual living standards or socioeconomic status.

Adolescent↗

PubMed1996

The angiotensin-I converting enzyme (ACE) gene I/D polymorphism and ACE levels in Pima Indians.

An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene is associated with plasma ACE levels in white populations. The occurrence of the I/D polymorphism and relationship to ACE levels was examined in a Pima Indian group (n = 305). The frequency of the D allele was lower in Pimas than whites (0.29 v 0.52 respectively). ACE levels were significantly associated with genotype in both groups (p = 0.0001), which accounted for 6.5% of the variation in ACE levels in Pimas and 18% in whites. The association of the I/D polymorphism with ACE levels confirms the relationship across ethnic groups. The low frequency of the D allele in Pima Indians shows that ethnic differences should be accounted for when studying the ACE gene.

Adult↗

PubMed1996

Angiotensin-converting enzyme insertion/deletion polymorphism and cerebrovascular disease.

BACKGROUND AND PURPOSE: There is evidence that an allelic variation in the angiotensin-converting enzyme (ACE) gene may confer an increased risk of vascular disease. The roles of the ACE insertion/deletion polymorphism and circulating ACE levels are unknown in cerebrovascular disease. METHODS: We studied an insertion/deletion polymorphism within intron 16 of the ACE gene by polymerase chain reaction and plasma ACE activity in 467 cases of stroke, the pathological type of which was established by cranial CT, and 231 control subjects. ACE genotype and activity were related to stroke type and mortality at 4 weeks and 3 months. RESULTS: No difference in genotype frequency was observed between all subjects with stroke and control subjects or between control subjects and subjects with cerebral infarction or cerebral hemorrhage. Plasma ACE activity was significantly lower in stroke patients at presentation (64.1 IU/L) than in control subjects (79.6 IU/L; P<.0001). Twenty-one patients (4.5%) with cerebral infarction died within 4 weeks and 56 patients (12%) within 3 months. These patients had significantly lower plasma ACE activity than patients who survived. There was some evidence that risk of death within 4 weeks increased with the number of D alleles (P=.02). Among survivors, plasma ACE activity showed a mean increase of 6.9 IU/L (95% confidence interval, 3.0 to 10.8) between levels at presentation and at 3 months (73.6 IU/L), the latter being similar to ACE activity in control subjects. CONCLUSIONS: Low ACE activity at sroke presentation and possession of the D allele may be associated with increased risk of early death from acute cerebral infarction.

Adult↗

PubMed1995

Analysis of breast cancer pedigrees using affected sibship methods.

Haplotype-sharing was examined in sets of affected siblings in the Breast Cancer Linkage Consortium pedigrees [Easton et al., 1993], using both identity-by-descent and identity-by-state methods. Linkage of the disease susceptibility locus to markers on chromosome 17 was confirmed. Substantial genetic heterogeneity was found, with more young cases being attributable to the putative gene. No differences were found between breast and ovarian cancer, and there was no evidence against a simple dominant mode of inheritance.

Age of Onset↗

PubMed1992

Genetic mapping based on radiation hybrid data.

Radiation hybrid mapping is a recently developed technique for constructing high-resolution maps of mammalian chromosomes. The chromosome of interest is exposed to X rays, which cause it to break into numerous fragments. The fragments are randomly recovered into hamster cells. The resulting hybrids are then analyzed for the presence or absence of DNA markers of interest. A simple method for using this information to order the markers on the chromosome is developed here. For any particular ordering of the loci, the least number of breaks consistent with the data can be determined. The best order is taken to be that which minimizes this number of obligatory breaks. Some statistical properties of the method are examined, both theoretically and by use of a simulation study. Except for some extreme cases, the method gives good results, which compare well with results obtained by a full maximum likelihood analysis. The method is used to order a set of 14 loci on chromosome 21 with encouraging results.

Animals↗

PubMed1990

Dosimetric intercomparison in the British Institute of Radiology fractionation study of 3F/week versus 5F/week in radiotherapy of laryngo-pharynx cancer.

A dose intercomparison was carried out by the National Physical Laboratory between the seven radiotherapy centres which contributed the largest number of patients to the British Institute of Radiology fractionation study of three fractions per week versus five fractions per week in clinical cancer treatment. Six of the centres showed remarkable agreement within the acceptable limits of error of the measurements. In one centre there appeared to be a physical dose discrepancy of 2.8% which was materially less than could be detected clinically.

Humans↗

PubMed1982