• Journal of the Korean Ceramic Society
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• v.30 no.8
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• pp.657-663
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• 1993

BaTiO3 sputtering targets of 3 inch diameter were prepared by sintering the CIP (Cold Isotatic Pressing) compacts at 136$0^{\circ}C$ for 3hrs. The apparent density and grain size were 97% and 30${\mu}{\textrm}{m}$, respectively. After BaTiO3 films were deposited on Si and Pt/Ti/SiO2/Si substrates using these targets, films were annealed at various conditions and the crystallization behavior, reaction with the substrate and the electrical properties were investigated. The films on both substrates required 5~20hrs furnace annealing for crystallization at the temperatures from $600^{\circ}C$ to 80$0^{\circ}C$. For the films on Si substrate, interaction between the film and the substrate was suppressed upt o $700^{\circ}C$ for 10 hrs and the relative dielectric constant was 30. As the annelaing temperature and time were increased, the relative dielectric constants of the films decreased due to the formation of silicate phases through the reaction with the substrate. For the BaTiO3 films on Pt/Ti/SiO2/Si substrate, the reaction with the substrate was further reduced when the annealing condition was identical to that for Si substrate, but the reaction between the layers in Pt electrode took place above $700^{\circ}C$. When the films were annealed at $600^{\circ}C$ where the stability of Pt electrode was sustained, relative dielectric constant was increased to 110 since the reaction with substrate was effectively reduced even for a longer annealing time and the crystallization was enhanced.

• Journal of Korean Society of Steel Construction
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• v.23 no.4
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• pp.493-501
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• 2011

The $45^{\circ}$cone failure theory has been used for concrete anchor bolt design, but the CCD (concrete capacity design) method was adopted as a new design method in 2000. The method was allowed to be used, however, only for anchors with a diameter of less than 50 mm and an embedment depth of less than 635 mm because it is based on the experiment results from medium-sized to small anchor bolts. Therefore, it is necessary to develop a rational concrete breakout capacity equation for medium-sized to large anchor bolts. In this study, tension tests on an M56 cast-in-place single anchor bolt with an effective embedment depth of 400-450 mm were carried out for the five test specimens. Based on the test results together with the other recent test results, the applicability of the concrete breakout capacity equation in the current design code to the large to medium-sized anchor bolts with an embedment depth of 280-1,200 mm was estimated.

• Korean Journal of Clinical Laboratory Science
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• v.48 no.2
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• pp.74-81
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• 2016

Ureaplasma species can normally colonize in the bodies of healthy individuals. Their colonization is associated with various diseases including non-gonococcal urethritis, chorioamnionitis, neonatal meningitis, and prematurity. In 2012, the sum of the resistant and intermediate resistant rates of Ureaplasma spp. to ofloxacin and ciprofloxacin was 66.08% and 92.69%, respectively. DNA point mutations in the genes encoding DNA gyrase (topoisomerase II) and topoisomerase IV are commonly responsible for fluoroquinolone resistance. Each enzyme is composed of two subunits encoded by gyrA and gyrB genes for DNA gyrase and parC and parE genes for topoisomerase IV. In the current study, these genes were sequenced in order to determine the role of amino acid substitutions in Ureaplasma spp. clinical isolates. From December 2012 to May 2013, we examined mutation patterns of the quinolone resistance-determining region (QRDR) in Ureaplasma spp. DNA sequences in the QRDR region of Ureaplasma clinical isolates were compared with those of reference strains including U. urealyticum serovar 8 (ATCC 27618) and U. parvum serovar 3 (ATCC 27815). Mutations were detected in all ofloxacin- and ciprofloxacin-resistant isolates, however no mutations were detected in drug-susceptible isolates. Most of the mutations related to fluoroquinolone resistance occurred in the parC gene, causing amino acid substitutions. Newly found amino acid substitutions in this study were Asn481Ser in GyrB; Phe149Leu, Asp150Met, Asp151Ile, and Ser152Val in ParC; and Pro446Ser and Arg448Lys in ParE. Continuous monitoring and accumulation of mutation data in fluoroquinolone-resistant Ureaplasma clinical isolates are essential to determining the tendency and to understanding the mechanisms underlying antimicrobial resistance.

• Journal of Marine Bioscience and Biotechnology
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• v.1 no.2
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• pp.76-83
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• 2006

Epidemiological studies have indicated that the ubiquitous consumption of seaweeds is a protective factor against some types of cancer. Previous results showed that the administration of seaweed powder or extract reduced the incidence rate of chemically induced tumorigenesis using in vivo animal model. Recently, we reported that the extracts of Gloiopeltis furcata, a kind of Korean edible seaweed, caused he cell growth inhibition of various human cancer cell lines, among them methanol extract exhibited a relatively strong antiproliferative activity. However, the molecular mechanisms of this seaweed in malignant cells have been poorly studied until now. To elucidate this problem, we investigated the effects of methanol extract of G. furcata (MEGF) on the growth inhibition in several human cancer cell lines, and further we analyzed the effects of this extract were tested on the activity of apoptosis induction in human leukemic cells. The results demonstrated that MEGF treatment resulted in the morphological changes and the growth inhibition in a dose-dependent manner. Furthermore, MEGF potently suppresses the growth of human leukemic U937 cells by induction of apoptosis, which was associated with induction of cyclin-dependent kinase inhibitor p21(WAF1/CIP1) in a tumor suppressor p53-independent fashion and up-regulation of Fas/FasL system. Further studies will be needed to identify the active compounds that confer the anticancer activity of MEGF. Once such compounds are identified, the mechanisms by which they exert their effects can begin to be characterized.

