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Biomedical subjects

B G Greenberg

Publications and source records attributed to B G Greenberg.

At least 19 recordsLinked to original sources

Development and application of a prediction model for dental caries.

The development and validation of a caries prediction model comprising 13 sociodemographic and dental examination variables on Grade 1 and Grade 5 children in the National Preventive Dentistry Demonstration Program are described. The objective was to derive a method of predicting children at high risk to caries early in order that preventive measures might be undertaken. True high risk children were defined in two ways: highest 25% of children based on their 4-yr DMFS increment, and their total DMFS score at the end of the study. In both cases, children predicted to be at high risk were defined as the 25% with the highest discriminant score. Discriminant function and logistic regression analyses were used to determine the extent to which the 13 variables collectively discriminated between true high risk and non-high risk children so defined. Sensitivity was approximately 0.50 and specificity around 0.82, using the 4-yr increment as the criterion for defining true high risk, and approximately 0.64 and 0.88, respectively, using the final DMFS score for defining true high risk.

Child

Application of life table methodology in determining dental caries rates.

Probabilities of caries risk over time measured from eruption of first and second molars are illustrated using life table methodology. Life table rates based on 4,365 children in the National Preventive Dentistry Demonstration Program indicate that both fluoridation and sealants are effective in preventing caries on occlusal and buccal/lingual surfaces of molars. Effectiveness would probably have been greater on occlusal surfaces if sealants had been applied closer to the time of eruption. Similarities and differences between conventional DMFS indices and life table probabilities are discussed.

Actuarial Analysis

Statistical age-period-cohort analysis: a review and critique.

Descriptive and statistical age-period-cohort (APC) analysis methods have received considerable attention in the literature. The statistical modeling of APC data often involves the popular multiple classification model, a model containing the effects of age groups (rows), periods of observation (columns), and birth cohorts (diagonals of the age-by-period table). The identifiability problem inherent to this model is discussed, and its adverse effects on the results of APC modeling exercises are illustrated numerically. Potential problems attendant with the use of two-factor models are described, and other possible modeling approaches currently in use are discussed. Interpretational limitations due to certain innate characteristics of typical APC data sets are also detailed. Given all the documented potential sources for error, the current state-of-the-art regarding the statistical modeling of APC data should be considered to be at an early stage of development.

Adult

Statistical methods in the study of toxic shock syndrome.

Analysis of statistical methods used in matched case-control studies of toxic shock syndrome shows that matching has implications for validity and precision of the studies and for the choice of analysis techniques. The studies considered accounted for the matching in the analysis, either by the Mantel-Haenszel or Miettinen-Pike-Morrow approach to 1-to-M matched designs, or by the use of conditional maximum likelihood fitting of logistic regression models. Methods of dealing with confounding and effect modification in the (matched) logistic regression model are presented in the context of studies of toxic shock syndrome. The varied statistical techniques used in these studies were generally appropriate to the matched design except that nonmatching variables were not thoroughly considered as effect modifiers or confounders.

Carboxymethylcellulose Sodium

Predominance of early endometrial cancers after long-term estrogen use.

Clinical stage and pathological characteristics of endometrial cancer cases were related to several aspects of estrogen prescribing. In comparing 256 cases with 321 community control subjects, estrogen use of less than 3 1/2 years' duration did not increase the risk of endometrial cancer for any stage, grade, histological type, or extent of ivasion. With long-term estrogen use (3 1/2 years or more), relative risks were significantly increased (5.2 to 7.6) for the early cancers--those clinically stage IA, histologically grade 1, and invading the endometrium only. These increases were seen with both high-dose (greater than 0.625 mg) and low-dose (less than or equal to 0.625 mg) preparations. Risks were only minimally increased for the more advanced cancers. However, long-duration estrogen use did produce an increased risk of advanced cancer when administration was continuous rather than cyclic.

Adenocarcinoma

"Alternative" controls in a case-control study of endometrial cancer and exogenous estrogen.

To address the issue of detection bias among endometrial cancer cases and controls, women admitted to the North Carolina Memorial Hospital for dilatation and curettage (D&C) during 1970-1976 were selected as one of three control groups in a study of endometrial cancer and exogenous estrogen. Study subjects included 256 cases, 316 D&C controls, 224 gynecology controls and 321 community controls. The D&C controls had a higher frequency of estrogen use than either of the other control groups or the cases. These differences existed for both blacks and whites. When white cases were compared to either gynecology or community controls, relative risks were increased for long duration estrogen use and for recent use prior to diagnosis. With D&C controls, relative risks were not significantly different from unity irrespective of duration or recency of estrogen use. Exclusion of hyperplasias from the D&C controls had no substantive effect of these results. Bleeding was a presenting complaint for 92% of cases, 82% of D&C controls and 22% of gynecology controls. Both among cases and gynecology controls, there was no statistically significant association between bleeding and estrogen use, whereas this association was evident among D&C controls, and specifically among those who did not have pathologic evidence of endometrial hyperplasia. These data support the presence of detection bias among D&C controls but they do not provide evidence of this bias among endometrial cancer cases.

Aged

Exogenous estrogens and endometrial cancer.

Reports in the lay press that exogenous estrogens cause endometrial cancer are unjustified with the present evidence. The epidemiologic method used to identify retrospectively an increased association of estrogens with endometrial cancer cannot prove causality. Mortality from endometrial carcinoma has not increased in this country and may actually be starting to decline.

Breast Neoplasms