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Biomedical subjects

D Dix

Publications and source records attributed to D Dix.

At least 37 records · Page 2Linked to original sources
PubMed1979

Glycohemoglobin and glucose tolerance tests compared as indicators of borderline diabetes.

We concurrently measured glycohemoglobin and performed 3-h oral (100 g) glucose tolerance tests on 69 ambulatory patients suspected of having abnormal carbohydrate metabolism. The patients were divided into two groups: (a) The 37 patients for whom the results were normal had plasma glucose concentrations of 0.70--1.15 milligram during fasting and 0.70--1.23 g/L 2 h after glucose ingestion. (b) Borderline diabetics exceeded one or both of these limits. The range of glycohemoglobin in the normal group was 3.0--4.7% of total hemoglobin. Of the 21 borderline diabetics, 11 had increased glycohemoglobin (4.8--8.0%). The difference in tolerance test results between borderline diabetics with and without increased glycohemoglobin was insufficient to predict the status of glycohemoglobin. We suggest a tentative definition for latent diabetes: increased glycohemoglobin in the presence of normal or borderline-abnormal glucose concentration in plasma collected during fasting.

Adolescent↗
PubMedDate not supplied

The oral glucose tolerance test: an objective method of interpretation.

Oral glucose tolerance test results from a positively-skewed, unimodal distribution were analyzed in such a way as to uncover a natural division within the set of results for each time point. The division in results was obtained from a break in the curve formed when plasma glucose concentration was plotted vs the percentile of the population described by those concentrations. The percentile at which the break occurs separated normal from abnormal glucose concentrations objectively. Previously natural divisions between normal and abnormal glucose concentrations had been found only in bimodal distributions from atypical populations such as the Pima Indians and Nauruans of Micronesia. The glucose concentrations at which separations in our unimodal distribution occur compare well with the available data from the atypical populations. According to one measure of reliability, the 3-h time point was more effective than the more commonly utilized 2-h point in distinguishing normal from abnormal plasma glucose concentration.

Adolescent↗
PubMedDate not supplied

On the role of aging in carcinogenesis.

We have studied cancer age-incidence patterns for the most common cancers in Connecticut from 1935 to 1994 and in locations throughout the world in the 1975 and 1990 eras. We defined "Age 1/2" as the age at which half the incidence occurs in any given year or era. In every population, we found the cancers could be ranked in the same order according to "Age 1/2", i.e., testis < ovary, corpus uterus, breast < stomach, colon, rectum, prostate. This order of cancers according to "Age 1/2" does not correlate with the order according to age-standardized rates, and "Age 1/2" values exhibit less than 10% the variability of age-standardized rates over time and place. We conclude that the determinant of "Age 1/2" is independent of the determinant of age-standardized rates and suggest that "Age 1/2" is determined by host genes that may vary among tissues of tumor origin but are common to all people.

Adolescent↗
PubMedDate not supplied

On the role of aging in cancer incidence: analysis of the skin cancer data.

Worldwide age-incidence patterns for melanoma, non-melanoma skin cancer, and the group of all cancers except non-melanoma skin cancer from 1971 to 1976 were normalized for differences in frequency of occurrence and compared. The percentage of total cancer incidence that occurred in young subjects was greater for melanoma and less for non-melanoma skin cancer than for the group of all cancers. The risk for melanoma was apparent by age 15, much earlier than for non-melanoma skin cancer and the group of all cancers. While the risk for non-melanoma skin cancer and the group of all cancers increased continuously with advancing age, the risk for melanoma was constant beyond age 35. We conclude that risk for melanoma is unusually concentrated among the young, and, therefore, that protection from sun exposure is particularly important for this group.

Age Factors↗
PubMedDate not supplied

On the role of aging in cancer incidence: cohort analyses of the lung cancer data.

