• Proceedings of the Korean Nuclear Society Conference
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• 1996.05c
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• pp.231-237
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• 1996

Defect equilibrium equations were modelled, and the relations of P $o_2$, venus x were derived using the mass action law. The dominant defect species active in a specified region were determined by fitting the curve of experimental data to the calculated curve of log P $o_2$, versus log x for each theoretical model. The calculated curve for (2:1:2) and (Er')$^{x}$ in the hyperstoichiometric $U_{1-y}$E $r_{y}$ $O_{2＋x}$ and that for (2Er'quot;)$^{x}$ $_{dec}$ in the hypostoichiometric $U_{1-y}$E $r_{y}$ $O_{2－x}$ are in good agreement with the present experimental results. The sintering behavior of Er-doped U $O_2$ is observed with erbium content in oxidizing and reducing atmospheres. For sintering in oxidizing atmosphere, sintered density decreases as increasing y in $U_{1-y}$E $r_{y}$ $O_{2＋x}$. However, in hydrogen atmosphere, sintered density decreases as increasing y at lower erbium content but the density increases again above y=0.10. In oxidizing sintering conditions, the formation of (Er'U')$^{x}$ clusters hinders the diffusion of cations, and hence the sinterability of Er-doped U $O_2$ decreases. In reducing atmosphere of Er-doped U $O_2$ for higher Er concent, the oxygen vacancies make (Er')$^{x}$ cluster decompose by charge compensation and the concentration of mobile cations increases, thereby improving the sinterability.ntration of mobile cations increases, thereby improving the sinterability.ability.

• Proceedings of the KIEE Conference
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• 2000.07e
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• pp.35-39
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• 2000

$ZnIn_2S_4$ and $ZnGaInS_4:Er^{3+}$ single crystals crystallized in the rhombohedral (hexagonal) space group $C_{3v}^5(R3m)$, with lattice constants $a=3.852{\AA},\;c=37.215{\AA}$ for $ZnIn_2S_4$, and $a=3.823{\AA}$, and $c=35.975{\AA}$ for $ZnIn_2S_4:Er^{3+}$. The optical absorption measured near the fundamental band edge showed that the optical energy band structure of there compounds had a direct and indirect band gap, the direct and indirect energy gaps are found to be 2.778 and 2.682 eV for $ZnIn_2S_4$, and 2.725 and 2.651eV for $ZnIn_2S_4:Er^{3+}$ at 293 K. The photoluminescence spectra of $ZnIn_2S_4:Er^{3+}$ measured in the wavelength ranges of $500nm{\sim}900nm$ at 10 K. Eight sharp emission peaks due to $Er^{3+}$ ion are observed in the regions of $549.5{\sim}550.0nm,\;661.3{\sim}676.5nm$, and $811.1{\sim}834.1nm$, and $1528.2{\sim}1556.0nm$ in $CdGaInS_4:Er^{3+}$ single crystal. These PL peaks were attributed to the radiative transitions between the split electron energy levels of the $Er^{3+}$ ions occupied at $C_{2v}$, symmetry of the $ZnIn_2S_4$ single crystals host lattice.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1431-1437
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• 2012

The growth of many breast tumors is stimulated by IGF-1, which activates signal transduction pathways inducing cell proliferation. $ER{\alpha}$ is important in this process. The aim of the study was to investigate relationships in vitro among inhibitory effects of luteolin on the growth of MCF-7 cells, IGF-1 pathway and $ER{\alpha}$. Our results showed that luteolin could effectively block IGF-l-stimulated MCF-7 cell proliferation in a dose- and time-dependent manner and block cell cycle progression and induce apoptosis evidenced by the flow cytometric detection of sub-G1DNA content. Luteolin markedly decreased IGF-l-dependent IGF-IR and Akt phosphorylation without affecting Erk1/2 phosphorylation. Further experiments pointed out that $ER{\alpha}$ was directly involved in IGF-l induced cell growth inhibitory effects of luteolin, which significantly decreased $ER{\alpha}$ expression. Knockdown of $ER{\alpha}$ in MCF-7 cells by an $ER{\alpha}$-specific siRNA decreased the IGF-l induced cell growth inhibitory effects of luteolin. $ER{\alpha}$ is thus a possible target of luteolin. These findings indicate that the inhibitory effect of luteolin on the growth of MCF-7 cells is via inhibiting IGF-l mediated PI3K-Akt pathway dependent of $ER{\alpha}$ expression.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3223-3228
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• 2016

