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Register a new userEffect sizes of the differences between means without assuming the variance equality and between a mean and a constant
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Satoshi Aoki
Publication date
2019
fields
Mathematical Statistics
and research's language is
English
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Hedges d, an existing unbiased effect size of the difference between means, assumes the variance equality. However, the assumption of the variance equality is fragile, and is often violated in practical applications. Here, we define e, a new effect size of the difference between means, which does not assume the variance equality. In addition, another novel statistic c is defined as an effect size of the difference between a mean and a known constant. Hedges g, our c, and e correspond to Students unpaired two-sample t test, Students one-sample t test, and Welchs t test, respectively. An R package is also provided to compute these effect sizes with their variance and confidence interval.
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Comparing the differences in outcomes (that is, in dependent variables) between two subpopulations is often most informative when comparing outcomes only for individuals from the subpopulations who are similar according to independent variables. The independent variables are generally known as scores, as in propensity scores for matching or as in the probabilities predicted by statistical or machine-learned models, for example. If the outcomes are discrete, then some averaging is necessary to reduce the noise arising from the outcomes varying randomly over those discrete values in the observed data. The traditional method of averaging is to bin the data according to the scores and plot the average outcome in each bin against the average score in the bin. However, such binning can be rather arbitrary and yet greatly impacts the interpretation of displayed deviation between the subpopulations and assessment of its statistical significance. Fortunately, such binning is entirely unnecessary in plots of cumulative differences and in the associated scalar summary metrics that are analogous to the workhorse statistics of comparing probability distributions -- those due to Kolmogorov and Smirnov and their refinements due to Kuiper. The present paper develops such cumulative methods for the common case in which no score of any member of the subpopulations being compared is exactly equal to the score of any other member of either subpopulation.
Many predictions are probabilistic in nature; for example, a prediction could be for precipitation tomorrow, but with only a 30 percent chance. Given both the predictions and the actual outcomes, reliability diagrams (also known as calibration plots) help detect and diagnose statistically significant discrepancies between the predictions and the outcomes. The canonical reliability diagrams are based on histogramming the observed and expected values of the predictions; several variants of the standard reliability diagrams propose to replace the hard histogram binning with soft kernel density estimation using smooth convolutional kernels of widths similar to the widths of the bins. In all cases, an important question naturally arises: which widths are best (or are multiple plots with different widths better)? Rather than answering this question, plots of the cumulative differences between the observed and expected values largely avoid the question, by displaying miscalibration directly as the slopes of secant lines for the graphs. Slope is easy to perceive with quantitative precision even when the constant offsets of the secant lines are irrelevant. There is no need to bin or perform kernel density estimation with a somewhat arbitrary kernel.
Causal variance decompositions for a given disease-specific quality indicator can be used to quantify differences in performance between hospitals or health care providers. While variance decompositions can demonstrate variation in quality of care, causal mediation analysis can be used to study care pathways leading to the differences in performance between the institutions. This raises the question of whether the two approaches can be combined to decompose between-hospital variation in an outcome type indicator to that mediated through a given process (indirect effect) and remaining variation due to all other pathways (direct effect). For this purpose, we derive a causal mediation analysis decomposition of between-hospital variance, discuss its interpretation, and propose an estimation approach based on generalized linear mixed models for the outcome and the mediator. We study the performance of the estimators in a simulation study and demonstrate its use in administrative data on kidney cancer care in Ontario.
We study the least squares estimator in the residual variance estimation context. We show that the mean squared differences of paired observations are asymptotically normally distributed. We further establish that, by regressing the mean squared differences of these paired observations on the squared distances between paired covariates via a simple least squares procedure, the resulting variance estimator is not only asymptotically normal and root-$n$ consistent, but also reaches the optimal bound in terms of estimation variance. We also demonstrate the advantage of the least squares estimator in comparison with existing methods in terms of the second order asymptotic properties.
The detection of differentially expressed (DE) genes is one of the most commonly studied problems in bioinformatics. For example, the identification of DE genes between distinct disease phenotypes is an important first step in understanding and developing treatment drugs for the disease. It can also contribute significantly to the construction of a discriminant rule for predicting the class of origin of an unclassified tissue sample from a patient. We present a novel approach to the problem of detecting DE genes that is based on a test statistic formed as a weighted (normalized) cluster-specific contrast in the mixed effects of the mixture model used in the first instance to cluster the gene profiles into a manageable number of clusters. The key factor in the formation of our test statistic is the use of gene-specific mixed effects in the cluster-specific contrast. It thus means that the (soft) assignment of a given gene to a cluster is not crucial. This is because in addition to class differences between the (estimated) fixed effects terms for a cluster, gene-specific class differences also contribute to the cluster-specific contributions to the final form of the test statistic. The proposed test statistic can be used where the primary aim is to rank the genes in order of evidence against the null hypothesis of no DE. We also show how a P-value can be calculated for each gene for use in multiple hypothesis testing where the intent is to control the false discovery rate (FDR) at some desired level. With the use of real and simulated data sets, we show that the proposed contrast-based approach outperforms other methods commonly used for the detection of DE genes both in a ranking context with lower proportion of false discoveries and in a multiple hypothesis testing context with higher power for a specified level of the FDR.
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