• Journal of the Korean Crystal Growth and Crystal Technology
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• v.18 no.1
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• pp.27-32
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• 2008

Novel long persistent phosphors of $CaZrO_3:Er^{3+}$ have been synthesized by traditional solid state reaction method. The long persistent phosphor crystalline particles were characterized by the X-ray diffraction (XRD), photoluminescence spectrophotometer, thermoluminescence (TL) and luminance meter. The results reveal that the samples are composed of single $CaZrO_3$ phase. The broadband emission spectra of 446 nm peak and 550 nm peak was revealed by synthesized at high temperature in $N_2$ gas. Green long persistent phosphors have been observed in the sys_em for over 6 h after UV irradiation (254 nm). The main emission peak was ascribed to $Er^{3+}$ ions transition from $^5D_{5/2}{\rightarrow}^4F_{9/2},\;^2H_{12/2},\;^4S_{3/2}{\rightarrow}^4I_{13/2}\;and\;^2G_{9/2}{\rightarrow}^4I_{13/2}$, and the afterglow may be ascribed to the suitable trap centers in the $CaZrO_3$ host lattice.

• Journal of Periodontal and Implant Science
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• v.38 no.1
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• pp.67-74
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• 2008

Purpose: The aim of this study was to evaluate the effect of Er:YAG laser on microstructure and roughness of $TiO_2$ blasting implant surface. Materials and Methods: Ten $TiO_2$ blasting implant were used in this experiment. One implant was control group, and nine $TiO_2$ blasting implant surfaces were irradiated with Er:YAG laser under 100 mJ/pulse, 140 mJ/pulse, and 180 mJ/pulse condition for 1 min, 1.5 min, and 2 min respectively. Optical interferometer and scanning electron microscopy was utilized to measure roughness and microstructure of specimens. Results: The surface roughness was decreased after Er:YAG laser irradiation in all groups, but there was no significant difference. 100 mJ/pulse and 140 mJ/pulse group did not alter the $TiO_2$ blasting implant surface in SEM study while 180 mJ/pulse group altered the $TiO_2$ blasting implant surface. Implant surfaces showed melting, microfracture and smooth surface in 180 mJ/pulse group. Conclusion: Detoxification of implant surface using Er:YAG laser must be irradiated with proper energy output and irradiation time to prevent implant surface alteration.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.28 no.5
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• pp.454-469
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• 2006

Today, there is considerable evidence to support a cause-effect relationship between microbial colonization and the pathogenesis of implant failures. The presence of bacteria on implant surfaces may result in an inflammation of the peri-implant mucosa, and, if left untreated, it may lead to a progressive destruction of alveolar bone supporting the implant, which has been named as peri-impantitis. Several maintenance regimens and treatment strategies for failing implants have been suggested. Recently, in addition to these conventional tools, the use of different laser systems has also been proposed for treatment of peri-implant infections. As lasers can perform excellent tissue ablation with high bactericidal and detoxification effects, they are expected to be one of the most promising new technical modalities for treatment of failing implants. It is introduced that Er,Cr:YSGG laser, operating at 2780nm, ablates tissue by a hydrokinetic process that prevents temperature rise. We studied the change of the titanium implant surface under scanning electron microscopy after using Er,Cr:YSGG laser at various energies, irradiation time. In this study, Er,Cr:YSGG laser irradiation of implant fixture showed different effects according to implant surface. Er,Cr:YSGG laser in TPS surface with RBM not alter the implant surface under power setting of 4 Watt(W) and irradiation time of 30sec. But in TPS surface with $Ca_3P$ coating alter above power setting of 2W and irradiation time of 10sec. TPS surface with RBM showed microfracture in 4W, 30sec and TPS surface with $Ca_3P$ coating showed destruction of fine crystalline structure, melting in excess of 2W, 10sec. We concluded that proper power setting, air, water of each implant surface must be investigated and implant surface must be irradiated under the damaged extent.

