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Specifically, our study power was enhanced by selecting a genetically enriched study population predisposed to breast cancer, by using a counter-matched design, and by developing a dose reconstruction method to reduce the error in estimating individual radiation exposure derived from imperfect and old medical records.
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When developing a dose-verification system, we needed to know which TLDs are sufficiently stable to use as postal dosimeters.
We developed a dose finding trial to assess toxicity, differentiating activity, and clinical impact of the combination of bryostatin-1 and GM-CSF.
The MTD was defined as the dose at which three or more out of six patients developed a dose limiting toxicity.
Therefore, our objective was to develop a dose selection method for PK studies in hemodialysis patients using the simulation-extrapolation of an optimal PK dose from the PK parameters of a subpharmacological dose.
We have previously developed a dose-dependent glycan array binding assay [10], [21] to quantitatively characterize glycan receptor binding affinity of HA by calculating an apparent binding constant Kd'.
No patient developed a dose-limiting toxicity.
One patient who received the 36 mg/m dose on day 8 developed a dose-limiting toxicity (grade 3 fatigue).
By integrating the results of the studied patients, they developed a dosing regimen for propofol sedation in ICU patients.
For this reason, we developed a dosing procedure that enables us to trace and subtract the fluctuating fragmentation behavior.
If one patient at a given dose level developed a dose-limiting toxicity, three additional patients were to be treated at that level.
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