• Korean Journal of Materials Research
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• v.19 no.7
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• pp.349-355
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• 2009

Metal thin film patterns on a LTCC substrate, which was connected through inner via and metal paste for electrical signals, were formed by a screen printing process that used electric paste, such as silver and copper, in a conventional method. This method brought about many problems, such as non uniform thickness in printing, large line spaces, and non-clearance. As a result of these problems, it was very difficult to perform fine and high resolution for high frequency signals. In this study, the electric signal patterns were formed with the sputtered metal thin films (Ti, Cu) on an LTCC substrate that was coated with protective oxide layers, such as $TiO_2$ and $SiO_2$. These electric signal patterns' morphology, surface bonding strength, and effect on electro plating were also investigated. After putting a sold ball on the sputtered metal thin films, their adhesion strength on the LTCC substrate was also evaluated. The protective oxide layers were found to play important roles in creating a strong design for electric components and integrating circuit modules in high frequency ranges.

• Proceedings of the Korea Water Resources Association Conference
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• 2015.05a
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• pp.225-225
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• 2015

Drought events usually evolve slowly in time and their impacts generally span a long period of time. This indicates that the sequence of drought is not completely random. The Hidden Markov Model (HMM) is a probabilistic model used to represent dependences between invisible hidden states which finally result in observations. Drought characteristics are dependent on the underlying generating mechanism, which can be well modelled by the HMM. This study employed a HMM with Gaussian emissions to fit the Standardized Precipitation Index (SPI) series and make multi-step prediction to check the drought characteristics in the future. To estimate the parameters of the HMM, we employed a Bayesian model computed via Markov Chain Monte Carlo (MCMC). Since the true number of hidden states is unknown, we fit the model with varying number of hidden states and used reversible jump to allow for transdimensional moves between models with different numbers of states. We applied the HMM to several stations SPI data in South Korea. The monthly SPI data from January 1973 to December 2012 was divided into two parts, the first 30-year SPI data (January 1973 to December 2002) was used for model calibration and the last 10-year SPI data (January 2003 to December 2012) for model validation. All the SPI data was preprocessed through the wavelet denoising and applied as the visible output in the HMM. Different lead time (T= 1, 3, 6, 12 months) forecasting performances were compared with conventional forecasting techniques (e.g., ANN and ARMA). Based on statistical evaluation performance, the HMM exhibited significant preferable results compared to conventional models with much larger forecasting skill score (about 0.3-0.6) and lower Root Mean Square Error (RMSE) values (about 0.5-0.9).

• Journal of the Korean Society for Railway
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• v.19 no.4
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• pp.498-505
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• 2016

As a basic study to develop maintenance-effective optimal ballast track in preparation for upgrading a conventional line to a high speed railway, a full-scale test that combined the components of ballast track was conducted and the characteristic of track settlement was analyzed. As a result of the full-scale test, reduction in maintenance via an increase of the elasticity of only the pad was insignificant; however, the effect increased significantly with increasing of the weight of the sleeper or with increasing of the weight of the sleeper and the thickness of the ballast together with use of a pad with high resiliency. An optimal type of ballast track, in line with upgrading the speed of a conventional line, shall be developed through cost efficiency analysis considering the maintenance cost depending on the track settlement as well as the initial construction cost.

• Korean Journal of Veterinary Research
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• v.59 no.3
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• pp.133-139
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• 2019

Autophagy is a fundamental cellular process that maintains homeostasis and cell integrity, under stress conditions. Although the involvement of autophagy in various conditions has been elucidated, the role of autophagy in renal structure is not completely clarified. Our aim was to investigate the cytoprotective effect of autophagy against acute kidney injury (AKI) through cisplatin deteriorative pathway, which leads to AKI via renal cell degradation. For in vivo experiments, male Sprague Dawley rats were divided in to 2 groups (n = 6/group) as control, Cis-5D. Following a single intraperitoneal injection of cisplatin, rats were sacrificed after 5 days. Blood urea nitrogen (BUN), creatinine (Cr) and histological alterations were examined. Further, expression of key regulators of autophagy, light-clain 3 (LC3), p62, and Beclin1, was evaluated by immunohistochemistry (IHC). The rats exhibited severe renal dysfunction, indicated by elevated BUN, Cr. Hematoxylin and eosin staining revealed histological damages in cisplatin-treated rats. Furthermore, IHC analysis revealed increased expression of LC3, Beclin1 and decreased expression of p62. Furthermore, expression of aforementioned autophagy markers was restricted to proximal tubule. Taken together, our study demonstrated that cisplatin can cause nephrotoxicity and lead to AKI. This phenomenon accelerated autophagy in renal proximal tubules and guards against AKI.

