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In experiment 1, 500 g/day of Q was found to be the minimal dose that decreased feed intake in heifers.
Formal regulatory review of a proposed human study requires an assessment of the minimal dose that shows some metabolic/clinical effect [30].
Each batch of recombinant RANKL was tested in dose response studies and the minimal dose that promoted maximal osteoclast differentiation of WT marrow (typically 50 ng/ml) was used for all of the experiments with the exception of the dose-response studies reported here, where the maximum dose tested (100 ng/ml) was twice the dose used for differentiation studies.
with different inocula in Todd-Hewitt broth: 1×106, 5×106, 1×107, 5×107, 1×108 cfu/ml (spectrophotometrically measured) to determine the minimal dose that produced a 100% mortality rate over a 7-day follow-up period (i.e., the minimal lethal dose).
The dose we tested corresponded to the minimal dose that has been shown to be active on CFTR function.
Each year, ICS was adjusted to the minimal dose that maintained the patient's asthma in control and the efficacy and tolerability of SCIT was evaluated accordingly.
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We used log2 to reflect the minimal dose spacing, that is, doubling, typically used for in vivo toxicology studies.
Each individual UVR dose was approximately one-fourth of the mouse minimal erythemic dose, that is, 1.0 kJ/m.
This calculation was defined as an optimization problem: find the minimal predicted dose that ensures a certain level of receptor occupancy, given a certain number of doses per day, a certain coverage time, and the predicted human PK parameters.
As this investigation required the use of tamoxifen to induce Cre-recombinase-mediated gene recombination in liver, we needed to determine the minimal dose of tamoxifen that would 1) reduce serum IGF-1 levels by at least 50% in the iLID mice without affecting bone remodeling per se and 2) not affect circulating IGF-1 levels in floxed controls.
Thus, localized administration of HU210 or oral administration of CB1 agonists with limited CNS availability, such as CT-3 (ajulemic acid), produced analgesia both in pain models [ 42, 43] and in the clinic at a dose that causes minimal CNS side effects [ 44].
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