• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.16 no.3
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• pp.211-221
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• 2006

This study was performed to compare with desorption efficiency and storage stability of CSC and CMS tubes for Ketones in workplace air. 1. The best desorbing solution for CSC tube was 1 % or 3 % dimethylformamide(DMF) in carbon disulfide($CS_2$). The desorption efficiencies were 96.40 % for cyclohexanone, 94.86 % for acetone, 96.96 % for methyl ethyl ketone(MEK), 103.44 % for methyl isobutyl ketone(MIBK), 100.17 % for methyl amyl ketone(MAK), 100.43 % for methyl butyl ketone(MBK), 97.01 % for toluene and 99.33 % for trichloroethylene(TCE). 2. The best desorbing solution for CMS tube was 1 % or 3 % DMF in $CS_2$. The desorption efficiencies were 96.42 % for cyclohexanone, 98.53 % for acetone, 99.67 % for MEK, 105.48 % for MIBK, 100.13 % for MAK, 100.13 % for MBK, 95.42 % for toluene and 98.15 % for TCE. 3. In the storage condition at room temperature($20^{\circ}C$), the recovery rates of cyclohexanone and MEK on CSC tube were rapidly decreased 30.9 % and 50.9 % after 4 weeks, respectively. The recovery rates of all of 6 ketones and 2 nonpolar solvents were shown over 80 % after 1 week in the storage condition of refrigerate temperature($-4^{\circ}C$), and were kept over 80 % after 4 weeks in the storage condition of freezer temperature($-20^{\circ}C$). 4. The recovery rates of cyclohexanone on CMS tube were 80.6 % for 1 week after and 60.5 % for 4 weeks after at room temperature($20^{\circ}C$). The recovery rates of cyclohexanone were shown 80.6 % for 1 week after and 60.5 % for 4 weeks after at $-4^{\circ}C$, and of 6 ketones and 2 non-polar solvents were kept stable over 85 % at $-4^{\circ}C$ and over 97 % at $-20^{\circ}C$ for 4 weeks after. In conclusion, the best desorbing solution was 1 % or 3 % DMF in $CS_2$ and more appropriate sorbent tube for ketones and non-polar solvents was CMS than CSC. We recommend CSC tube would be useful if the samples analyzed within 1 week because CMS tubes are more expensive than CSC tubes. However, if the storage time is needed more than 3 weeks, CMS tubes should be suitable and the storage condition should be below $-20^{\circ}C$.

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.95.2-95.2
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• 2007

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• BMB Reports
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• v.49 no.8
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• pp.437-442
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• 2016

We aimed to study the role of protein L-isoaspartyl methyltransferase (PIMT) in neuronal differentiation using basic fibroblast growth factor (bFGF)-induced neuronal differentiation, characterized by cell-body shrinkage, long neurite outgrowth, and expression of neuronal differentiation markers light and medium neurofilaments (NF). The bFGF-mediated neuronal differentiation of PC12 cells was induced through activation of mitogen-activated protein kinase (MAPK) signaling molecules [MAPK kinase 1/2 (MEK1/2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p90RSK], and phosphatidylinositide 3-kinase (PI3K)/Akt signaling molecules PI3Kp110β, PI3Kp110γ, Akt, and mTOR. Inhibitors (adenosine dialdehyde and S-adenosylhomocysteine) of protein methylation suppressed bFGF-mediated neuronal differentiation of PC12 cells. PIMT-eficiency caused by PIMT-specific siRNA inhibited neuronal differentiation of PC12 cells by suppressing phosphorylation of MEK1/2 and ERK1/2 in the MAPK signaling pathway and Akt and mTOR in the PI3K/Akt signaling pathway. Therefore, these results suggested that PIMT was critical for bFGF-mediated neuronal differentiation of PC12 cells and regulated the MAPK and Akt signaling pathways.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.139-145
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• 2018

