• Title/Summary/Keyword: hER

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THE EFFECT OF Er,Cr:YSGG IRRADIATION ON MICROTENSILE BOND STRENGTH OF COMPOSITE RESIN RESTORATION (Er,Cr:YSGG 조사가 복합레진 수복의 미세인장 결합강도에 미치는 영향)

  • Son, Jeong-Hye;Kim, Hyeon-Cheol;Hur, Bock;Park, Jeong-Kil
    • Restorative Dentistry and Endodontics
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    • v.35 no.2
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    • pp.134-142
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    • 2010
  • The purpose of this study was to evaluate the effect of Er,Cr:YSGG laser irradiation with hypersensitivity mode on microtensile bond strength of composite resin. Twenty extracted permanent molars were randomly assigned to six groups, according to the irradiation of Er,Cr:YSGG laser, adhesive system (Optibond FL or Clearfil SE bond) and application time of etchant (15 sec or 20 sec). Then composite resin was build up on each conditioned surface. The restored teeth were stored in distilled water at room temperature for 24 h and twelve specimens for each group were prepared. All specimens were subjected to microtensile bond strength and the fracture modes were evaluated. Also, the prepared dentin surface and laser irradiated dentin surface were examined under SEM. The results were as follows: 1. The microtensile bond strength of laser irradiated group was lower than that of no laser irradiated group. 2. Regardless of laser irradiation, the microtensile bond strength of Optibond FL was higher than that of Clearfil SE bond. And the microtensile bond strength of 20 sec etching group was higher than that of 15 sec etching group when using Optibond FL. 3. The SEM image of laser irradiated dentin surface showed prominent peritubular dentin, opened dentinal tubules and no smear layer.

1,25-dihydroxyvitamin D3 affects thapsigargin-induced endoplasmic reticulum stress in 3T3-L1 adipocytes

  • Dain Wi;Chan Yoon Park
    • Nutrition Research and Practice
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    • v.18 no.1
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    • pp.1-18
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    • 2024
  • BACKGROUND/OBJECTIVES: Endoplasmic reticulum (ER) stress in adipose tissue causes an inflammatory response and leads to metabolic diseases. However, the association between vitamin D and adipose ER stress remains poorly understood. In this study, we investigated whether 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) alleviates ER stress in adipocytes. MATERIALS/METHODS: 3T3-L1 cells were treated with different concentrations (i.e., 10-100 nM) of 1,25(OH)2D3 after or during differentiation (i.e., on day 0-7, 3-7, or 7). They were then incubated with thapsigargin (TG, 500 nM) for an additional 24 h to induce ER stress. Next, we measured the mRNA and protein levels of genes involved in unfold protein response (UPR) and adipogenesis using real-time polymerase chain reaction and western blotting and quantified the secreted protein levels of pro-inflammatory cytokines. Finally, the mRNA levels of UPR pathway genes were measured in adipocytes transfected with siRNA-targeting Vdr. RESULTS: Treatment with 1,25(OH)2D3 during various stages of adipocyte differentiation significantly inhibited ER stress induced by TG. In fully differentiated 3T3-L1 adipocytes, 1,25(OH)2D3 treatment suppressed mRNA levels of Ddit3, sXbp1, and Atf4 and decreased the secretion of monocyte chemoattractant protein-1, interleukin-6, and tumor necrosis factor-α. However, downregulation of the mRNA levels of Ddit3, sXbp1, and Atf4 following 1,25(OH)2D3 administration was not observed in Vdr-knockdown adipocytes. In addition, exposure of 3T3-L1 preadipocytes to 1,25(OH)2D3 inhibited transcription of Ddit3, sXbp1, Atf4, Bip, and Atf6 and reduced the p-alpha subunit of translation initiation factor 2 (eIF2α)/eIF2α and p-protein kinase RNA-like ER kinase (PERK)/PERK protein ratios. Furthermore, 1,25(OH)2D3 treatment before adipocyte differentiation reduced adipogenesis and the mRNA levels of adipogenic genes. CONCLUSIONS: Our data suggest that 1,25(OH)2D3 prevents TG-induced ER stress and inflammatory responses in mature adipocytes by downregulating UPR signaling via binding with Vdr. In addition, the inhibition of adipogenesis by vitamin D may contribute to the reduction of ER stress in adipocytes.