Reports indicate that 15-deoxy-delta-12,14-prostaglandin-J2 (15d-PGJ2) has anticancer activities, but its mechanisms of action have yet to be fully elucidated. We therefore investigated the effects of 15d-PGJ2 on the human breast cancer cell lines, MCF-7 (estrogen receptor $ER{\alpha}+/ER{\beta}+$) and MDA-MB-231 ($ER{\alpha}-/ER{\beta}+$). Cellular proliferation and cytotoxicity were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays while apoptosis was determined by fluorescence microscopy and flow cytometry using annexin V-propidium iodide (PI) staining. ER expression was determined by Western blotting. Intracellular calcium was stained with Fluo-4 AM while intracellular caspase activities were detected with Caspase-$FLICA(R)$ and measured by flow cytometry. We showed that 15d-PGJ2 caused a significant increase in apoptosis in MCF-7 and MDA-MB-231 cells. $ER{\alpha}$ protein expression was reduced in treated MCF-7 cells but pre-incubation with the $ER{\alpha}$ inhibitor' ICI 182 780' did not affect the percentage of apoptotic cells. The expression of $ER{\beta}$ was unchanged in both cell lines. In addition, 15d-PGJ2 increased intracellular calcium ($Ca^{2+}$) staining and caspase 8, 9 and 3/7 activities. We therefore conclude that 15d-PGJ2 induces caspase-dependent apoptosis that is associated with an influx of intracellular $Ca^{2+}$ with no involvement of ER signaling.

• Molecules and Cells
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• v.28 no.1
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• pp.67-71
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• 2009

Estrogen receptor ${\alpha}$ ($ER{\alpha}$) mediates the mitogenic effects of estrogen. $ER{\alpha}$ signaling regulates the normal growth and differentiation of mammary tissue, but uncontrolled $ER{\alpha}$ activation increases the risk to breast cancer. Estrogen binding induces ligand-dependent $ER{\alpha}$ activation, thereby facilitating $ER{\alpha}$ dimerization, promoter binding and coactivator recruitment. $ER{\alpha}$ can also be activated in a ligand-independent manner by many signaling pathways, including protein kinase A (PKA) signaling. However, in several $ER{\alpha}$-positive breast cancer cells, PKA inhibits estrogen-dependent cell growth. FoxH1 represses the transcriptional activities of estrogen receptors and androgen receptors (AR). Interestingly, FoxH1 has been found to inhibit the PKA-induced and ligand-induced activation of AR. In the present study, we examined the effects of PKA activation on the ability of FoxH1 to represses $ER{\alpha}$ transcriptional activity. We found that PKA increases the protein stability of FoxH1, and that FoxH1 inhibits PKA-induced and estradiol-induced activation of an estrogen response element (ERE). Furthermore, in MCF7 cells, FoxH1 knockdown increased the PKA-induced and estradiol-induced activation of the ERE. These results suggest that PKA can negatively regulate $ER{\alpha}$, at least in part, through FoxH1.

• Bulletin of the Korean Chemical Society
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• v.25 no.10
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• pp.1503-1507
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• 2004

New synthetic methodology of the saturated and unsaturated Er(III)-chelated prototype complexes based on benzoate and pentafluorobenzoate ligands was developed through ligand-exchange reaction. The saturated 8-coordinated Er(III) complexes exhibit stronger near-IR emission than those of the unsaturated 6-coordinated Er(III) complexes, obtained from the direct photoexcitation of Er ions with 488 nm. Three $H_2O$ molecules coordinated in the unsaturated 6-coordinated complexes seriously quenched the near IR emission by the harmonic vibration relaxation decay of O-H bonds. Also, the stronger emission of the Er(III) complexes was obtained by the indirect photoexcitation of ligands than by the direct photoexcitation of the Er(III) ions, due to the energy transfer between the excited ligand and the erbium ion. Furthermore, the saturated Er(III)-chelated complex with C-F bonds shows much stronger near IR emission than that of the saturated Er(III)-chelated complex with C-H bonds. It is attributed to the influence of C-F bonds on near IR emission.