• The Korean Journal of Emergency Medical Services
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• v.24 no.3
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• pp.161-169
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• 2020

Purpose: This study aims to identify changes in patients' transport time and chief complaints visiting the emergency room via emergency medical services from the "pre-COVID-19 period" compared to the "COVID-19 early-stage period". Methods: This retrospective observational study analyzed the emergency medical services reports at two time periods defined by the COVID-19 virus outbreak in Korea. The study was conducted in Busan, the Republic of Korea, from January 19 through May 6, 2019. Results: The transfer time of patients transported during the "COVID-19 early-stage period" was significantly delayed compared to the "pre-COVID-19 period" (p<.05). We found a significant increase in transport time for patients complaining of respiratory infections compared to patients without symptoms (p<.05). During the "COVID-19 early-stage period", there was a significant increase in the number of patients with respiratory infections and patients complaining of general symptoms compared to the "COVID-19early-stage period" (p<.05). Conclusion: The spread of the COVID-19 virus infection delayed patient transport and increased the number of patients reporting respiratory infection symptoms. Emergency medical services will need administrative and economic support to transport the increased number of patients requiring services.

• Biomolecules & Therapeutics
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• v.29 no.2
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• pp.195-204
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• 2021

Cereblon (CRBN), a substrate receptor of cullin 4-RING E3 ligase (CRL4) regulates the ubiquitination and degradation of c-Jun, mediating the lipopolysaccharide-induced cellular response. However, the upstream signaling pathway that regulates this process is unknown. In this study, we describe how endoplasmic reticulum (ER) stress reversely regulates sequestosome-1 (p62)and c-Jun protein levels. Furthermore, our study reveals that expression of p62 attenuates c-Jun protein levels through the ubiquitinproteasome system. Conversely, siRNA knockdown of p62 elevates c-Jun protein levels. Immunoprecipitation and immunoblotting experiments demonstrate that p62 interacts with c-Jun and CRBN to form a ternary protein complex. Moreover, we find that CRBN knockdown completely abolishes the inhibitory effect of p62 on c-Jun. Using brefeldin A as an inducer of ER stress, we demonstrate that the p62/c-Jun axis participates in the regulation of ER stress-induced apoptosis, and that CRBN is required for this regulation. In summary, we have identified an upstream signaling pathway, which regulates p62-mediated c-Jun degradation. Our findings elucidate the underlying molecular mechanism by which p62/c-Jun axis regulates the ER stress-induced apoptosis, and provide a new molecular connection between ER stress and apoptosis.

• Molecules and Cells
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• v.45 no.4
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• pp.180-192
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• 2022

Nuclear receptor coactivator 6 (NCOA6) is a transcriptional coactivator of nuclear receptors and other transcription factors. A general Ncoa6 knockout mouse was previously shown to be embryonic lethal, but we here generated liver-specific Ncoa6 knockout (Ncoa6 LKO) mice to investigate the metabolic function of NCOA6 in the liver. These Ncoa6 LKO mice exhibited similar blood glucose and insulin levels to wild type but showed improvements in glucose tolerance, insulin sensitivity, and pyruvate tolerance. The decrease in glucose production from pyruvate in these LKO mice was consistent with the abrogation of the fasting-stimulated induction of gluconeogenic genes, phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose-6-phosphatase (G6pc). The forskolin-stimulated inductions of Pck1 and G6pc were also dramatically reduced in primary hepatocytes isolated from Ncoa6 LKO mice, whereas the expression levels of other gluconeogenic gene regulators, including cAMP response element binding protein (Creb), forkhead box protein O1 and peroxisome proliferator-activated receptor γ coactivator 1α, were unaltered in the LKO mouse livers. CREB phosphorylation via fasting or forskolin stimulation was normal in the livers and primary hepatocytes of the LKO mice. Notably, it was observed that CREB interacts with NCOA6. The transcriptional activity of CREB was found to be enhanced by NCOA6 in the context of Pck1 and G6pc promoters. NCOA6-dependent augmentation was abolished in cAMP response element (CRE) mutant promoters of the Pck1 and G6pc genes. Our present results suggest that NCOA6 regulates hepatic gluconeogenesis by modulating glucagon/cAMP-dependent gluconeogenic gene transcription through an interaction with CREB.