Neurotoxin-Induced Pathway Perturbation in Human Neuroblastoma SH-EP Cells

  • Do, Jin Hwan
    • Molecules and Cells
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    • v.37 no.9
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    • pp.672-684
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    • 2014
  • The exact causes of cell death in Parkinson's disease (PD) remain unknown despite extensive studies on PD.The identification of signaling and metabolic pathways involved in PD might provide insight into the molecular mechanisms underlying PD. The neurotoxin 1-methyl-4-phenylpyridinium ($MPP^+$) induces cellular changes characteristic of PD, and $MPP^+$-based models have been extensively used for PD studies. In this study, pathways that were significantly perturbed in $MPP^+$-treated human neuroblastoma SH-EP cells were identified from genome-wide gene expression data for five time points (1.5, 3, 9, 12, and 24 h) after treatment. The mitogen-activated protein kinase (MAPK) signaling pathway and endoplasmic reticulum (ER) protein processing pathway showed significant perturbation at all time points. Perturbation of each of these pathways resulted in the common outcome of upregulation of DNA-damage-inducible transcript 3 (DDIT3). Genes involved in ER protein processing pathway included ubiquitin ligase complex genes and ER-associated degradation (ERAD)-related genes. Additionally, overexpression of DDIT3 might induce oxidative stress via glutathione depletion as a result of overexpression of CHAC1. This study suggests that upregulation of DDIT3 caused by perturbation of the MAPK signaling pathway and ER protein processing pathway might play a key role in $MPP^+$-induced neuronal cell death. Moreover, the toxicity signal of $MPP^+$ resulting from mitochondrial dysfunction through inhibition of complex I of the electron transport chain might feed back to the mitochondria via ER stress. This positive feedback could contribute to amplification of the death signal induced by $MPP^+$.

Anisotropic Hyperfine Structures of Nd3+ and Er3+ in VTE-Treated Ferroelectric LiNbO3 Crystals (VTE 처리된 강유전 LiNbO3 단결정 내의 Nd3+와 Er3+ 초미세 구조의 비등방성)

  • Park, I.W.;Choh, S.H.;Kim, Y.M.;Chon, U.;Kim, S.S.;Kim, W.J.;Kim, B.G.;Sohn, J.M.
    • Journal of the Korean Magnetics Society
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    • v.15 no.2
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    • pp.118-124
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    • 2005
  • We have obtained sharp and clearly resolved ESR spectra of $Nd^{3+}$ and $Er^{3+}$ in vapor transport equilibrium (VTE) treated $LiNbO_3$ crystals, consequently have determined more accurate spin Hamiltonian parameters, than those in congruent samples. The anisotropic hyperfine structures of $^{143}Nd^{3+}$ and $^{145}Nd^{3+}$ in the VTE-treated crystals at liquid helium temperature have been analyzed. It is proposed that both rare earth ions favor the lithium site in $LiNbO_3$ from the consideration of the determined anisotropic g-values.

Korean Red Ginseng inhibits apoptosis in neuroblastoma cells via estrogen receptor ${\beta}$-mediated phosphatidylinositol-3 kinase/Akt signaling

  • Nguyen, Cuong Thach;Luong, Truc Thanh;Kim, Gyu-Lee;Pyo, Suhkneung;Rhee, Dong-Kwon
    • Journal of Ginseng Research
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    • v.39 no.1
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    • pp.69-75
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    • 2015
  • Background: Ginseng has been shown to exert antistress effects both in vitro and in vivo. However, the effects of ginseng on stress in brain cells are not well understood. This study investigated how Korean Red Ginseng (KRG) controls hydrogen peroxide-induced apoptosis via regulation of phosphatidylinositol-3 kinase (PI3K)/Akt and estrogen receptor (ER)-${\beta}$ signaling. Methods: Human neuroblastoma SK-N-SH cells were pretreated with KRG and subsequently exposed to $H_2O_2$. The ability of KRG to inhibit oxidative stress-induced apoptosis was assessed in MTT cytotoxicity assays. Apoptotic protein expression was examined byWestern blot analysis. The roles of ER-${\beta}$, PI3K, and p-Akt signaling in KRG regulation of apoptosis were studied using small interfering RNAs and/or target antagonists. Results: Pretreating SK-N-SH cells with KRG decreased expression of the proapoptotic proteins p-p53 and caspase-3, but increased expression of the antiapoptotic protein BCL2. KRG pretreatment was also associated with increased ER-${\beta}$, PI3K, and p-Akt expression. Conversely, ER-${\beta}$ inhibition with small interfering RNA or inhibitor treatment increased p-p53 and caspase-3 levels, but decreased BCL2, PI3K, and p-Akt expression. Moreover, inhibition of PI3K/Akt signaling diminished p-p53 and caspase-3 levels, but increased BCL2 expression. Conclusion: Collectively, the data indicate that KRG represses oxidative stress-induced apoptosis by enhancing PI3K/Akt signaling via upregulation of ER-${\beta}$ expression.

