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This disparity between trials could be attributed to a many factors, including differences between interventions, measurement techniques, and cohorts.
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This discrepancy between the trials could be dependent upon the specific drug used and the design of the trials [ 118- 124].
The difference between these trials could be that in our trial we used a more reliable score: we have shown that individual items from the Centor score and score 1 did not perform optimally in our two previous diagnostic cohorts in terms of identifying patients with low likelihood of streptococcal infection.
Differences in hypoglycemic events between the two trials could be in part explained by reduced nutritional intake in surgical patients and the fact that in the previous trial we dosed the TDD of insulin as 0.4 units/kg for BG between 140 mg/dL and 200 mg/dL and 0.5 unit/kg for BG between 200 mg/dL and <400 mg/dL.
High pCR rates in unrandomised trials and differences in pCR rates between treatments in randomised trials could be explained by high proportions of ER-negative patients and imbalances in ER status between treatment arms, respectively.
If high quality trials could be found, comparisons between all of the studies and studies with high quality would be conducted.
The differences between the naturalistic studies and the randomised trials could be resolved if there were at least the inclusion of some standard measures of what one would expect to change as a result of using an ePHR.
Only four trials could be rated as low RoB on all domains considered, preventing us from reliably assessing the relationship between overall trial risk of bias and outcomes.
* The trials could be held in secret.
The United States Olympic trials could be another matter.
Additional trials could be helpful to clarify this point.
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