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Prefrontal regions showed consistent bilateral reduction in oscillatory power (Fig. 2C), typically reaching maximal reduction after ∼20 min (Fig. 3B).
As observed, the administration of 100 mg/day of ASA induced, already after 1 week, a significant reduction of the vasodilatory response to ischemia that reached the maximal reduction after 4 weeks of treatment (RHI from 1.72 ± 0.30 to 1.33 ± 0.26, P < 0.0001); normal value ≥ 1.67.
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As shown in Figure 5, when the cultures were exposed to SI 34 10 μM, a time-dependent decrease of the cyclin D1 expression was observed with the maximal reduction detected after 72 h of treatment (P < 0.05 vs untreated cultures).
Fasting blood glucose was also decreased in the two recent canagliflozin studies, but showed a slight progressive decrease after the maximal reduction was observed at weeks 4 [ 5] and 6 [ 6].
The maximal reduction in MAP was observed after 3.5 h after AEH oral administration.
A maximal reduction of proliferation was achieved after treatment with 500 n M 17-AAG for 48 h, where Kyse70 and Kyse450 showed 80 and 84% inhibition, respectively.
Circulating fetuin-A levels were decreased in both endotoxemic (Fig. 1A) and septic (Fig. 1B) mice in a time-dependent fashion, with maximal reduction (by 50 60%) 24 48 h after onset of these diseases.
The maximal reduction was observed within 2 h after the treatment, with steady recovery thereafter.
In fact we demonstrated that the combination of the two inhibitors seems to give the maximal reduction of IL-1 β release after PM10 exposure.
For calibration, maximal reduction state of NAD(P H was achieved after the addition of 2 mmol/l sodium cyanide, and minimal reduction state was achieved after the addition of 200 μmol/l DNP.
This coincided with a maximal reduction in P-gp expression 20 days after single-dose irradiation and a complete loss of P-gp expression 10 days after the start of fractionated irradiation (5 × 4 Gy).
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