Effect of galactose-ethanol feeding on growth in rats.
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Adenosine Diphosphate↗
Biomedical subjects
N Keiding
Publications and source records attributed to N Keiding.
Maximum likelihood estimation of the size distribution of liver cell nuclei from the observed distribution in a plane section.
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Biopsy↗
The role of frailty models and accelerated failure time models in describing heterogeneity due to omitted covariates.
In survival analysis, deviations from proportional hazards may sometimes be explained by unaccounted random heterogeneity, or frailty. This paper recalls the literature on omitted covariates in survival analysis and shows in a case study how unstably frailty models might behave when asked to account for unobserved heterogeneity in standard survival analysis with no replications per heterogeneity unit. Accelerated failure time modelling seems to avoid these difficulties and also to yield easily interpretable results. We propose that it would be advantageous to upgrade the accelerated failure time approach alongside the hazard modelling approach to survival analysis.
Algorithms↗
The Manton-Woodbury model for longitudinal data with dropouts.
Often in longitudinal studies one is not able to obtain a complete set of measurements of the variable recorded over time for each person in the study. This could be caused by some of the persons dying (or leaving the study for some other reasons) while the study is going on. If there is any concern that such missing data (which have been termed dropouts) and the variables measured over time affect each other, a model for the joint distribution is needed. For a review of several such models see Hogan and Laird (in this volume). A model of the same kind was proposed by Woodbury and Manton and developed further later on. In this model it is possible to describe the evolution of the distribution of the variable measured over time when exposed to mortality selection. In contrast to other models, this allows for an explicit description of the interaction between the variable measured over time and the time to dropout. We describe the model and propose some generalizations. The theory is illustrated by some Monte Carlo simulations.
Adult↗
Event history analysis and inference from observational epidemiology.
Systematic inclusion of time in observational epidemiological studies may help strengthen the inference to be drawn, but new epidemiological challenges arise, such as time-dependent confounders - covariates which may change from being confounders to being intermediate variables. The focus of this presentation concerns two sets of tools: event history analysis and structural nested failure time models, both applied to a particularly intricate problem in observational epidemiology, of empirically assessing the graft-versus-leukaemia effect after bone marrow transplantation.
Bone Marrow Transplantation↗
Calculating expected mortality.
The widely used 'person-years method' of calculating expected mortality has been discussed recently by several authors. In studies where mortality is either lower or higher than the standard mortality of some reference population, the use of exposure to death as an estimator of the expected number of deaths will generally lead to bias, always exaggerating the difference between study and standard mortality. This bias is examined in a proportional hazards model. The recent suggestion by Hartz et al.1 of calculating the mortalities of individuals during their 'potential follow-up time' is claimed to be only rarely feasible in practice.
Biometry↗
Neurobehavioral deficits associated with PCB in 7-year-old children prenatally exposed to seafood neurotoxicants.
Prenatal exposure to polychlorinated biphenyls (PCBs) was examined by analysis of cord tissue from 435 children from a Faroese birth cohort. Analysis of 50 paired cord blood samples showed excellent correlation with the cord tissue concentration (r=.90). Among 17 neuropsychological outcomes determined at age 7 years, the cord PCB concentration was associated with deficits on the Boston Naming Test (without cues, two-tailed P=.09 not adjusted for mercury; with cues, P=.03), the Continuous Performance Test reaction time (P=.03), and, possibly, on long-term recall on the California Verbal Learning Test (P=.15). The association between cord PCB and cord-blood mercury (r=.42) suggested possible confounding. While no PCB effects were apparent in children with low mercury exposure, PCB-associated deficits within the highest tertile of mercury exposure indicated a possible interaction between the two neurotoxicants. PCB-associated increased thresholds were seen at two of eight frequencies on audiometry, but only on the left side, and no deficits occurred on evoked potentials or contrast sensitivity. The limited PCB-related neurotoxicity in this cohort appears to be affected by concomitant methylmercury exposure.
Child↗