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R R Regal

Publications and source records attributed to R R Regal.

7 recordsLinked to original sources
PubMed1992

The value of capture-recapture methods even for apparent exhaustive surveys. The need for adjustment for source of ascertainment intersection in attempted complete prevalence studies.

Almost all reported prevalence studies of which we are aware make exhaustive attempts to find diagnosed individuals and report all affected individuals, but make no attempt to estimate or adjust for missing cases. Yet very simple methods introduced in the planning stage of a prevalence study may enable investigators, or at least those subsequently reading their reports, to derive such adjusted estimates. If investigators keep track of the nature of the ascertainment of cases by source and collect and report data that allow calculation of the number of cases by source intersection, then they, or at least others, may derive estimates of missing cases and of the total population affected, by using readily available analogues of capture-recapture methods developed for wildlife populations censuses. Unfortunately, such methods are often inappropriately disparaged or ignored by epidemiologists. The derived estimates are sensitive to assumptions about dependence or independence ("interaction") of various sources, assumptions that sometimes are unprovable, and these estimates have some uncertainty because of statistical fluctuation. Moreover, most investigators who attempt exhaustive prevalence studies apparently believe that they have ascertained all cases and that there is no need to attempt to adjust for, let alone provide data pertinent to, the number of missing cases or to use a statistical method that will at best imply a certain imprecision to their result. Yet a survey that reports prevalence data without adjustment for, or data on, source intersection in essence makes an estimate of missing cases--zero--while providing no quantitative grounds for that claim. The results of all such surveys should be regarded with skepticism because, at best (if the case reports are accurate), they provide only a lower boundary of prevalence. We illustrate the grounds for these views by analyzing data from an apparently exhaustive prevalence study that used at least 14 distinct sources for ascertainment, including advertising, to find cases. Available limited data on source intersection provided in the report enable the plausible inference that the study missed about 25-40% of cases. We urge that no attempted complete prevalence studies be presented without data on ascertainment by source intersection.

Bias↗
PubMed1992

Interrelationships of relative risks of birth defects in embryonic and fetal deaths, in livebirths, and in all conceptuses.

Most studies of associations with birth defects are undertaken in livebirths. An observed association in livebirths different from unity may be compatible with no association in conceptuses if "balanced" by a particular relative risk in embryonic and fetal deaths. We derived formulae to address the following queries: (1) If one observes in livebirths a relative risk of birth defect, tau def,lb, then, with what combinations of relative risk of defect in embryonic and fetal deaths, tau def,efd, and in all conceptuses, tau def, is this value compatible? (2) What balancing relative risk in embryonic and fetal deaths is predicted if there is no causal association in all conceptuses? (3) Under what circumstances is there no relative risk in embryonic and fetal deaths that can balance an observed relative risk in livebirths? We present an expression for tau def,efd in terms of five other variables: tau def,lb, tau def, and tau efd (the relative risk of embryonic or fetal death), and the lethalities of the average (unexposed) conceptus and of the (unexposed) defective conceptus. This equation enables one to derive the balancing relative risk in embryonic and fetal deaths, bal tau def,efd, which is the value of tau def,efd when tau def = 1.0. If bal tau def,efd is negative, no such balancing relative risk exists, and any observed association in livebirths is incompatible with a null association in all conceptuses, that is, the association cannot be explained completely by differential selection of conceptuses with defect.

Abortion, Spontaneous↗
PubMed1991

The effects of model selection on confidence intervals for the size of a closed population.

One encounters in the literature estimates of some rates of genetic and congenital disorders based on log-linear methods to model possible interactions among sources. Often the analyst chooses the simplest model consistent with the data for estimation of the size of a closed population and calculates confidence intervals on the assumption that this simple model is correct. However, despite an apparent excellent fit of the data to such a model, we note here that the resulting confidence intervals may well be misleading in that they can fail to provide an adequate coverage probability. We illustrate this with a simulation for a hypothetical population based on data reported in the literature from three sources. The simulated nominal 95 per cent confidence intervals contained the modelled population size only 30 per cent of the time. Only if external considerations justify the assumption of plausible interactions of sources would use of the simpler model's interval be justified.

Confidence Intervals↗
PubMed1991

Conceptus viability, malformation, and suspect mutagens or teratogens in humans. The Yule-Simpson paradox and implications for inferences of causality in studies of mutagenicity or teratogenicity limited to human livebirths.

If a genetic disorder or a congenital malformation is associated with embryonic or fetal death, then this may distort reported associations of environmental or biological factors with genetic and congenital disorders. We illustrate how such distortion may occur in humans as a manifestation of the Yule-Simpson (or Simpson) statistical paradox. We analyze the reported negative association of maternal smoking and Down syndrome in livebirths and demonstrate that under plausible conditions, valid negative associations both in livebirths and in embryonic or fetal deaths can occur, despite the fact that in all conceptuses there may be no association whatsoever. A similar analogous manifestation of the Yule-Simpson paradox may hold for positive associations. That is, positive relative risks may occur for an alleged mutagen or teratogen in separate studies both of livebirths, and of embryonic and fetal deaths, despite the absence of any effect in all conceptuses. These considerations illustrate the need for data on genetic disorders and malformations in embryonic and fetal deaths, and the need for a synthesis of such data with those from studies in livebirths before valid inferences may be made about mutagenic or teratogenic effects of environmental or biological factors.

Congenital Abnormalities↗
PubMed1988

Relation of blood flow to VO2, PO2, and PCO2 in dog gastrocnemius muscle.

We pump-perfused gastrocnemius-plantaris muscle preparations at constant pressure to study the relationship of muscle blood flow (Q) to muscle oxygen consumption (VO2), venous oxygen tension (PVO2), and venous carbon dioxide tension (PVCO2) during steady-state exercise at different rates. Tests were performed under four experimental conditions produced by altering the perfusate blood-gas status with a membrane lung. The consistency of the relationship of Q to other variables was evaluated by statistical analysis of fitted curves. Not one of the above listed variables had the same relationship with Q in all four of the experimental conditions we tested. However, we did find that a consistent relationship existed among Q, PVO2, and PVCO2 in our data. That relationship is well described by the equation (Q-23).[PVO2 - (0.5.PVCO2) - 3] = 105 (when Q is expressed in ml.100 g-1.min-1 and PVO2 and PVCO2 in mmHg). One interpretation of this result is that both PO2 and PCO2 are important variables in the control of blood flow in skeletal muscle the combined influence of which could account for nearly all of the hyperemia response to steady-state muscle exercise.

Animals↗