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Fixed effect meta-analysis considers that variation between studies is due purely to random variation.
The discrepancies between studies is due in part to the more stringent criteria applied in our study.
There was evidence of heterogeneity between studies in the three epidemic states with an I 2 of 80 87% (P < 0.001), indicating that the variation in RRHCV/HIV between studies is due to differences in effect size, and not chance.
Thus, a fixed effects model can be used to synthesize the data, since the assumption underlying a fixed effects model is that the treatment effect is the same in each study, and variation between studies is due to sampling (i.e., chance) [ 3, 7].
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This was used to test whether the differences between studies was due to chance.
These were used to test whether the differences obtained between studies were due to chance.
They concluded that a large variation between studies was due to different instruments used for assessing the preventability [ 23].
Approximately 62% of the variability between studies was due to moderate heterogeneity, with an I 61%9595% CI 5 84), Cochran Q test P value = 0.024 (Supplementary Fig. 1).
We suggest that the disagreement between the two studies is due to several factors, the first being the differences in the phylogenetic markers analyzed.
The discrepancy between the two studies is due to improved gene models provided by the more recent release of the P. trichocarpa Phytozome 7.0 database (http://www.phytozome.net).net
We also can not exclude the possibility that inconsistent results between epidemiological studies are due to measurement errors associated with dietary assessment, as these are inherent in a retrospective study design [ 19].
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