• The Journal of Korean Academy of Prosthodontics
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• v.48 no.2
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• pp.143-150
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• 2010

Purpose: The purpose of this study is to fabricate the new zirconia block (CNU block) and to evaluate fit of core and porcelain veneered zirconia crown. Material and methods: The experimental blocks were fabricated from the commercial ytrria-stabilized zirconia powder (KZ-3YE Type A). The powder was uniaxial pressing and the green bodies were conducted using the Cold Isostatic Pressing. The zirconia blocks were presintered at $1040^{\circ}C$ and the final sintering was performed at $1450^{\circ}C$. The Kavo Everest ZS $blank{(R)}$ (KaVo, Biberach/ $Ri{\beta}$.) was used as a control group. The linear shrinkage of CNU block and Kavo block were compared. Twenty-one cores for porcelain veneered crowns were fabricated with CAD/CAM system ($Everest{(R)}$, Biberach/ $Ri{\beta}$.). Group I; seven cores fabricated from Kavo blocks, Group II; seven cores fabricated from CNU blocks, Group III; seven cores from CNU blocks and porcelain veneering for crowns. All specimens were cemented and sectioned into two planes; diagonal and bucco-lingual. The measurement of the marginal, internal, and occlusal fit was carried out using SEM ($S-4800^{(R)}$) at $30{\times}$. The results were analyzed by one-way ANOVA test. Results: The linear shrinkage of the CNU block and the KaVo block was 19.00% and 20.09%. The marginal gap of cores ($29.67{\pm}6.58{\mu}m$) fabricated from CNU blocks showed significantly smaller than that of the cores of Kavo blocks ($36.84{\pm}7.18{\mu}m$) (P < .05). The internal gaps of the porcelain veneered crowns ($32.23{\pm}6.33{\mu}m$) were larger than those of the other two groups ($37.57{\pm}6.81{\mu}m$ and $38.14{\pm}6.81{\mu}m$). Conclusion: No statistically significant difference was found in between experimental groups and control group. The experimental groups in marginal gap showed significantly smaller than the control group.

• Tuberculosis and Respiratory Diseases
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• v.57 no.5
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• pp.449-460
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• 2004

Background : PS-341 is a novel, highly selective and potent proteasome inhibitor, which showed cytotoxicity against some tumor cells. Its anti-tumor activity has been suggested to be associated with modulation of the expression of apoptosis-associated proteins, such as p53, $p21^{WAF/CIP1}$, $p27^{KIP1}$, NF-${\kappa}B$, Bax and Bcl-2. c-Jun N-terminal kinase (JNK) and glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) are important modulators of apoptosis. However, their role in PS-341-induced apoptosis is unclear. This study was undertaken to elucidate the role of JNK and GSK-$3{\beta}$ in the PS-341-induced apoptosis in lung cancer cells. Method : NCI-H157 and A549 cells were used in the experiments. The cell viability was assayed using the MTT assay and apoptosis was evaluated by proteolysis of PARP. The JNK activity was measured by an in vitro immuno complex kinase assay and by phosphorylation of endogenous c-Jun. The protein expression was evaluated by Western blot analysis. Dominant negative JNK1 (DN-JNK1) and GSK-$3{\beta}$ were overexpressed using plasmid and adenovirus vectors, respectively. Result : PS-341 reduced the cell viability via apoptosis, activated JNK and increased the c-Jun expression. Blocking of the JNK activation by overexpression of DN-JNK1, or pretreatment with SP600125, suppressed the apoptosis induced by PS-341. The activation of caspase 3 was mediated by JNK activation. Blocking of the caspase 3 activation suppressed PS-341-induced apoptosis. PS-341 activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, but its blockade enhanced the PS-341-induced cell death via apoptosis. GSK-$3{\beta}$ was inactivated by PS-341 via the PI3K/Akt pathway. Overexpression of constitutively active GSK-$3{\beta}$ enhanced PS-341-induced apoptosis; in contrast, this was suppressed by dominant negative GSK-$3{\beta}$ (DN-GSK-$3{\beta}$). Inactivation of GSK-$3{\beta}$ by pretreatment with lithium chloride or the overexpression of DN-GSK-$3{\beta}$ suppressed both the JNK activation and c-Jun up-regulation induced by PS-341. Conclusion : The JNK/caspase pathway is involved in PS-341-induced apoptosis, which is negatively regulated by the PI3K/Akt-mediated inactivation of GSK-$3{\beta}$ in lung cancer cells.