• The Transactions of the Korean Institute of Electrical Engineers C
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• v.48 no.2
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• pp.92-97
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• 1999

The mechanical and electrical properties of the hot-pressed and annealed $\beta-Sic$+39vol.%$ZrB_2$ electroconductive ceramic composites were investigated as a function of the liquid forming additives of $Al_2O_3+Y_2O_3(6:4wt%)$. In this microstructures, no reactions and elongated $\alpha$-SiC grains with equiaxed $ZrB_2$, gains were observed between $\beta-SiC$ and $ZrB_2$, and the relative density was over 97.6% of the theoretical density. Phase analysis of the composites by XRD revealedmostly of $\alpha$-SiC(6H, 4H), $ZrB_2$, and weakly $\beta-SiC$(15R) phase. The fracture toughness decreased with increasing $Al_2O_3+Y_2O_3$ contents and showed the highest of $6.37MPa.m^{\fraction ane-half}$ for composite added with 4wt% $Al_2O_3+Y_2O_3$ additives at room temperature. The electrical resistivity increased with increasing $Al_2O_3+Y_2O_3$contents and showed the lowest of $1.51\times10^{-4}\Omega.cm$ for composite added with $Al_2O_3+Y_2O_3$ additives at $25^{\circ}C$. This reason is the increasing tendency of pore formation according to amount of liquid forming additives $Al_2O_3+Y_2O_3$. The electrical resistivity of the composites was all positive temperature coefficient resistance(PTCR) against temperature up to $700^{\circ}C$.

• Korean Journal of Veterinary Research
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• v.48 no.3
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• pp.251-258
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• 2008

The neurotoxicity of C-terminal fragments of amyloid precusor protein (CT) is known to play some roles in Alzheimer's disease progression. In this study, we investigated the effects of the recombinant C-terminal 105 amino acid fragment of amyloid precusor protein (CT105) on cholinergic function using CT105-injected rat. To study the effects of CT105 on septohippocampal pathway, choline acetyltransferase (ChAT) positive neurons were examined in the medial septum and in the diagonal band after an injection of CT105 peptide into the lateral ventricle. Immunohistological analysis revealed that the number of ChAT-immunopositive cells decreased significantly in both medial septum and diagonal band. In addition, CT105 decreased ChAT-immunopositive cells in the hippocampal area, particulary in the dentate gyros. To study the effect of amyloid beta peptide ($A{\beta}$) and CT105 on the cholinergic system, each peptide was injected into the left lateral ventricle, and acetylcholine (ACh) levels were monitored in hippocampus. ACh level in the hippocampal area was reduced to 60% of control level in $A{\beta}$-treated group, and the level was reduced to 15% of control level in CT105-treated group, at one week after the injection. ACh level was further reduced to 35% of control in $A{\beta}$-treated group, whereas the level was slightly increased to 30% of control in CT105-treated group at 4 weeks after the injection. Taken together, the results in the present study suggest that CT105 impairs the septohippocampal pathway by reducing acetylcholine synthesis and release, which results in damage of learning and memory.

• Animal cells and systems
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• v.9 no.2
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• pp.79-85
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• 2005

Oxidized abasic residues arise as a major class of DNA damage by a variety of agents involving free radical attack and oxidation of deoxyribose sugar components. 2-deoxyribonolactone (dL) is a C1'-oxidized abasic lesion implicated in DNA strand scission, mutagenesis, and covalent DNA-protein cross-link (DPC). We show here that mammalian cell-free extract give rise to stable DPC formation that is specifically mediated by dL residue. When a duplex DNA containing dL at the site-specific position was incubated with cell-free extracts of Po ${\beta}-proficient$ and -deficient mouse embryonic fibroblast cells, the formation of major dL-mediated DPC was dependent on the presence of DNA polymerase (Pol) ${\beta}$. Formation of dL-specific DPC was also observed with histones and FEN1 nuclease, although the reactivity in forming dL-mediated DPC was significantly higher with Pol ${\beta}$ than with histones or FEN1. DNA repair assay with a defined DPC revealed that the dL lesion once cross-linked with Pol ${\beta}$ was resistant to nucleotide excision repair activity of cell-free extract. Analysis of nucleotide excision repair utilizing a model DNA substrate containing a (6-4) photoproduct suggested that excision process for DPC was inhibited because of DNA single-strand incision at 5' of the lesion. Consequently DPC mediated by dL lesion may not be readily repaired by DNA excision repair pathway but instead function as unusual DNA damage causing a prolonged DNA strand break and trapping of the major base excision repair enzyme.

