• The Korean Journal of Rheology
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• v.11 no.2
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• pp.97-104
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• 1999

This paper presents vibration control of a drive feeding system consisting of a new type of CD-ROM(compact discread only memory) mount using electro-rheologocal(ER) fluid. Chemically treated starch particles and silicon oil are used for ER fluid. and its field-dependent yield stresses are experimentally distilled under both the shear and the flow modes. On the basis of the yield stress, an appropriate size of ER CD-ROM mount adapted to conventional feeding system is designed and manufactured. Vibration isolation performance of the proposed mount is evaluated in the frequency domain and compared with that of conventional rubber mount. The ER CD-ROM mount is then installed to the drive feeding system and the system equation of motion is derived. Following the formulating the sky-hook controller, computer simulation is undertaken in order to evaluate vibration suppression of the feeding system subjected to various disturbances(excitations).

• Journal of Life Science
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• v.26 no.4
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• pp.490-495
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• 2016

Brefeldin A (BFA), a lactone antibiotic isolated from the fungus Eupenicillium brefeldianum, inhibits the transport of secreted and membrane proteins from the endoplasmic reticulum (ER) to the Golgi apparatus. BFA disrupts Golgi function, the accumulation of unfolded proteins in ER, and the induction of ER stress. Prolonged ER stress induces apoptosis at least in part through the transcription factor C/EBP (CCAAT/enhancer binding protein) homologous protein (CHOP),which is activated by the unfolded protein response (UPR). In this paper, we demonstrate that BFA-induced endoplasmic reticulum stress leads to different CHOP expression in primary astrocyte cells and C6 glioma cells. BFA induced lower CHOP expression levels in primary astrocyte cells than in C6 glioma cells; however, other ER stress inducers (thapsigargin and tunicamycin) resulted in similar expression patterns in these two cell types. Interestingly, the three different ER stress inducers (BFA, thapsigargin, and tunicamycin) induced similar levels of CHOP mRNA expression in primary astrocyte cells. The ubiquitin-proteasome inhibitor MG132 also markedly up-regulated the BFA-mediated CHOP protein expression in primary astrocyte cells. BFA also induced higher proteasome activity in primary astrocyte cells than in C6 glioma cells. Taken together, our results suggest that higher proteasomal activity might down-regulate BFA-induced CHOP expression in primary astrocyte cells.

• Proceedings of the Materials Research Society of Korea Conference
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• 2003.03a
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• pp.223-223
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• 2003

광통신에는 광신호의 전송과 광신호 처리에 처리 과정에서 광 손실을 수반하므로 각 요소별로 광신호 증폭이 반드시 필요하다. 또한 광통신망의 완전 광화를 위해서는 제조 공정이 간단하여 가격이 저렴하고, 높은 신뢰성과 높은 증폭 효율을 가지면서 다른 부품과의 집적화가 가능한 광도파로형 광증폭기가 요구되고 있다 그러나 실리카는 광통신 파장대인 1.55$\mu\textrm{m}$대역의 증폭이 가능한 Er 이온에 대한 용해도가 50ppm 이하로 낮아 lmol% 이상 고농도로 Er 이온을 첨가하여 높은 증폭 효율을 얻는데 한계를 가지고 있다. 따라서 본 연구에서는 Er 이온에 대하여 높은 용해 특성을 가지고 있어 고농도 Er 이온 도핑이 가능한 알루미나에 Er을 1-2 mol% 첨가하여 광발광 특성을 조사하였다. Er이 첨가된 알루미나 나노 졸은 Al(NO$_3$)$_3$ㆍ9$H_2O$와 Er(NO$_3$)$_3$.5$H_2O$가 일정 양 용해된 수용액에 NH$_4$OH를 가하여 침전물을 얻고 여과 및 수세하여 졸 입자의 함량이 약 5wt%가 되게 이온교환수와 해교제인 초산을 소량 가하여 10$0^{\circ}C$에서 약 50시간 열처리하는 방법으로 제조하였다. Er이 첨가된 알루미나 코팅막은 Er 이 첨가된 알루미나 나노 졸에 GPS(3-glycidoxypropyltriethoxysilane)를 Al에 대하여 7 mol% 가하여 스핀 코팅법으로 제조하였다. Si 기판에 코팅하고, 상온에서 90$0^{\circ}C$까지 각 1시간 열처리한 코팅막의 광 발광 특성은 Er 이온의 첨가량과 열처리로 변화된 알루미나 코팅막의 결정상과 연계하여 논의 될 것이다. X-선 회절법으로 분석한 알루미나 코팅막의 온도에 따른 결정상은 boehmite 상에서 약 50$0^{\circ}C$이후에 ${\gamma}$-Al$_2$O$_3$로 전이하고 있다.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.4113-4117
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• 2012