Lung cancer age-specific mortality rates for male and female cohorts born in the United States between 1903 and 1928 increase from age 32 to 52 according to an equation of the form log (mortality rate) = m(age) + b, where m and b are constants. Variation exists among the cohorts in the magnitudes of m and b, but correlation coefficients between age-mortality patterns among all cohorts are highly positive (r greater than 0.98, p less than 0.01), indicating that the form of the equation is similarly appropriate for each cohort. Because cigarette smoking behavior has varied among cohorts and between sexes, we conclude that the form of the equation, i.e., the exponential nature of the lung cancer age-mortality pattern, is independent of environmental carcinogenicity and is best attributed to some aspect of the intrinsic aging process.

Adult↗
PubMedDate not supplied

On the role of aging in cancer incidence: analysis of the lung cancer data.

Age-specific lung cancer mortality rates for U.S. males and females from 1935 to 1978 were normalized to describe the percentage of total mortality in a given era which occurred at a given age interval. Correlation coefficients between age-mortality patterns for various eras were calculated and found to be highly positive. We conclude that the shape of the lung cancer age-mortality pattern has remained remarkably constant despite dramatic changes in the carcinogenicity of the lung environment, and suggest that shape is determined by an invariant influence which is best attributed to some aspect of the aging process.

Adult↗
PubMedDate not supplied

The incidence of female cancers: correlations with etiologic implications.

Correlation coefficients were calculated between incidence rates for the most frequent female cancers in populations throughout the world. Positive correlations were generally weak, and we conclude that most female cancers do not share a dominant etiologic factor which is inherent in cancer incidence rates. However, most cancers do exhibit similar age-incidence patterns. We also conclude that the determinant of shape in cancer age-incidence patterns is common to most female cancers, internationally invariant, and independent of the determinants of cancer incidence rates. Breast cancer exhibits an unusual age-incidence pattern with a peculiar dependence on the frequency of breast cancer occurrence.

Age Factors↗
PubMedDate not supplied

The incidence of female breast and genital cancer: analysis of the age-dependence.

Worldwide age-incidence patterns for female breast and genital cancers were normalized for differences in frequency of tumor occurrence and compared. The percentage of total cancer incidence which occurred in elderly subjects differed between populations but was similar for cancer of the breast, ovary, and corpus uteri within a given population. In addition, cancers of the breast, ovary, and corpus uteri exhibited similar ranges of distribution about the worldwide median incidence at all age intervals and strong positive correlations between crude incidence rates in the populations studied. Despite these and other similarities, breast cancer exhibited a correlation between crude incidence rate and percentage of total incidence which occurred in elderly subjects which was not apparent in the genital cancers. We cannot exclude the possibility that this correlation is coincidental. However the possibility of identifying factors predisposing to or protecting against breast cancer is attractive. The results of this study suggest that such factors would apply to breast but not to genital tissue.

Adult↗
PubMedDate not supplied

The incidence of breast cancer: analysis of the age dependence.

The incidence of female breast cancer was studied as a function of age in 71 different populations throughout the world. Incidence data was normalized for differences in frequency of occurrence. Median normalized incidence increased exponentially from age 20 to 45. After age 45 the rate of incidence decreased, and we suggest that menopause may be responsible for the rate reduction. Populations were not randomly distributed about the total population median normalized incidence at the various age intervals. Populations were classified according to their age-incidence patterns in 3 groups: Group 1 (with median % incidence after age 69=50): Group 2 (with median % incidence after age 69=47), and Group 3 (with median % incidence after age 69=31). At most age intervals, the normalized incidence in Group 1 populations was less than the total median, while the normalized incidence in Group 3 populations was greater than the total median. Although we cannot exclude the possibility that the variation in age-incidence patterns among the population groups is an artifact of tumor registration errors, evidence suggests that such an artifact is unlikely. Breast cancer occurs more frequently in Group I populations than it does in Group 3 populations. We suggest that Group 3 populations may share an element of protection from, or that Group I populations may share an element of risk for, breast cancer.

Adult↗