Peste des petits ruminants virus infection induces endoplasmic reticulum stress and apoptosis via IRE1-XBP1 and IRE1-JNK signaling pathways

  • Shuyi Yuan;Yanfen Liu;Yun Mu;Yongshen Kuang;Shaohong Chen;Yun-Tao Zhao;You Liu
    • Journal of Veterinary Science
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    • v.25 no.2
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    • pp.21.1-21.15
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    • 2024
  • Background: Peste des petits ruminants (PPR) is a contagious and fatal disease of sheep and goats. PPR virus (PPRV) infection induces endoplasmic reticulum (ER) stress-mediated unfolded protein response (UPR). The activation of UPR signaling pathways and their impact on apoptosis and virus replication remains controversial. Objectives: To investigate the role of PPRV-induced ER stress and the IRE1-XBP1 and IRE1-JNK pathways and their impact on apoptosis and virus replication. Methods: The cell viability and virus replication were assessed by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay, immunofluorescence assay, and Western blot. The expression of ER stress biomarker GRP78, IRE1, and its downstream molecules, PPRV-N protein, and apoptosis-related proteins was detected by Western blot and quantitative reverse transcription-polymerase chain reaction, respectively. 4-Phenylbutyric acid (4-PBA) and STF-083010 were respectively used to inhibit ER stress and IRE1 signaling pathway. Results: The expression of GRP78, IRE1α, p-IRE1α, XBP1s, JNK, p-JNK, caspase-3, caspase-9, Bax and PPRV-N were significantly up-regulated in PPRV-infected cells, the expression of Bcl-2 was significantly down-regulated. Due to 4-PBA treatment, the expression of GRP78, p-IRE1α, XBP1s, p-JNK, caspase-3, caspase-9, Bax, and PPRV-N were significantly downregulated, the expression of Bcl-2 was significantly up-regulated. Moreover, in PPRV-infected cells, the expression of p-IRE1α, p-JNK, Bax, and PPRV-N was significantly decreased, and the expression of Bcl-2 was increased in the presence of STF-083010. Conclusions: PPRV infection induces ER stress and IRE1 activation, resulting in apoptosis and enhancement of virus replication through IRE1-XBP1s and IRE1-JNK pathways.

Effects of Red Ginseng-Ejung-tang and White Ginseng-Ejung-tang Water Extract on Hydrogen Peroxide Production in RAW 264.7 Cells (백삼(白蔘)과 홍삼(紅蔘)이 포함된 이중탕(理中湯)의 마우스 대식세포 내 hydrogen peroxide 생성에 미치는 영향)

  • Park, Wan-Su
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.25 no.1
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    • pp.78-83
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    • 2011
  • The purpose of this study is to investigate whether the intracellular hydrogen peroxide productions of mouse macrophage RAW 264.7 are modulated by Red Ginseng-Ejung-tang water extract (ER) and White Ginseng-Ejung-tang water extract (EG). Red Ginseng-Ejung-tang were composed of Red Ginseng, Atractylodes rhizome white, Zingiberis Rhizoma Siccus, and Glycyrrhizae Radix. White Ginseng-Ejung-tang were composed of White Ginseng, Atractylodes rhizome white, Zingiberis Rhizoma Siccus, and Glycyrrhizae Radix. The intracellular hydrogen peroxide productions were measured by dihydrorhodamine 123 assay with spectrofluorometer (excitation 485 nm; emission 535 nm). For 4, 20, 24, 44, 48, 68, and 72 h incubation, ER significantly increased hydrogen peroxide productions of RAW 264.7 at the concentration of 25, 50, 100, and $200{\mu}g/mL$ (P <0.05). EG for 4, 20, 24, 44, and 48 h incubation significantly increased hydrogen peroxide productions of RAW 264.7 at the concentration of 25, 50, 100, and $200{\mu}g/mL$ (P <0.05). For 68 and 72 h incubation, EG at the concentration of 50, 100, and $200{\mu}g/mL$ significantly increased hydrogen peroxide productions in RAW 264.7 (P <0.05). These results suggest that ER and EG have the immune-enhancing properties related with their increasing effects on the intracellular hydrogen peroxide production of macrophage.