The present study was undertaken to investigate the influence of hypothermia on endothelium-independent vascular smooth muscle contractility and to determine the mechanism underlying the relaxation. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Hypothermia significantly inhibited fluoride-, thromboxane $A_{2-}$, phenylephrine-, and phorbol ester-induced vascular contractions regardless of endothelial nitric oxide synthesis, suggesting that another pathway had a direct effect on vascular smooth muscle. Hypothermia significantly inhibited the fluoride-induced increase in pMYPT1 level and phorbol ester-induced increase in pERK1/2 level, suggesting inhibition of Rho-kinase and MEK activity and subsequent phosphorylation of MYPT1 and ERK1/2. These results suggest that the relaxing effect of moderate hypothermia on agonist-induced vascular contraction regardless of endothelial function involves inhibition of Rho-kinase and MEK activities.

• Journal of Life Science
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• v.19 no.8
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• pp.1073-1080
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• 2009

A number of studies have demonstrated that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risks of colorectal, oesophageal and lung cancers. NSAIDs have been shown to exert their anti-cancer effects through inducing apoptosis in cancer cells. The susceptibility of tumor cells to anti-tumor drug-induced apoptosis appears to depend on the balance between pro-apoptotic and anti-apoptotic programs such as nuclear factor kB (NF-kB), phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) and MEK1/2-ERK1/2 pathways. We examined the effects of pro-survival PI3K and ERK1/2 signal pathways on cell cycle arrest and apoptosis in response to NSAIDs including sulindac sulfide and NS398. We show that simultaneous inhibition of the Akt/PKB and ERK1/2 signal cascades could synergistically enhance the potential pro-apoptotic activities of sulindac sulfide and NS398. Similar enhancement was observed in cells treated with sulindac sulfide or NS398 and 100 ${\mu}$M genistein, an inhibitor of receptor tyrosine kinases (RTKs) that are upstream of PI3K and MEK1/2 signaling. We further demonstrate that NAG-1 is induced and plays a critical role(s) in apoptosis by NSAIDs-based combined treatment. In sum, our results show that combinatorialtreatment of sulindac sulfide or NS398 and genistein results in a highlysynergistic induction of apoptotic cell death to increase the chemopreventive effects of the NSAIDs, sulindac sulfide and NS398.

• Biomolecules & Therapeutics
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• v.26 no.4
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• pp.374-379
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• 2018

In this study, we investigated the effects of pelargonidin, an anthocyanidin found in many fruits and vegetables, on endothelium-independent vascular contractility to determine the underlying mechanism of relaxation. Isometric contractions of denuded aortic muscles from male rats were recorded, and the data were combined with those obtained in western blot analysis. Pelargonidin significantly inhibited fluoride-, thromboxane A2-, and phorbol ester-induced vascular contractions, regardless of the presence or absence of endothelium, suggesting a direct effect of the compound on vascular smooth muscles via a different pathway. Pelargonidin significantly inhibited the fluoride-dependent increase in the level of myosin phosphatase target subunit 1 (MYPT1) phosphorylation at Thr-855 and the phorbol 12,13-dibutyrate-dependent increase in the level of extracellular signal-regulated kinase (ERK) 1/2 phosphorylation at Thr202/Tyr204, suggesting the inhibition of Rho-kinase and mitogen-activated protein kinase kinase (MEK) activities and subsequent phosphorylation of MYPT1 and ERK1/2. These results suggest that the relaxation effect of pelargonidin on agonist-dependent vascular contractions includes inhibition of Rho-kinase and MEK activities, independent of the endothelial function.

