• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.

• The Journal of Korean Academy of Prosthodontics
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• v.46 no.2
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• pp.148-156
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• 2008

Statement of problems: Self-etch adhesives exhibit some clinical benefits such as ease of manipulation and reduced technique-sensitivity. Nevertheless, some concern remains regarding the bonding effectiveness of self-etch adhesives to enamel, in particular when so-called 'mild' self-etch adhesives are employed. This study compared the microtensile bond strengths to ground enamel of the two-step self-etch adhesive Clearfil SE Bond (Kuraray) to the three-step etch-and- rinse adhesive Scotchbond Multi-Purpose (3M ESPE) and the one-step self-etch adhesive iBond (Heraeus Kulzer). Purpose: The purpose of this study was to determine the effect of a preceding phosphoric acid conditioning step on the bonding effectiveness of a two-step self-etch adhesive to ground enamel. Material and methods: The two-step self-etch adhesive Clearfil SE Bond non-etch group, Clearfil SE Bond etch group with prior 35% phosphoric acid etching, and the one-step self-etch adhesive iBond group were used as experimental groups. The three-step etch-and-rinse adhesive Scotchbond Multi-Purpose was used as a control group. The facial surfaces of bovine incisors were divided in four equal parts cruciformly, and randomly distributed into each group. The facial surface of each incisor was ground with 800-grit silicon carbide paper. Each adhesive group was applied according to the manufacturer's instructions to ground enamel, after which the surface was built up using Light-Core (Bisco). After storage in distilled water at $37^{\circ}C$ for 1 week, the restored teeth were sectioned into enamel beams approximately 0.8*0.8mm in cross section using a low speed precision diamond saw (TOPMET Metsaw-LS). After storage in distilled water at $37^{\circ}C$ for 1 month, 3 months, microtensile bond strength evaluations were performed using microspecimens. The microtensile bond strength (MPa) was derived by dividing the imposed force (N) at time of fracture by the bond area ($mm^2$). The mode of failure at the interface was determined with a microscope (Microscope-B nocular, Nikon). The data of microtensile bond strength were statistically analyzed using a one-way ANOVA, followed by Least Significant Difference Post Hoc Test at a significance level of 5%. Results: The mean microtensile bond strength after 1 month of storage showed no statistically significant difference between all adhesive groups (P>0.05). After 3 months of storage, adhesion to ground enamel of iBond was not significantly different from Clearfil SE Bond etch (P>>0.05), while Clearfil SE Bond non-etch and Scotchbond Multi-Purpose demonstrated significantly lower bond strengths (P<0.05), with no significant differences between the two adhesives. Conclusion: In this study the microtensile bond strength to ground enamel of two-step self-etch adhesive Clearfil SE Bond was not significantly different from three-step etch-and-rinse adhesive Scotchbond Multi-Purpose, and prior etching with 35% phosphoric acid significantly increased the bonding effectiveness of Clearfil SE Bond to enamel at 3 months.

• Korean Journal of Heritage: History & Science
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• v.49 no.2
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• pp.172-189
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• 2016

In this research, literature research on the Odong material, mixture ratio, casting method and casting facility was conducted on contemporary documents, such as Cheongong Geamul. Also, a long sword was produced using the Odong inlay technique. The sword reproduction steps were as follows; Odong alloying, silver soldering alloying, Odong plate and Silver plate production, hilt and sheath production, metal frame and decorative elements, such as a Dugup (metal frame), production, Odong inlay assembly and final assembly. For the Odong alloy production, the mixture ratio of the true Odong, which has copper and gold ratio of 20:1, was used. This is traditional ratio for high quality product according to $17^{th}$ century metallurgy instruction manual. The silver soldering alloy was produced with silver and brass(Cu 7 : Zn 3) ratio of 5:1 for inlay purpose and 5:2 ratio for simple welding purpose. The true Odong alloy laminated with silver plate was used to produce hilt and sheath. The alloy went through annealing and forging steps to make it into 0.6 mm thick plate and its backing layer, which is a silver plate, had the matching thickness. After the two plates were adhered, the laminated plate went through annealing, forging, engraving, silver inlaying, shaping, silver welding, finishing and polishing steps. During the Odong colouring process, its red surface turns black by induced corrosion and different hues can be achieved depending on its quality. To accomplish the silver inlay Odong techniques, a Hanji saturated with thirty day old urine is wrapped around a hilt and sheath material, then it is left at warm room temperature for two to three hours. The Odong's surface will turn black when silver inlay remains unchanged. Various scientific analysis were conducted to study composition of recreated Odong panel, silver soldering, silver plate and the colouring agent on Odong's surface. The recreated Odong had average out at Cu 95.57 wt% Au 4.16wt% and Cu 98.04 wt% Au 1.95wt%, when documented ratio in the old record is Cu 95wt% and Au 5wt%. The recreated Odong was prone to surface breakage during manufacturing process unlike material made with composition ratio written in the old record. On the silver plate of the silver and Odong laminate, 100wt% Ag was detected and between the two layers Cu, Ag and Au were detected. This proves that the adhesion between the two layers was successfully achieved. The silver soldering had varied composition of Ag depending on the location. This shows uneven composition of the silver welding. A large quantities of S, that was not initially present, was detected on the surface of the black Odong. This indicates that presence of S has influence on Odong colour. Additional study on the chromaticity, additional chemical compounds and its restoration are needed for the further understanding of the origin of Odong colour. The result of Odong alloy testing and recreation, Odong silver inlay long sword production, scientific analysis of the Odong black colouring agent will form an important foundation of knowledge for conservation of Odong artifact.