Data Hiding Using Sequential Hamming + k with m Overlapped Pixels

  • Kim, Cheonshik;Shin, Dongkyoo;Yang, Ching-Nung;Chen, Yi-Cheng;Wu, Song-Yu
    • KSII Transactions on Internet and Information Systems (TIIS)
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    • v.13 no.12
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    • pp.6159-6174
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    • 2019
  • Recently, Kim et al. introduced the Hamming + k with m overlapped pixels data hiding (Hk_mDH) based on matrix encoding. The embedding rate (ER) of this method is 0.54, which is better than Hamming code HC (n, n - k) and HC (n, n - k) +1 DH (H1DH), but not enough. Hamming code data hiding (HDH) is using a covering function COV(1, n = 2k -1, k) and H1DH has a better embedding efficiency, when compared with HDH. The demerit of this method is that they do not exploit their space of pixels enough to increase ER. In this paper, we increase ER using sequential Hk_mDH (SHk_mDH ) through fully exploiting every pixel in a cover image. In SHk_mDH, a collision maybe happens when the position of two pixels within overlapped two blocks is the same. To solve the collision problem, in this paper, we have devised that the number of modification does not exceed 2 bits even if a collision occurs by using OPAP and LSB. Theoretical estimations of the average mean square error (AMSE) for these schemes demonstrate the advantage of our SHk_mDH scheme. Experimental results show that the proposed method is superior to previous schemes.

Inhibitory Effect of Thapsigargin on the Activities of $H^+-ATPases$ in Tomato Roots (토마토 뿌리조직 $H^+-ATPase$ 활성에 미치는 Thapsigargin의 저해효과)

  • Cho, Kwang-Hyun;Kim, Young-Kee
    • Applied Biological Chemistry
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    • v.48 no.3
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    • pp.212-216
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    • 2005
  • Thapsigargin is a specific antagonist of SR/ER-type $Ca^{2+}-ATPase$ in animal tissue, and it was used to characterize the microsomal ATPases prepared from the roots of tomato. When $10\;{\mu}M$ thapsigargin was added, it inhibited the microsomal ATPase activity by 30%. The thapsigargin-induced inhibition was dose-dependent. Since the activity of $Ca^{2+}-ATPase$ is very low in the roots of tomato tissue, it is possible that thapsigargin inhibits the activities of major $H^+-ATPases$ located in plasma and vacuolar membranes. The inhibitory effect of thapsigargin was reduced when the vacuolar $H^+-ATPase$ activity was inhibited by ${NO_3}^-$. However, the effect of thapsigargin was not observed on the $H^+-ATPase$ activity located in the plasma membrane. These results suggest that thapsigargin inhibits the vacuolar $H^+-ATPase$ activity in the roots of tomato.

Structural Diversity of Five New Lanthanide Coordination Polymers Tuned by Different Salt Anions

  • Tao, Yinhua;Lou, Yongbing;Li, Yang;Chen, Jinxi
    • Bulletin of the Korean Chemical Society
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    • v.35 no.5
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    • pp.1417-1421
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    • 2014
  • Five new lanthanide coordination polymers, $[Ln_2(1,4-NDC)_2(1,4-HNDC)_2(phen)_2]_n$ (Ln = Er (1), Yb (2)), and $[Ln_2(1,4-NDC)_3(phen)_2(H_2O)_2]_n$ (Ln = Nd (3), Gd (4), Er (5)) ($1,4-H_2NDC$ = 1,4-naphthalenedicarboxylic acid, phen = 1,10-phenanthroline), have been successfully prepared via the reaction of corresponding trivalent lanthanide salt, $1,4-H_2NDC$ and phen in the presence of NaOH and pyridine under hydrothermal condition. Pyridine plays a key role in the synthesis of these lanthanide coordination polymers. Single-crystal X-ray diffraction analyses indicate that compounds 1-5 all form a 2-D network while different salt anions result in the diversity of crystal structures. These lanthanide coordination polymers showed a considerable thermal stability in TGA analyses.