• Clinical and Experimental Reproductive Medicine
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• v.28 no.2
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• pp.111-120
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• 2001

Objective: To verify the expression of leptin receptor (OB-R) in oocytes and preimplantation embryos, the involvement of mitogen activated protein kinase (MAPK or Erk1/2) in the leptin signaling, and effect of leptin on the oocyte maturation in mice. Method: RT-PCR analysis of OB-R was conducted in germinal vesicle (GV)-intact and MII stage oocytes, and 1, 2, 8-cell embryos and blastocysts. Germinal vesicle breakdown (GVB), polar body extrusion, monitored in the presence or absence of leptin ($1{\mu}M$). Following the leptin treatment, temporal changes in MAPK activity were verified by immunoprecipitation and in vitro kinase assay in MII oocytes. Results: The expression of OB-R mRNA was found in GV and MII oocyte but not in the embryos. MAPK activity of the MII oocytes was significantly increased by brief incubation in the HTF supplemented with leptin ($1{\mu}M$). Priming of PD098059, a MEK inhibitor to leptin treatment attenuated the activation of MAPK by leptin in MII oocytes. Following 24 hrs of culture of the GV oocytes, leptin significant increased the GVB and 1 st polar body extrusion. Conclusion: This result suggested that functional interaction between leptin and OB-R resulted in potentiation of MAPK (Erk1/2) activity in MII oocytes through MEK activation and that leptin might be a local regulator of meiotic maturation of the mouse oocytes.

• Proceedings of the Korean Society of Life Science Conference
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• 2006.09a
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• pp.98.2-98.2
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• 2006

• Journal of Life Science
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• v.21 no.3
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• pp.349-357
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• 2011

Inhibitors of EGFR (epidermal growth factor receptor) kinase activity may prove useful to therapeutically intervene in cancer and to treat other proliferative diseases. In this study, we investigated the inhibitive effects of two compounds named 63013 and 63033 possess a [1,4]-dioxino quinazoline structure that links the alkoxy side chains together and their structural characteristics are considered to allow better solubility than the dialkoxyquinazoline derivatives. The EGFR kinase activities of A431 human epidermoid carcinoma cells, stimulated by EGF were inhibited by treatment with 63013 and 63033 in a dose-dependent manner respectively. Consistent with the compound-mediated EGFR kinase suppression, the major EGF-related downstream target molecules, such as MEK1/2, MAPK p44/42, AKT and STAT3, were also suppressed by both compounds. Interestingly, both compounds led to cell growth inhibition at a lower concentration than that of Gefitinib (Iressa$^{(R)}$). Collectively, our study showed that both compounds may have good therapeutic potential as an EGFR kinase specific inhibitor to treat EGFR-related diseases.

• The Journal of Korean Medicine
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• v.25 no.3
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• pp.149-159
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• 2004

Backgrounds & Objectives : The water extract of Gyungokgo (GOG) has traditionally been used for treatment of general weakness and hemoptysis in oriental medicine. However, little is known about the mechanism by which the water extract of GOG rescues cells from these damages. This study was designed to investigate the protective mechanisms of GOG on H2O2­induced cell death in H9c2 cardiomyoblasts. Methods : In this study, we used H9c2 cells. Cells were treated with oxidative stress in the absence and presence of 1000㎍/ml GOG for 12hrs. Cells were treated with various concentrations of GOG for 12hrs. Cell viability was measured by MTT assay. Oxidative stress, which markedly decreased the viability of H9c2 cells, was characterized by apparent apoptotic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. Results : GOG significantly reduced H₂O₂-induced cell death and apoptotic characteristics. The cotreatment of GOG and H₂O₂ in H9c2 cells also induced the phosphorylation of ERKs in a time-dependent manner. Moreover, PD098059, a MEK1 (upstream activator of ERK) inhibitor attenuated the protective effect of GOG on H₂O₂-induced cytotoxicity in H9c2 cardiomyoblast cells. Conclusions : These results suggest that MEK/ERK pathways play important roles in the protective effects of GOG in H9c2 cells. Taken together, they suggest that the protective effects of the water extracts of GOG against oxidative damages may be mediated by the regulation of HO-1, Fas/FasL and Bcl-XS proteins.