• Molecules and Cells
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• v.40 no.12
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• pp.916-924
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• 2017

MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently unclear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expression level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that $Gadd45{\beta}$ (growth arrest DNA damage-inducible gene $45{\beta}$) was a direct target gene of miR-206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of $Gadd45{\beta}$. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting $Gadd45{\beta}$.

• Molecules and Cells
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• v.39 no.8
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• pp.625-630
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• 2016

The RNA-binding protein Rbfox3 is a well-known splicing regulator that is used as a marker for post-mitotic neurons in various vertebrate species. Although recent studies indicate a variable expression of Rbfox3 in non-neuronal tissues, including lung tissue, its cellular function in lung cancer remains largely unknown. Here, we report that the number of RBFOX3-positive cells in tumorous lung tissue is lower than that in normal lung tissue. As the transforming growth factor-${\beta}$ (TGF-${\beta}$) signaling pathway is important in cancer progression, we investigated its role in RBFOX3 expression in A549 lung adenocarcinoma cells. TGF-${\beta}1$ treatment inhibited RBFOX3 expression at the transcriptional level. Further, RBFOX3 depletion led to a change in the expression levels of a subset of proteins related to epithelial-mesenchymal transition (EMT), such as E-cadherin and Claudin-1, during TGF-${\beta}1$-induced EMT. In immunofluorescence microscopic analysis, mesenchymal morphology was more prominent in RBFOX3-depleted cells than in control cells. These findings show that TGF-${\beta}$-induced RBFOX3 inhibition plays an important role in EMT and propose a novel role for RBFOX3 in cancer progression.

• Korean Journal of Acupuncture
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• v.30 no.4
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• pp.305-318
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• 2013

Objectives : The aim of this study was to examine the effect of electroacupuncture(EA) at an acupoint, HT8(Sobu), on normal humans by using power spectral analysis. We examined the effect on the Heart Rate Variability(HRV), and the balance of the autonomic nervous system. Methods : Thirty-two healthy volunteers participated in this study. EEG(Electroencephalogram) power spectrum exhibits site-specific and state-related differences in specific frequency bands. A thirty-two channel EEG study was carried out on thirty-two subjects(14 males; mean age=23.5 years old, 18 females; mean age=21.5 years old). HRV and EEG were simultaneously recorded before and after acupuncture. Results : In the ${\alpha}$(alpha) band, during the HT8-acupoint treatment, the power values in the ${\alpha}$(alpha) band significantly decreased(p<0.05) at 28 channels. In the ${\beta}$(beta) band significantly decreased(p<0.05) at 26 channels. In ${\delta}$(delta) band significantly decreased(p<0.05) at 18 channels. In ${\theta}$(theta) band significantly decreased(p<0.05) at 20 channels. ${\alpha}/{\beta}$ values were increased at 6 channels and decreased at 10 channels.${\beta}/{\theta}$ values were increased at 10 channels and decreased at 19 channels. Mean-RR(RR-interval), Complexity, RMSSD(Root mean square of successive differences), SDSD(Standard deviations differences between adjacent normal R-R intervals), norm HF showed a significantly increased and mean-HRV, norm LF, LHR(LF/HF Ratio) showed a significantly decreased after HT8-acupoint treatment(p<0.05). Conclusions : These results suggest that EA at the HT8 mostly causes significant changes on alpha(28 channels), beta(26 channels), delta(18 channels), theta(20 channels) bands and mean-HRV, mean-RR, complexity, RMSSD, SDSD, norm LF, norm HF and LHR. If practicing EA at the HT8, it will regulate the function of the cerebral cortex, decrease activity of the sympathetic and increase parasympathetic nervous activity.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7617-7623
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• 2014

Objective: The mechanism of action of fatty acid synthase (FASN) in drug tolerance of breast cancer cells with epithelial-mesenchymal transition (EMT) features was investigated. Methods: The breast cancer cell line MCF-7-MEK5 with stably occurring EMT and tumour necrosis factor-${\alpha}$ (TNF-${\alpha}$) tolerance was used as the experimental model, whereas MCF-7 acted as the control. Tumour cells were implanted into nude mice for in vivo analysis, and cerulenin was used as a FASN inhibitor. RT-PCR, real-time quantitative PCR and Western blot were employed to detect the expression of FASN, TNFR-1, TNFR-2, Wnt-1, ${\beta}$-catenin and cytC at the RNA and protein levels. Results: Compared with MCF-7, TNFR-1 expression in MCF-7-MEK5 was slightly changed, TNFR-2 was decreased, and FASN, Wnt-1, ${\beta}$-catenin and cytC were increased. The expression of Wnt-1 and ${\beta}$-catenin in MCF-7-MEK5 decreased after cerulenin treatment, whereas cytC expression increased. Conclusions: The important function of FASN in the drug tolerance of breast cancer may be due to the following mechanisms: FASN downregulated TNFR-2 expression through lipid rafts to make the cells less sensitive to TNF-${\alpha}$, and simultaneously activated the Wnt-$1/{\beta}$-catenin signalling pathway. Thus, cytC expression increased, which provided cells with anti-apoptotic capacity and induced drug tolerance.

