These conflicting findings might be explained by dose-related differences in the hemodynamic and immunologic effects of dopexamine [ 12].
This cannot be explained by lower dose, as the median lopinavir dose received by children in the pharmacokinetic study was 19.0 mg/kg or 537 mg/m q.d., which is comparable or higher than the doses received by children in the other studies.
The association between increasing cumulative albumin dose and decreasing mortality could not be explained by vasoconstrictor dose or type, treatment duration, age, baseline serum creatinine, bilirubin or albumin, baseline mean arterial pressure, or study design, size or time period.
Indeed, the observed threshold of benefit of folic acid with MTX toxicity, can be explained by a dose of 5 10 mg per week to adequately correct this deficit.
This difference found between the tumor entities is difficult to interpret, but might be explained by different dose distributions.
The lower reactogenicity induced with the Montanide formulation could also be explained by the dose of adjuvant, 0.5 ml here against 1 ml in the MSP3 study, and the intrinsic character of the antigen/adjuvant mixture.
Repeated operations for radionecrosis were observed and may be explained by inhomogeneous dose distribution and slight migration of seeds over time.
A patient-level meta-analysis suggested that some of the differences might be explained by the dose of dopexamine employed [ 13].
However, only 30% of the variation of change in Pmsf can be explained by the dose of i.v. fluid given.
Interestingly, in those studies, the therapeutic effect of IL-10 on anti Col II antibodies was associated with contradictory results that could be explained by the dose and timing of the IL-10 treatments.
