• Journal of the Korean Chemical Society
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• v.64 no.6
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• pp.327-333
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• 2020

Performance of a portable GC that can be utilized for the real time determination of volatile organic compounds in air was evaluated. It employs purified/compressed ambient air as the carrier gas eliminating the need for high pressure gas tanks. The compact system with dimensions of 35 × 26 × 15 ㎤ and weight of 5 kg is powered by either a 24 V DC external adapter or battery pack. Chromatograms of the mixture sample including benzene, toluene, ethylbenzene, and oxylene at concentrations of 1 ppmv and 20 ppmv represent a good reproducibility: 3.79% and 0.48% relative standard deviations (RSDs) for peak area variations; 0.40% and 0.08% RSDs for retention times. The method detection limit was 0.09 ppmv. A 30 m long, 0.28 mm I.D. column operated at an optimal condition yielded a peak capacity of 61 with good resolution for a 10 min isothermal analysis. The relative standard deviations (RSD) of the peak area variations and retention times during consecutive measurements over 27 h were less than 2.4%RSD and 0.5%RSD, respectively. Thus, this instrument makes it suitable for continuous and field analysis of low-concentration VOC mixtures in the indoor/outdoor environment as well as the spillage accident of hazardous chemicals.

• Biomolecules & Therapeutics
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• v.20 no.1
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• pp.43-49
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• 2012

Stimulation of mast cells through the high affinity IgE receptor (Fc${\varepsilon}$RI) induces degranulation, lipid mediator release, and cytokine secretion leading to allergic reactions. Although various signaling pathways have been characterized to be involved in the Fc${\varepsilon}$RI-mediated responses, little is known about the precious mechanism for the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in mast cells. Here, we report that rapamycin, a specific inhibitor of mammalian target of rapamycin (mTOR), reduces the expression of TNF-${\alpha}$ in rat basophilic leukemia (RBL-2H3) cells. IgE or specific antigen stimulation of RBL-2H3 cells increases the expression of TNF-${\alpha}$ and activates various signaling molecules including S6K1, Akt and p38 MAPK. Rapamycin specifically inhibits antigeninduced TNF-${\alpha}$ mRNA level, while other kinase inhibitors have no effect on TNF-${\alpha}$ mRNA level. These data indicate that mTOR signaling pathway is the main regulation mechanism for antigen-induced TNF-${\alpha}$ expression. TNF-${\alpha}$ mRNA stability analysis using reporter construct containing TNF-${\alpha}$ adenylate/uridylate-rich elements (AREs) shows that rapamycin destabilizes TNF-${\alpha}$ mRNA via regulating the AU-rich element of TNF-${\alpha}$ mRNA. The antigen-induced activation of S6K1 is inhibited by specific kinase inhibitors including mTOR, PI3K, PKC and $Ca^{2+}$chelator inhibitor, while TNF-${\alpha}$ mRNA level is reduced only by rapamycin treatment. These data suggest that the effects of rapamycin on the expression of TNF-${\alpha}$ mRNA are not mediated by S6K1 but regulated by mTOR. Taken together, our results reveal that mTOR signaling pathway is a novel regulation mechanism for antigen-induced TNF-${\alpha}$ expression in RBL-2H3 cells.