• BMB Reports
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• v.43 no.11
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• pp.738-743
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• 2010

The c-Jun $NH_2$-terminal kinase (JNK) signaling pathway participates in many physiological functions. In the current study we reported the cloning and characterization of five novel JNK2 transcript variants, which were designated as $JNK2\alpha3$, $JNK2\alpha4$, $JNK2\beta3$, $JNK2\gamma1$ and $JNK2\gamma2$, respectively. Among them, $JNK2\alpha4$ and $JNK2\gamma2$ are potential non-coding RNA because they contain pre-mature stop codons. Both $JNK2\alpha3$ and $JNK2\beta3$ contain an intact kinase domain, and both encode a protein product of 46 kDa, the same as those of $JNK2\alpha1$ and $JNK2\beta1$. $JNK2\gamma1$ contains a disrupted kinase domain and it showed a disable function. When over-expressed in mammalian cells, $JNK2\alpha3$ showed higher activity on AP-1 than that of $JNK2\beta3$ and $JNK2\gamma1$. Furthermore, $JNK2\alpha3$ and $JNK2\beta3$ showed different levels of substrate phosphorylation, although they both could promote the proliferation of 293T cells. Our results further demonstrate that JNK2 isoforms preferentially target different substrates and may regulate the expression of various target genes.

• BMB Reports
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• v.50 no.1
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• pp.1-2
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• 2017

Acquiring a selective growth advantage by breaking the proliferation barrier established by gatekeeper genes is a centrally important event in tumor formation. Removal of the mammalian Hippo kinase Mst1 and Mst2 in hepatocytes leads to rapid hepatocellular carcinoma (HCC) formation, indicating that the Hippo signaling pathway is a critical gatekeeper that restrains abnormal growth in hepatocytes. By rigorous genetic approaches, we identified an interacting network of the Hippo, Wnt/${\beta}$-catenin and Notch signaling pathways that control organ size and HCC development. We found that in hepatocytes, the loss of Mst1/2 leads to the activation of Notch signaling, which forms a positive feedback loop with Yap/Taz (transcription factors controlled by Mst1/2). This positive feedback loop results in severe liver enlargement and rapid HCC formation. Blocking the Yap/Taz-Notch positive feedback loop by Notch inhibition in vivo significantly reduced the Yap/Taz activities, hepatocyte proliferation and tumor formation. Furthermore, we uncovered a surprising inhibitory role of Wnt/${\beta}$-catenin signaling to Yap/Taz activities, which are important in tumor initiation. Genetic removal of ${\beta}$-catenin in the liver of the Mst1/2 mutants significantly accelerates tumoriogenesis. Therefore, Wnt/${\beta}$-catenin signaling, known for its oncogenic property, exerts an unexpected function in restricting Yap/Taz and Notch activities in HCC initiation. The molecular interplay between the three signaling pathways identified in our study provides new insights in developing novel therapeutic strategies to treat liver tumors.

• Journal of Korea Water Resources Association
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• v.45 no.6
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• pp.531-544
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• 2012

This study suggested the parameter estimation method for given rainfall events to be properly expressed by the beta distribution. For this purpose, this study compared the characteristics of probability density function with the parameter proposed considering the cases with and without addition to the rainfall peak, and the cases of using the real hyetograph and the rearranged hyetograph about the rainfall peak. As an example, this study analyzed the independent rainfall events at Seoul in 2010 and the annual maximum independent rainfall events from 1961 to 2010. The results derived are as follows. First, this study confirmed the necessity of additional consideration on rainfall peak to mimic the real hyetograph of rainfall events by the beta distribution. Second, this study confirmed the case of using rearranged hyetograph about the rainfall peak derived a better beta distribution to well mimic the characteristics of real rainfall than the case using the real hyetograph.