• Tuberculosis and Respiratory Diseases
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• v.52 no.5
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• pp.485-496
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• 2002

Background : The NF-${\kappa}B$ transcription factors control various biological processes including the immune response, acute phase reaction and cell cycle regulation. NF-${\kappa}B$ complexes are retained in the cytoplasm in the basal state and various stimuli cause a translocation of the NF-${\kappa}B$ complexes into the nucleus where they bind to the ${\kappa}B$ elements and regulate the transcription of the target genes. Recent reports also suggest that NF-${\kappa}B$ proteins are involved in oncogenesis, tumor growth and metastasis. High expression of NF-${\kappa}B$ expression was reported in many cancer cell lines and tissues. The constitutive activation of NF-${\kappa}B$ was also reported in several cancer cell lines supporting its role in cancer development and survival. The anti-apoptotic action of NF-${\kappa}B$ is important for cancer survival. NF-${\kappa}B$ also controls the expression of several proteins that are important for cellular adhesion (ICAM-1, VCAM-1) suggesting a role in cancer metastasis. In lung cancer, high expression levels of the NF-${\kappa}B$ subunit p50 and c-Rel were reported. In fact, high expression does not mean a high activity, and the activation pattern of NF-${\kappa}B$ in lung cancer has not been reported. Materials and Methods : In this study, the NF-${\kappa}B$ nuclear binding activity in the basal and TNF-${\alpha}$ stimulated states were exmined in various lung cancer cell lines and compared with the normal bronchial epithelial cell line. Twelve lung cancer cell lines including the non-small cell and small cell lung cancer cell lines (A549, NCI-H358, NCI-H441, NCI-H552, NCI-H2009, NCI-H460, NCI-H1229, NCI-H1703, NCI-H157, NCI-H187, NCI-H417, NCI-H526) and BEAS-2B bronchial epithelial cell line were used. To evaluate the NF-${\kappa}B$ expression and DNA binding activity, western blot analysis and an electrophoretic mobility shift assay with the nuclear protein extracts. Results : The basal expressions of the p65 and p50 subunits were observed in the BEAS-2B cell line and all lung cancer cell lines except for NCI-H358 and NCI-H460. The expression levels of p65 and p50 were increased 30 minutes after stimulation with TNF-${\alpha}$ in BEAS-2B and in 10 lung cancer cell lines. In the NCI-H358 and NCI-H460 cell lines, p65 expression was not observed in the basal and stimulated states and the two p50 related protein levels were higher after stimulation with TNF-${\alpha}$ These new proteins were smaller than p50 and are thought to be variants of p50. In the basal state, NF-${\kappa}B$ was nearly activated in the BEAS-2B and all lung cancer cell lines. The DNA binding activity of the NF-${\kappa}B$ complexes was markedly higher after stimulation with TNF-${\alpha}$ In the BEAS-2B and all lung cancer cell line except for NCI-H358 and NCI-H460, the activated NF-${\kappa}B$ complex was a p65/p50 heterodimer. In the NCI-H358 and NCI-H460 lung cancer cell lines, the NF-${\kappa}B$ complex was variant of a p50/p50 homodimer. Conclusion : The NF-${\kappa}B$ activation pattern in the lung cancer cell lines and the normal bronchial epithelial cell lines was similar except for the activation of a variant of the p50/p50 homodimer in some lung cancer cell linse.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.