• BMB Reports
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• v.53 no.6
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• pp.311-316
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• 2020

Cholestasis is a condition in which the bile duct becomes narrowed or clogged by a variety of factors and bile acid is not released smoothly. Bile acid-induced liver injury is facilitated by necrotic cell death, neutrophil infiltration, and inflammation. Metformin, the first-line treatment for type 2 diabetes, is known to reduce not only blood glucose but also inflammatory responses. In this study, we investigated the effects of metformin on liver injury caused by cholestasis with bile acid-induced hepatocyte injury. Static bile acid-induced liver injury is thought to be related to endoplasmic reticulum (ER) stress, inflammatory response, and chemokine expression. Metformin treatment reduced liver injury caused by bile acid, and it suppressed ER stress, inflammation, chemokine expression, and neutrophil infiltration. Similar results were obtained in mouse primary hepatocytes exposed to bile acid. Hepatocytes treated with tauroursodeoxycholic acid, an ER stress inhibitor, showed inhibition of ER stress, as well as reduced levels of inflammation and cell death. These results suggest that metformin may protect against liver injury by suppressing ER stress and inflammation and reducing chemokine expression.

• Journal of Ginseng Research
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• v.20 no.3
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• pp.325-330
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• 1996

Dynamic parameters of physiology including embryo ratio (ER), embryo length to endosperm length, dry weight ratio between embryo and endosperm (DWR) and respiration rate (RR) in American send (Panax quinquefolium L.) seed were investigated. According to the changes of ER during seed stratification, the duration of embryo afterripening could be divided into three stages as \circled1 embryo slow growth stage (ESGS), ER increased from 7.31% to 20.48% (0.16% day-1): \circled2 embryo rapid growth stage (ERGS), ER increased to 80.98% (0.61% day-1) (75G5+ ERGS=morphological afterripening stage (MP,5)) and \circled3pysiological afterripening stage (PAS), ER Increased to 88.50% (0.094 day-1) only. DWR Increased slowly from 0.20% to 2.76clp (0.016% day-1) in MAS and rapidly to 8.81% (0.061% day-1) in PAS. The RR correlated significantly with ER as well (r=0.8934 > rot, 0.6610). The steep increment of both DWR and RR in PAS indicated that the PAS was not a static stage although the ER was not changed too much. All of these may provide some information for understanding the dormancy mechanisms of American sting seed.

• Bulletin of the Korean Chemical Society
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• v.30 no.1
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• pp.219-223
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• 2009

$TiO_2$ doped with $Er^{3+\;and\;Yb^{3+}$ was used for fabricating a scattering layer and a nano-crystalline $TiO_2$ electrode layer to be used in dye-sensitized solar cells. The material was prepared using a new sol-gel combustion hybrid method with acetylene black as fuel. The $Er^{3+}$-$Yb^{3+}$ co-doped titanium oxide powder synthesized at 700oC had embossed structure morphology with a size between 27 to 54 nm that agglomerated to produce micron size particles, as observed by the scanning electron micrographs. The XRD patterns showed that the $Er^{3+}$-$Yb^{3+}$ co-doped titanium oxide had an amorphous structure, while using the same method without doping $Er^{3+}\;or\;Yb^{3+},\;TiO_2$ was obtained in the crystallite form with thea dominance of rutile phase. Fabricating a bilayer structure consisting of nano-crystalline $TiO_2$ and the synthesized $Er^{3+}$-$Yb^{3+}$ co-doped titanium oxide showed better scattering property, with an overall increase of 15.6% in efficiency of the solar cell with respect to a single nano-crystalline $TiO_2$ layer.

• Molecules and Cells
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• v.38 no.10
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• pp.851-858
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• 2015

Disturbed blood flow with low-oscillatory shear stress (OSS) is a predominant atherogenic factor leading to dysfunctional endothelial cells (ECs). Recently, it was found that disturbed flow can directly induce endoplasmic reticulum (ER) stress in ECs, thereby playing a critical role in the development and progression of atherosclerosis. Ursodeoxycholic acid (UDCA), a naturally occurring bile acid, has long been used to treat chronic cholestatic liver disease and is known to alleviate endoplasmic reticulum (ER) stress at the cellular level. However, its role in atherosclerosis remains unexplored. In this study, we demonstrated the anti-atherogenic activity of UDCA via inhibition of disturbed flow-induced ER stress in atherosclerosis. UDCA effectively reduced ER stress, resulting in a reduction in expression of X-box binding protein-1 (XBP-1) and CEBP-homologous protein (CHOP) in ECs. UDCA also inhibits the disturbed flow-induced inflammatory responses such as increases in adhesion molecules, monocyte adhesion to ECs, and apoptosis of ECs. In a mouse model of disturbed flow-induced atherosclerosis, UDCA inhibits atheromatous plaque formation through the alleviation of ER stress and a decrease in adhesion molecules. Taken together, our results revealed that UDCA exerts anti-atherogenic activity in disturbed flow-induced atherosclerosis by inhibiting ER stress and the inflammatory response. This study suggests that UDCA may be a therapeutic agent for prevention or treatment of atherosclerosis.