Breast cancer is a prevalent heterogeneous malignant disease. Gene expression profiling by DNA microarray can classify breast tumors into five different molecular subtypes: luminal A, luminal B, HER-2, basal and normal-like which have differing prognosis. Recently it has been shown that immunohistochemistry (IHC) markers including estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (Her2), can divide tumors to main subtypes: luminal A (ER+; PR+/-; HER-2-), luminal B (ER+;PR+/-; HER-2+), basal-like (ER-;PR-;HER2-) and Her2+ (ER-; PR-; HER-2+). Some subtypes such as basal-like subtype have been characterized by poor prognosis and reduced overall survival. Due to the importance of the ER signaling pathway in mammary cell proliferation; it appears that epigenetic changes in the $ER{\alpha}$ gene as a central component of this pathway, may contribute to prognostic prediction. Thus this study aimed to clarify the correlation of different IHC-based subtypes of breast tumors with $ER{\alpha}$ methylation in Iranian breast cancer patients. For this purpose one hundred fresh breast tumors obtained by surgical resection underwent DNA extraction for assessment of their ER methylation status by methylation specific PCR (MSP). These tumors were classified into main subtypes according to IHC markers and data were collected on pathological features of the patients. $ER{\alpha}$ methylation was found in 25 of 28 (89.3%) basal tumors, 21 of 24 (87.5%) Her2+ tumors, 18 of 34 (52.9%) luminal A tumors and 7 of 14 (50%) luminal B tumors. A strong correlation was found between $ER{\alpha}$ methylation and poor prognosis tumor subtypes (basal and Her2+) in patients (P<0.001). Our findings show that $ER{\alpha}$ methylation is correlated with poor prognosis subtypes of breast tumors in Iranian patients and may play an important role in pathogenesis of the more aggressive breast tumors.

• Macromolecular Research
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• v.17 no.9
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• pp.672-681
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• 2009

A series of inert and photo-stable Er(III)-encapsulated complexes based on ${\pi}$-extended dendritic anthracene ligands bearing G3-aryl-ether dendron ([G3-AnX]-$CO_2H$), which retain different ${\pi}$-bridging systems, such as single (X= S), double (X= D) and triple (X= T) bonds was designed and synthesized to establish the structure-property relationship. The near infrared emission intensities of Er(III)-encapsulated complexes were enhanced dramatically by increasing the ${\pi}$-conjugated extension of anthracene ligands. The time-resolved luminescence spectra show monoexponential decays with a lifetime of $2.0{\sim}2.4ms$ for $Er^{3+}$ ions in thin films, and calculated intrinsic quantum yields of $Er^{3+}$ ions are in the range of $0.025{\sim}0.03%$. As a result, all Er(III)-encapsulated dendrimer complexes exhibit the near IR emission with the following order: $Er^{3+}-[G3-AnD]_3$(terpy) > $Er^{3+}-[G3-AnS]_3$(terpy) ${\approx}$ $Er^{3+}-[G3-AnT]_3$(terpy), because $Er^{3+}-[G3-AnD]_3$(terpy) has a higher relatively spectral overlap J value and energy transfer efficiency. In addition, the lack of detectable phosphorescence and no significant spectral dependence of the ${\pi}$-extended anthracene moieties on the solvent polarity support energy transfer from their singlet state to the central $Er^{3+}$ ion taking place in $Er^{3+}-[G3-AnX]_3$(terpy).

• Biomolecules & Therapeutics
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• v.32 no.3
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• pp.341-348
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• 2024

Endoplasmic reticulum (ER) stress plays a crucial role in liver diseases, affecting various types of hepatic cells. While studies have focused on the link between ER stress and hepatocytes as well as hepatic stellate cells (HSCs), the precise involvement of hepatic macrophages in ER stress-induced liver injury remains poorly understood. Here, we examined the effects of ER stress on hepatic macrophages and their role in liver injury. Acute ER stress led to the accumulation and activation of hepatic macrophages, which preceded hepatocyte apoptosis. Notably, macrophage depletion mitigated liver injury induced by ER stress, underscoring their detrimental role. Mechanistic studies revealed that ER stress stimulates macrophages predominantly via the PERK signaling pathway, regardless of its canonical substrate ATF4. hnRNPA1 has been identified as a crucial mediator of PERK-driven macrophage activation, as the overexpression of hnRNPA1 effectively reduced ER stress and suppressed pro-inflammatory activation. We observed that hnRNPA1 interacts with mRNAs that encode UPR-related proteins, indicating its role in the regulation of ER stress response in macrophages. These findings illuminate the cell type-specific responses to ER stress and the significance of hepatic macrophages in ER stress-induced liver injury. Collectively, the PERK-hnRNPA1 axis has been discovered as a molecular mechanism for macrophage activation, presenting prospective therapeutic targets for inflammatory hepatic diseases such as acute liver injury.

