Acta pharmacologica Sinica
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Acta Pharmacol. Sin. · Dec 2011
Magnesium sulfate enhances non-depolarizing muscle relaxant vecuronium action at adult muscle-type nicotinic acetylcholine receptor in vitro.
To investigate the effect of magnesium sulfate and its interaction with the non-depolarizing muscle relaxant vecuronium at adult muscle-type acetylcholine receptors in vitro. ⋯ Clinical enhancement of vecuronium-induced muscle relaxation by magnesium sulfate can be attributed partly to synergism between magnesium sulfate and non-depolarizing muscle relaxants at adult muscle-type acetylcholine receptors.
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Acta Pharmacol. Sin. · Oct 2011
Comparative StudyComparison between cerebral state index and bispectral index as measures of electroencephalographic effects of sevoflurane using combined sigmoidal E(max) model.
The cerebral state index (CSI) was recently introduced as an electroencephalographic monitor for measuring the depth of anesthesia. We compared the performance of CSI to the bispectral index (BIS) as electroencephalographic measures of sevoflurane effect using two combined sigmoidal E(max) models. ⋯ The overall performance of the BIS and CSI during sevoflurane anesthesia was similar despite major differences in their algorithms. However, the CSI was more consistent and more sensitive to changes in sevoflurane concentration, whereas the measured BIS seemed to respond faster. The newly developed combined E(max) model adequately described the clinical data, including the pharmacodynamic plateau.
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Acta Pharmacol. Sin. · Oct 2011
Effects of Rhein lysinate on H2O2-induced cellular senescence of human umbilical vascular endothelial cells.
To observe the effect of Rhein lysinate (RHL) on cellular senescence of human umbilical vascular endothelial cells (HUVECs) and elucidate its action mechanism. ⋯ RHL protected HUVECs against cellular senescence induced by H2O2, via up-regulation of Sirt1 expression and down-regulation of the expression of acetyl-p53 and p16(INK4a).
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Acta Pharmacol. Sin. · Jun 2011
ReviewTargeting F508del-CFTR to develop rational new therapies for cystic fibrosis.
The mutation F508del is the commonest cause of the genetic disease cystic fibrosis (CF). CF disrupts the function of many organs in the body, most notably the lungs, by perturbing salt and water transport across epithelial surfaces. F508del causes harm in two principal ways. ⋯ We emphasize the use of high-throughput screening to identify lead compounds for therapy development. These compounds include CFTR correctors that restore the expression of F508del-CFTR at the apical membrane of epithelial cells and CFTR potentiators that rescue the F508del-CFTR gating defect. Initial results from clinical trials of CFTR correctors and potentiators augur well for the development of small molecule therapies that target the root cause of CF: mutations in CFTR.