• Molecules and Cells
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• v.45 no.6
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• pp.413-424
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• 2022

Suppressor of mothers against decapentaplegic homolog (SMAD) 4 is a pluripotent signaling mediator that regulates myriad cellular functions, including cell growth, cell division, angiogenesis, apoptosis, cell invasion, and metastasis, through transforming growth factor β (TGF-β)-dependent and -independent pathways. SMAD4 is a critical modulator in signal transduction and functions primarily as a transcription factor or cofactor. Apart from being a DNA-binding factor, the additional SMAD4 mechanisms in tumor suppression remain elusive. We previously identified methyl malonyl aciduria cobalamin deficiency B type (MMAB) as a critical SMAD4 binding protein using a proto array analysis. This study confirmed the interaction between SMAD4 and MMAB using bimolecular fluorescence complementation (BiFC) assay, proximity ligation assay (PLA), and conventional immunoprecipitation. We found that transient SMAD4 overexpression down-regulates MMAB expression via a proteasome-dependent pathway. SMAD4-MMAB interaction was independent of TGF-β signaling. Finally, we determined the effect of MMAB downregulation on cancer cells. siRNA-mediated knockdown of MMAB affected cancer cell metabolism in HeLa cells by decreasing ATP production and glucose consumption as well as inducing apoptosis. These findings suggest that SMAD4 controls cancer cell metabolism by regulating MMAB.

• Archives of Craniofacial Surgery
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• v.23 no.5
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• pp.220-227
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• 2022

Background: Frontal sinus fractures are relatively rare. Their surgical management significantly differs depending on whether the posterior wall is invaded and the clinical features vary. A bicoronal incision or endoscopic approach can be used. However, the minimally invasive approach has been attracting attention, leading us to introduce a simple and effective surgical method using multiple-threaded Kirschner wires. Methods: All patients had isolated anterior wall fractures without nasofrontal duct impairment. The depth from the skin to the posterior wall was measured using computed tomography to prevent injury. The edge of the bone segment on the skin was marked, a threaded Kirschner wire was inserted into the center of the bone segment, and multiple Kirschner wires were gently reduced simultaneously. Results: Surgery was performed on 11 patients. Among them, seven patients required additional support for appropriate fracture reduction. Therefore, a periosteal elevator was used as an adjunct through a small sub-brow incision because the reduction was incomplete with the Kirschner wire alone. The reduction results were confirmed using facial bone computed tomography 1 to 3 days postoperatively. The follow-up period was 3 to 12 months. Conclusion: The patients had no complications and were satisfied with the surgical results. Here we demonstrated an easy and successful procedure to reduce a pure anterior wall frontal sinus fracture via non-invasive threaded Kirschner wire reduction.

• Journal of Microbiology and Biotechnology
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• v.31 no.8
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• pp.1098-1108
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• 2021

The literature indicates that LINC00174 promotes the growth of colorectal cancer (CRC) cells, but its research needs to be enriched. We tried to explore the function and mechanism of LINC00174 in CRC cell proliferation and migration. Bioinformatics analysis predicted the binding relationship and expressions of lncRNA, miRNA and mRNA. Clinical study analyzes the relationship between LINC00174 and clinical data characteristics of CRC patients. The expressions of LINC00174, miR-3127-5p and E2F7 were verified by RT-qPCR, and the combination of the two was verified by dual luciferase analysis and RNA immunoprecipitation as needed. Western blot was used to detect the expression of EMT-related protein and E2F7 protein. Functional experiments were used to evaluate the function of the target gene on CRC cells. LINC00174 was up-regulated in CRC clinical samples and cells and was related to the clinical characteristics of CRC patients. High-expression of LINC00174, contrary to the effect of siLINC00174, promoted cell viability, proliferation, migration and invasion, up-regulated the expressions of N-Cadherin, Vimentin, E2F7, and inhibited the expression of E-Cadherin. MiR-3127-5p was one of the targeted miRNAs of LINC00174 and was down-regulated in CRC samples. In addition, miR-3127-5p mimic partially reversed the malignant phenotype of CRC cells induced by LINC00174. Besides, E2F7 was a target gene of miR-3127-5p, and LINC00174 repressed miR-3127-5p to regulate E2F7. Our research reveals that LINC00174 affected the biological characteristics of CRC cells through regulated miR-3127-5p/ E2F7 axis.