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The Table includes the distribution of study variables in the study population, study sample and sample with mortality data.
The following comparisons were examined within each of the intervention and control groups: 1) population versus study sample and 2) study sample versus sample with mortality data.
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Table 2 presents a comparison between the enrolled sample and the sample with known mortality status.
The strengths of BEP are its simplicity, based on a relatively large sample with overall mortality 51/623 (8.2%).
However, the correlation was not as strong among the samples with higher mortality values of >40%.
This possibility was confirmed by the fact that, for those samples with high mortality, the measured TUs in sediment were also low, ranging from non-detected to 0.1.
Relative quantities of Mycoplasma sp. were calculated using previously published methods[26] for a subset of samples representing 10 animals with high fold differences (>10) sampled during an outbreak with mortality, 10 animals with low fold differences (<10) sampled during an outbreak, and 10 randomly selected samples from outside the outbreaks.
This may lead to improved outcomes for these patients, including greater survival, and may partly explain why HER-2 overexpression showed no association with mortality in our sample of women with localized disease.
With this sample size, mortality was not impacted by VAP. Discussion In this large cohort, VAP occurs early during VA-ECLS support while identified pathogens are those known to be involved for late-onset VAP.
However, they were not associated with mortality in our study sample.
For example, a doubling or halving of mortality by an intervention (or with a risk factor), even in the absence of effect modification, will have lower statistical power in a sample with lower baseline risk of mortality outcomes (as a healthier sample portends).
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