• Molecules and Cells
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• v.38 no.2
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• pp.145-150
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• 2015

Continuous intra- and extracellular stresses induce disorder of $Ca^{2+}$ homeostasis and accumulation of unfolded protein in the endoplasmic reticulum (ER), which results in ER stress. Severe long-term ER stress triggers apoptosis signaling pathways, resulting in cell death. Neural epidermal growth factor-like like protein 2 (NELL2) has been reported to be important in protection of cells from cell death-inducing environments. In this study, we investigated the cytoprotective effect of NELL2 in the context of ER stress induced by thapsigargin, a strong ER stress inducer, in Cos7 cells. Overexpression of NELL2 prevented ER stress-mediated apoptosis by decreasing expression of ER stress-induced C/EBP homologous protein (CHOP) and increasing ER chaperones. In this context, expression of anti-apoptotic Bcl-xL was increased by NELL2, whereas NELL2 decreased expression of pro-apoptotic proteins, such as cleaved caspases 3 and 7. This anti-apoptotic effect of NELL2 is likely mediated by extracellular signal-regulated kinase (ERK) signaling, because its inhibitor, U0126, inhibited effects of NELL2 on the expression of anti- and pro-apoptotic proteins and on the protection from ER stress-induced cell death.

• Journal of the Korean Ceramic Society
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• v.39 no.9
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• pp.835-839
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• 2002

Stoichiometric $LiNbO_3$(LN) single crystals of 1 mm diameter and 30∼40 mm length with co-doped the $Er_2O_3$ and MgO were grown by the Micro-Pulling Down(${\mu}$-PD) method. The grown crystals were investigated for the change of the up-conversion property by the $Er_2O_3$ and MgO addition and the optical damage by the MgO concentration. Also, the crystals were studied the defects using the optical microscope and it is identified the homogeneities of the distribution of the $Er_2O_3$ and MgO concentration by the Electron Probe Micro Analysis(EPMA).

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2002.08a
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• pp.97-100
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• 2002

$CdGaInS_{4}:Er^{3+}$ single crystal crystallized in the rhombohedral. with lattice constants a = 3.899 $\AA$ and c = 36.970 $\AA$ for $CdGaInS_{4}:Er^{3+}$. The optical absorption measured near the fundamental band edge showed that the optical energy band structure of this compound had a direct and indirect band gaps. the direct and indirect energy gaps are found to be 2.665 and 2.479eV for $CdGaInS_{4}:Er^{3+}$ at 10 K. The photoluminescence spectra of $CdGaInS_{4}:Er^{3+}$ measured in the wavelength ranges of 500 nm~900 nm and 1500~1600 nm at 10 K. Eight sharp emission peaks due to $Er^{3+}$ ion are observed in the regions of 549.5~560.0nm. 661.3~676.5nm. 811.1~ 834.1 nm and 1528.2~1556.0 nm in $CdGaInS_{4}:Er^{3+}$ single crystal. These PL peaks were attributed to the radiative transitions between the split electron energy levels of the $Er^{3+}$ ions occupied at $C_{2v}$ symmetry of the $CdGaInS_4$ single crystals host lattice.

• Development and Reproduction
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• v.23 no.1
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• pp.43-54
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• 2019

We examined the effects of endoplasmic reticulum (ER) stress inhibitor treatment during the micromanipulation of porcine somatic cell nuclear transfer (SCNT) on the in vitro development of SCNT embryos. ER stress inhibitors such as salubrinal (200 nM) and tauroursodeoxycholic acid (TUDCA; $100{\mu}M$) were added to the micromanipulation medium and holding medium. The expression of X-box binding protein 1 (Xbp1), ER-stress-associated genes, and apoptotic genes in SCNT embryos was confirmed at the one-cell and blastocyst stages. Levels of Xbp1 splicing and expression of ER-stress-associated genes in SCNT embryos at the one-cell stage decreased significantly with TUDCA treatment (p<0.05). The expression of ER-stress-associated genes also decreased slightly with the addition of both salubrinal and TUDCA (Sal+TUD). The expression levels of caspase-3 and Bcl2-associated X protein (Bax) mRNA were also significantly lower in the TUDCA and Sal+TUD treatments (p<0.05). At the blastocyst stage, there were no differences in levels of Xbp1 splicing, and transcription of ER-stress-associated genes and apoptosis genes between control and treatment groups. However, the blastocyst formation rate (20.2%) and mean blastocyst cell number ($63.0{\pm}7.2$) were significantly higher (p<0.05) for embryos in the TUDCA treatment compared with those for control (12.6% and $41.7{\pm}3.1$, respectively). These results indicate that the addition of ER-stress inhibitors, especially TUDCA, during micromanipulation can inhibit cellular damage and enhance in vitro development of SCNT embryos by reducing stress levels in the ER.