Sentence examples for creating propensity from inspiring English sources
In the primary analysis, missing weight measurements will be assumed missing at random, but additional analyses will be conducted related to missing data (e.g. comparing baseline characteristics of completers vs non-completers and creating propensity scores).
We did not create propensity scores for the 2.3% of patients missing key covariates.
We created propensity score-matched pairs (n = 133) and evaluated differences in health perception.
To evaluate the robustness of the results, we created propensity score matched cohorts of patients.
Using the Greed 5 1 digit-matching algorithm, we created propensity score-matched pairs without replacements (a 1 2 match).
A time dependent logistic regression model was built to create propensity scores of being treated with PD compared to HD as the initial dialysis modality.
1,846 patients were included to create propensity score matched treatment groups for platinum/pemetrexed versus docetaxel (95 pairs), paclitaxel (118 pairs), gemcitabine (199 pairs), and vinorelbine (72 pairs -contained doublet, respairs -contained
31 In a study of a dose-response effect of enzyme replacement therapy in patients with Gaucher disease type 1, Grabowski and colleagues created propensity scores to summarize multiple confounders and then used the scores to match patients who received different doses of enzyme therapy.
Using the parameter estimates for creating a propensity score, the following formula was reached for the propensity score: Propensity score = 4.8383+ dyslipidemia x (0.5314)+ thrombolytic use x (−1.0176)+ use of glycoprotein IIb/IIIa inhibitor drugs x (−1.3345)+ age x (−0.0306)+ weight x (0.0246)+ vessel diameter x (−1.1752).
Consequently, we implemented a propensity score matching method to reduce this bias 16 by first creating a propensity score to represent the relationship between multiple characteristics and the matching outcome: being in the prison group (treatments) or not (controls).
The link between maternal and offspring obesity can be explained by the 'early-life hyper nutrition' pathway where exposure to over-nutrition during fetal or early postnatal life may lead to perturbations of adipogenesis and/or appetite control mechanisms, creating a propensity to later obesity [ 8].