• Journal of Life Science
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• v.19 no.8
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• pp.1159-1163
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• 2009

It has been postulated that endoplasmic (ER) stress is involved in the development of several diseases. However, the detailed molecular mechanisms have not been fully understood. Therefore, we characterized a genetic network of genes induced by ER stress using cDNA microarray and gene set expression coherence analysis (GSECA), and identified gene function as well as several transcription regulators associated with ER stress. We analyzed time-dependent gene expression profiles in thapsigargin-treated Sk-Hep1 using an oligonucleotide expression chip, and then selected functional gene sets with significantly high expression coherence which was processed into functional clusters according to the expression similarities. The functions related to sugar binding, lysosome, ribosomal protein, ER lumen, and ER to golgi transport increased, whereas the functions with mRNA processing, DNA replication, DNA repair, cell cycle, electron transport chain and helicase activity decreased. Furthermore, functional clusters were investigated for the enrichment of regulatory motifs using GSECA, and several transcriptional regulators associated with regulation of ER-induced gene expression were found.

• Journal of the Korean Ceramic Society
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• v.39 no.9
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• pp.829-834
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• 2002

Ferroelectric properties of $ErMnO_3$ thin films deposited on Si(100) substrate using Sol-gel process with metal salts were investigated. $ErMnO_3$ thin films with a (001) preferred orientation were crystallized at 800$^{\circ}C$. The $ErMnO_3$ thin film post-annealed at 800$^{\circ}C$ for 1 h showed the dielectric constant(k) of 26 and the dielectric loss(tan ${\delta}$) of 0.032 at the frequency range from 1 to 100 KHz. The grain size of $ErMnO_3$ thin film post-annealed at 800 for 1 h was 10∼30 nm. The remanent polarization($P_r$) of the $ErMnO_3$ thin films increased with increasing (001) preferred orientation. The $ErMnO_3$ thin films post-annealed at 800$^{\circ}C$ for 1 h showed the remanent polarization($P_r$) of 400 nC/$cm^2$, with the increase of post-annealing time at 800$^{\circ}C$, the coercive field($E_c$) of thin films was lowered because the dense and homogeneous thin films were obtained.

• Journal of Life Science
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• v.31 no.9
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• pp.796-805
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• 2021

Hepatic endoplasmic reticulum (ER) stress contributes to the development of steatosis and insulin resistance. The components of unfolded protein response (UPR) regulate lipid metabolism. Recent studies have reported an association between ER stress and aberrant cellular lipid control; moreover, research has confirmed the involvement of sterol regulatory element-binding proteins (SREBPs)-the central regulators of lipid metabolism-in the process. However, the exact role of SREBPs in controlling lipid metabolism during ER stress and its contribution to fatty liver disease remain unknown. Here, we show that SREBP-1c deficiency protects against ER stress-induced hepatic steatosis in mice by regulating UPR, inflammation, and fatty acid oxidation. SREBP-1c directly regulated inositol-requiring kinase 1α (IRE1α) expression and mediated ER stress-induced tumor necrosis factor-α activation, leading to a reduction in expression of peroxisome proliferator-activated receptor γ coactivator 1-α and subsequent impairment of fatty acid oxidation. However, the genetic ablation of SREBP-1c prevented these events, alleviating hepatic inflammation and steatosis. Although the mechanism by which SREBP-1c deficiency prevents ER stress-induced inflammatory signaling remains to be elucidated, alteration of the IRE1α signal in SREBP-1c-depleted Kupffer cells might be involved in the signaling. Overall, the results suggest that SREBP-1c plays a crucial role in the regulation of UPR and inflammation in ER stress-induced hepatic steatosis.

• Bulletin of the Korean Chemical Society
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• v.29 no.6
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• pp.1107-1114
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• 2008

It is important to identify selective ligands for the estrogen receptor subtypes ER$\alpha$ or ER$\beta$ to evaluate them as pharmaceutical targets in breast cancer. To develop ER$\beta$-selective ligands as PET imaging agents, a series of aryl indazole estrogen analogues substituted at the C3 position with fluoroethyl and fluoropropyl groups were synthesized and evaluated for their relative binding affinities and selectivities for ER$\alpha$ vs ER$\beta$. The fluoroethylated indazole estrogen (FEIE, 1i) and fluoropropylated indazole estrogen (FPIE, 1h) showed 41- fold and 17-fold ER$\beta$/ER$\alpha$ selectivity, respectively. However, their binding affinities to ER$\alpha$ and ER$\beta$ were very low.