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Articles by S. H Cho
Total Records ( 2 ) for S. H Cho
  G. Y Kim , J. W Lee , S. H Cho , J. M Seo and J. H. Kim
 

Objective— The leukotriene B4 (LTB4) receptor BLT2 is expressed in endothelium, but no clear physiological function for it has yet been identified, especially in vascular angiogenesis. The purpose of this study is to characterize the potential function of BLT2 in vascular endothelial growth factor (VEGF)-induced angiogenesis.

Methods and Results— VEGF significantly upregulates BLT2 expression in human umbilical vein endothelial cells (HUVECs), and BLT2 knockdown by siRNA or inhibition of BLT2 by a specific BLT2 antagonist LY255283 attenuates VEGF-induced angiogenesis, which was determined by its effect on the formation of tube-like structures and on transmigration. The role of BLT2 in VEGF-induced angiogenesis was more evident in vivo, where BLT2 inhibition by LY255283 almost completely blocked VEGF-induced vessel formation in Matrigel-plug assays. In addition, we found that VEGF upregulates synthesis of the BLT2 ligand, 12(S)-hydroxyeicosatetraenoic acid (HETE). siRNA knockdown of 12-lipoxygenase (12-LO) expression attenuates VEGF-induced angiogenesis in HUVECs, and the addition of 12(S)-HETE to the 12-LO knockdown-HUVECs restores VEGF-induced angiogenesis. The activation of BLT2 itself by either 12(S)-HETE or LTB4 evoked significant angiogenic phenotypes, both in vitro and in vivo.

Conclusion— Our findings indicate that BLT2 plays an essential role in mediating VEGF-induced angiogenesis.

  J. A Jung , B. M Choi , S. H Cho , S. M Choe , J. L Ghim , H. M Lee , Y. J Roh and G. J. Noh
  Background

The aims of this study were to investigate the effectiveness, safety, pharmacokinetics, and pharmacodynamics of microemulsion propofol, AquafolTM (Daewon Pharmaceutical Co., Ltd, Seoul, Republic of Korea).

Methods

In total, 288 patients were randomized to receive 1% AquafolTM or 1% Diprivan® (AstraZeneca, London, UK) (n=144, respectively). A 30 mg test dose of propofol was administered i.v. over 2 s for assessing injection pain. Subsequently, a bolus of propofol 2 mg kg–1 (–30 mg) was administered. Anaesthesia was maintained with a variable rate infusion of propofol and a target-controlled infusion of remifentanil. Mean infusion rates of both formulations and times to loss of consciousness (LOC) and recovery of consciousness (ROC) were recorded. Adverse events and pharmacokinetic and pharmacodynamic characteristics were evaluated.

Results

Mean infusion rate of AquafolTM was not statistically different from that of Diprivan® (median: 6.2 vs 6.3 mg kg–1 h–1). Times to LOC and ROC were slightly prolonged in AquafolTM (median: 21 vs 18 s, 12.3 vs 10.8 min). AquafolTM showed similar incidence of adverse events to Diprivan®. AquafolTM (vs Diprivan®) caused more severe (median VAS: 72.0 vs 11.5 mm) and frequent (81.9 vs 29.2%) injection pain. The dose-normalized AUClast of AquafolTM and Diprivan® was 0.71 (0.19) and 0.74 (0.20) min litre–1. The V1 of both formulations were proportional to lean body mass. Sex was a significant covariate for k12 and Ce50 of AquafolTM, and for ke0 of Diprivan®.

Conclusions

AquafolTM was as effective and safe as Diprivan®, but caused more severe and frequent injection pain. AquafolTM demonstrated similar pharmacokinetics to Diprivan®.

 
 
 
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