• Clinical and Experimental Pediatrics
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• v.48 no.5
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• pp.539-544
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• 2005

Purpose : The aim of this study was to investigate the pathophysiologic role of serum E-selectin, vascular endothelial growth factor(VEGF)-induced cell adhesion mollecule in Kawasaki disease(KD) and to look for the evidence of direct relationship between the plasma levels of soluble E-selectin and the incidence of coronary artery lesion(CAL). Methods : Changes in plasma levels of sE-selectin(n=98) over time were measured by enzyme-linked immunosorbent assay(ELISA) in 23 patients with acute KD and 25 age-matched febrile children. Results : Compared with control values, the peak levels of plasma sE-selectin were significantly elevated($mean{\pm}S.E$. : $22.89{\pm}12.53ng/mL$ vs $10.65{\pm}3.42ng/mL$, P=0.01) in KD. 5 patients with CAL, plasma sE-selectin levels before treatment were higher than in 18 patients without CAL($mean{\pm}S.E$. : $39.43{\pm}15.08ng/mL$ and $19.00{\pm}8.32ng/mL$, respectively; P=0.01). Plasma sE-selectin declined rapidly in the majority of KD patients regardless of the presence of CAL. Plasma sE-selectin levels after treatment and convalesent period were similar in KD patients with and without CAL. The plasma levels sE-selectin were correlated with those of white blood cell count(r=0.299, P<0.05), CRP(r=0.430, P<0.05), serum albumin(r=-0.483, P<0.05), serum protein(r=-0.502, P<0.05) and hemoglobin(r=-0.372, P<0.05) not with those of ESR, platelet, or duration of fever. There were significant differences in the initial level of serum sE-selectin between KD with and without CAL($mean{\pm}S.E$. : $39.44{\pm}15.08ng/mL$ vs. $19.00{\pm}17.18ng/mL$) in multivariated linear tests. Conclusion : Plasma sE-selectin levels were significantly higher in KD than in other febrile illness. Higher plamsa levels of sE-selectin may have potential as a predictor of CAL in patients with KD.

• Restorative Dentistry and Endodontics
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• v.28 no.1
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• pp.89-99
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• 2003

The purpose of this study was to investigate the bonding of resin- based root canal sealer, AH26 when the sealer was applied as a thin layer between dentine and gutta-percha surface. In this study forty non-caries extracted human molars and resin-based root canal sealer(AH 26, DeTrey/Dentsply, Germany) were used. Disks of gutta-percha, 6mm in diameter.6mm thick (Diadent/Dentsply, Korea) for thermoplastic obturation were used and dentin surfaces were treated with 2% NaOCl(Group 1) or 2%NaOCl+17% EDTA(Group 3). Disks of gutta-Percha, 6mm in diameter.6mm thick (Diadent/Dentsply, Korea) for conventional obturation were used and dentin surface were treated with 2% NaOCl(Group 2) or 2%NaOCl+17% EDTA(Group 4). Enamel was removed by a horizontal section 1mm below the deepest portion of the central occlusal groove by using a watercooled low speed diamond saw. A second horizontal section was done around cementoenamel junction. Exposed dentin surface was cut to approximately $8{\times}8{\;}mm$ rectangular shape and was ground against 320, 400, 600 grade silicon carbide abrasive paper serially. After grinding, the dentine surface were soaked in a solution of 2% NaOCl for 30 minutes and twenty of specimens were treated with 17% EDTA solution for 1 minute. The treated specimens were washed and dried, Root canal sealer, AH26 was prepared according to the manufacture's instructions The Gutta-percha and dentin surface were coated with a thin layer of the freshly mixed seal or. The specimens were left overnight at room temperature. After their initial set, they were transferred to an incubator at $37$^{\circ}C$ for 72 h. After 72 hours, resin blocks were made. The resin block was serially sectioned vertically into stick of $1{\cdot}1mm$. Twenty sticks were prepared from each group. After that, tensile bond strength f3r each stick was measured with Microtensile Tester Failure patterns of the specimens at the interface between gutta-percha and dentin were observed under the SEM(x1000) and Stereomicroscope (LEICA M42O, Meyer Inst., TX U.S.A) at 1.25 x25 magnification. The results were statistically analysed by using a One-way ANOVA and Tukey's test. The results were as follows; 1. Tensile bond strengths($mean{\pm}SD$) were expressed with ascending order as follows: Group 1, $3.09{\pm}$ 1.05Mpa : Group 2, $6.23{\pm}1.16MPa$ : Group 3, $7.12{\pm}1.07MPa$ : Group 4, $10.32{\pm}2.06MPa$. 2. Tensile bond strengths of the group 2 and 4 used disks of gutta-percha for conventional obturation were significantly higher than that of the group 1 and 3 used fir thermoplastic obturation. (p < 0.05). 3. Tensile bond strengths of the group 3 and 4 treated with 2% NaOC1+17% EDTA were significantly higher than that of the group 1 and 2 treated with 2% NaOCl. (p < 0.05). 4. In analysis of failure patterns at the interface between sealer and gutta-percha, there were observed 49 (61%)cases of adhesive failure patterns and 31 (39%) cases of mixed failures patterns.

• Tuberculosis and Respiratory Diseases
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• v.55 no.4
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• pp.353-360
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• 2003

Background : Although most patients with tuberculous pleurisy respond well to anti-tuberculous drugs, some are known to progress into severe pleural thickening which needs decortication despite adequate anti-tuberculous treatment. Therefore, the purpose of this study was to identify factors associated with the development of severe pleural thickening in patients who finally underwent pleural decortication in tuberculous pleurisy. Patients and Methods : From retrospective medical records review, 121 patients initially diagnosed as tuberculous pleurisy without initial pleural fluid loculation were enrolled between January 1998 and December 2002. They were separated into two groups: 85 patients in group 1 who improved by anti-tuberculous drugs only, and 36 patients in group 2 who had progressed into pleural adhesion and finally underwent pleural decortication despite adequate (more than 6 months) anti-tuberculous treatment. Results : Males were more common in group 2 (M/F=31/5) than in group 1 (M/F=53/32) (p=0.010). Group 2 patients tended to have lower pleural fluid glucose level ($58{\pm}4$ mg/dL) than group 1 ($89{\pm}3$ mg/dL) (p=0.001) and higher pleural fluid adenosine deaminase level ($86{\pm}5$ IU/L) than group 1 ($76{\pm}3$ IU/L), (p=0.038). There were no significant differences in age, symptom duration, pleural fluid amount, or pleural fluid LDH level between groups 1 and 2. Conclusions : There was a relative risk of tuberculous pleurisy progression into severe pleural thickening which needed decortication in the case of male patients, low pleural fluid glucose or high adenosine deaminase level. But further, large-scale, prospective studies should be investigated.

• 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.