• Journal of the Korean Ceramic Society
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• v.37 no.8
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• pp.781-786
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• 2000

An Er-doped sulfide fiber was drawn, and its spectroscopic properties were analyzed. Compositions of a 1000 ppmwt Er3+-doped core and an undoped clad were Ge30-Ga1-Asg-S61 and Ge30-As8-S62, in at.%, respectively. Refractive index of the core composition was approximately 0.01 high than that of the clad. In order to enhance the mechanical stability as well as to prevent infiltration of impurity ions such as OH-, an UV-curable polymer was used for the coating. The optical loss of a fiber formed directly from a polymer coated core rod without cladding was ∼15 dB/m at 1.06$\mu\textrm{m}$. In the case of a fiber with core/clad structure, the optical loss was so high that the stimulated emission of erbium fluorescence was not evident. It is believed that presence of inhomogeneous core/clad interface and crystalline aggregates precipitated in the clad region were responsible for the high optical loss. On the other hand, fluorescence characteristics of Er3+ embedded in the core region were more or loss deteriorate compared to fiber preform, which is attributed to the redistribution of the Er ions along with the partial crystallization of the core glass during the fiberization process.

• Development and Reproduction
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• v.22 no.1
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• pp.73-83
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• 2018

This study investigates the endoplasmic reticulum (ER) stress and subsequent apoptosis in duced during somatic cell nuclear transfer (SCNT) process of porcine SCNT embryos. Porcine SCNT and in vitro fertilization (IVF) embryos were sampled at 3 h and 20 h after SCNT or IVF and at the blastocyst stage for mRNA extraction. The x-box binding protein 1 (Xbp1) mRNA and the expressions of ER stress-associated genes were confirmed by RT-PCR or RT-qPCR. Apoptotic gene expression was analyzed by RT-PCR. Before commencing SCNT, somatic cells treated with tunicamycin (TM), an ER stress inducer, confirmed the splicing of Xbp1 mRNA and increased expressions of ER stress-associated genes. In all the embryonic stages, the SCNT embryos, when compared with the IVF embryos, showed slightly increased expression of spliced Xbp1 (Xbp1s) mRNA and significantly increased expression of ER stress-associated genes (p<0.05). In all stages, apoptotic gene expression was slightly higher in the SCNT embryos, but not significantly different from that of the IVF embryos except for the Bax/Bcl2L1 ratio in the 1-cell stage (p<0.05). The result of this study indicates that excessive ER stress can be induced by the SCNT process, which induce apoptosis of SCNT embryos.

• BMB Reports
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• v.52 no.11
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• pp.665-670
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• 2019

Nucleotide-binding oligomerization domain protein 2 (NOD2), an intracellular pattern recognition receptor, plays important roles in inflammation and cell death. Previously, we have shown that NOD2 is expressed in vascular smooth muscle cells (VSMCs) and that NOD2 deficiency promotes VSMC proliferation, migration, and neointimal formation after vascular injury. However, its role in endoplasmic reticulum (ER) stress-induced cell death in VSMCs remains unclear. Thus, the objective of this study was to evaluate ER stress-induced viability of mouse primary VSMCs. NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer. In contrast, ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) were decreased in NOD2-overexpressed VSMCs. We found that the $IRE-1{\alpha}-XBP1$ pathway, one of unfolded protein response branches, was decreased in NOD2-deficient VSMCs and reversed in NOD2-overexpressed VSMCs in the presence of TM. Furthermore, NOD2 deficiency reduced the expression of XBP1 target genes such as GRP78, PDI-1, and Herpud1, thus improving cell survival. Taken together, these data suggest that the induction of ER stress through NOD2 expression can protect against TM-induced cell death in VSMCs. These results may contribute to a new paradigm in vascular homeostasis.