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D Dix

Publications and source records attributed to D Dix.

At least 37 records · Page 2Linked to original sources
PubMed1983

On estimating biological variation in diagnostic tests: application to the oral glucose tolerance test.

Biological variation (BV) in diagnostic tests can be conveniently estimated by the equation, BV = magnitude of reference limit - reference median magnitude of - 2(SD)A, where "reference limit" refers to either the 2.5th or 97.5th percentile in the reference population, magnitude of indicates absolute value, and (SD)A is the standard deviation of random analytical variation at the reference median. The value of (SD)A is calculated from the equation, (SD)A = (CV)A (reference median)/100, where (CV)A, the coefficient of variation of random analytical variation, is obtained from routine stable quality control material. The BV was calculated for plasma glucose concentration at the time points in the oral glucose tolerance test in an asymptomatic reference population and found to vary in the order: fasting less than 3 hour less than 1/2 hour less than 1 hour less than 2 hour. We present correlation coefficients between subject age and plasma glucose concentration that suggest that BV at the fasting, 1/2, 1, and 2 hour points might be reduced by subdividing reference populations according to subject age.

Adolescent↗
PubMed1982

Evaluation of extracranial cerebrovascular disease in the hypertensive patient with ocular pneumoplethysmography at 500 mm Hg.

OPG-300 is a reliable noninvasive method of detecting hemodynamically significant stenoses of the internal carotid circulation. An important limitation of the method is that patients with systemic blood pressure greater than 160 mm Hg cannot be studied; in our laboratory this represented 55 percent of the patients referred for testing. The addition of the 500 mm Hg vacuum modification now allows us to reliably test 95 percent of patients referred to our laboratory for evaluation of the extracranial cerebrovascular circulation.

Blood Pressure↗
PubMed1981

The oral glucose tolerance test: a comparison of the time points on the basis of limit values, normal dispersion, and reproducibility.

Time points in the glucose tolerance test (GTT) are compared on the basis of limit values, dispersion within a reference population, and reproducibility. We suggest using the distance between a limit value and the median reference value as a measure of the magnitude of abnormality. The distance between 140 mg/100 ml and the median fasting plasma glucose value is chosen as a standard distance and limits for other points in the GTT are calculated to equal this standard distance of abnormality. We suggest that the probability of correctly interpreting an individual result is directly related to the reproducibility of the test and inversely related to the percentage of the total range of values which is dispersed among the normal population. The ratio of reproducibility to percentage normal dispersion is proposed as an index of the probability of correctly interpreting an individual result. According to this index, and probability of correct interpretation varies in order: fasting plasma glucose concentration greater than 3-h greater than 2-h greater than 0.5-h greater than 1-h plasma glucose concentration.

Adolescent↗
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↗