LYCOS RETRIEVER 
Dexamethasone: Figs
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Dexamethasone attenuated ACh-induced, EC-dependent vasodilation. Superfusion of the chamber tissue with 10 µM ACh induced pronounced vasodilation of resistance arterioles (Fig. 1). This vasodilation was attenuated significantly in a dose-dependent fashion in animals that had received oral administration of dexamethasone for 1 wk (0.1–3.0 mg/kg body wt; Fig. 1A). In contrast, the endothelium-independent vasodilation by the NO donor SNAP was not affected significantly by dexamethasone at any of the tested doses (Fig.
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Dexamethasone down-regulates mTOR signaling and REDD2 expression but enhances REDD1 expression in L6 myoblasts. L6 myoblasts were exposed to dexamethasone ([D]ex) or vehicle control (con) as described in the legend to Fig. 2B. Cell homogenates were analyzed for the phosphorylation state of S6K1 (A) and 4E-BP1 (B) by changes in migration during SDS-PAGE. The , , , and forms of the proteins are denoted to the right of the respective blots. The results are representative of four studies performed.
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Dexamethasone was compared with placebo in four trials in adults and in three trials in children (Table 1, A and B, and Figure 1). In adults, dexamethasone 8 and 10 mg, orally or IV, was tested, in children, dexamethasone 0.5 mg/kg, 1 mg/kg, and 1.5 mg/kg IV. All results were statistically significant in favor of dexamethasone, except early nausea with dexamethasone 8 mg IV in a small trial with 25 treated adults (Table 1 A) and late vomiting with dexamethasone 0.5 mg/kg IV in a trial with a very low control event rate (the incidence of vomiting with placebo was only 9%) in children (Table 1 B). When data were combined to increase power, the number-needed-to treat to prevent early and late vomiting with any dose of dexamethasone compared with placebo in adults and children was 7.1 (95% CI 4.5 to 18) and 3.8 (95% CI 2.9 to 5). Two adult trials analyzed dexamethasone’s antinausea effect (Table 1 B); the number needed to treat was 4.3 (95% CI 2.3 to 26).
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Dexamethasone inhibited Ag-induced tyrosine phosphorylation of Btk (Fig. 6A), PLC1, (Fig. 6B), and PLC2 (Fig. 6C) in a dose-dependent manner without affecting the expression of these proteins in RBL-2H3 cells. However, the phosphorylation of PLC2 was inhibited to a much greater extent than the phosphorylation of PLC1 (Fig. 6D), a possible indication that these two isoforms are regulated differently.
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Dexamethasone suppresses iNOS gene transcription and promoter activation. To examine whether the suppressive effects of GC occurred at the level of transcription, nuclear run-on assays were performed. Shown in Fig. 4 is a representative nuclear run-on experiment looking at the effects of CM with or without dexamethasone on iNOS gene transcription. An average of several experiments indicates that CM stimulation increases iNOS transcription 8-to 10-fold in rat hepatocytes, and the addition of dexamethasone results in a 50% inhibition of iNOS transcription.
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Dexamethasone 8 mg added to granisetron 20 or 40 µg/kg was compared with placebo in two trials only, both in adults (Table 2, C and D, and Figure 2). Event rates with the combination therapy were very low, between 2% and 5% for both early and late outcomes. The number needed to treat point estimate to prevent early nausea and vomiting with the combination therapy compared with placebo was approximately 4 and to prevent late nausea and vomiting was 3.7 and 5.5.
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