1.A clinical study of splenectomy.
Choon Gon SHIN ; Jin Hyun PARK ; Byung Chul LEE
Journal of the Korean Surgical Society 1991;41(1):93-99
No abstract available.
Splenectomy*
2.The effect of different curing modes on composite resin/dentin bond strength in class icavities.
Shin Young BAEK ; Young Gon CHO ; Byeong Choon SONG
Journal of Korean Academy of Conservative Dentistry 2008;33(5):428-434
The purpose of this study was to compare the microtensile bond strength in Class I cavities associated with different light curing modes of same light energy density. Occlusal enamel was removed to expose a flat dentin surface and twenty box-shaped Class I cavities were prepared in dentin. Single Bond (3M Dental product) was applied and Z 250 was inserted using bulk technique. The composite was light-cured using one of four techniques; pulse delay (PD group), soft-start (SS group), pulse cure (PC group) and standard continuous cure (CC group). The light-curing unit capable of adjusting time and intensity (VIP, Bisco Dental product) was selected and the light energy density for all curing modes was fixed at 16 J/cm2. After storage for 24 hours, specimens were sectioned into beams with a rectangular cross-sectional area of approximately 1 mm2. Microtensile bond strength (microTBS) test was performed using a universal testing machine (EZ Test, Shimadzu Co.). The results were analyzed using oneway ANOVA and Tukey's test at significance level 0.05. The microTBS of PD group and SS group was higher than that of PC group and CC group. Within the limitations of this in vitro study, modification of curing modes such as pulse delay and soft start polymerization can improve resin/dentin bond strength in Class I cavities by controlling polymerization velocity of composite resin.
Bisphenol A-Glycidyl Methacrylate
;
Collodion
;
Dental Enamel
;
Dentin
;
Light
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Polymerization
;
Polymers
3.Long-Term Effects of Diesel Exhaust Particles on Airway Inflammation and Remodeling in a Mouse Model.
Byeong Gon KIM ; Pureun Haneul LEE ; Shin Hwa LEE ; Young En KIM ; Mee Yong SHIN ; Yena KANG ; Seong Hwan BAE ; Min Jung KIM ; Taiyoun RHIM ; Choon Sik PARK ; An Soo JANG
Allergy, Asthma & Immunology Research 2016;8(3):246-256
PURPOSE: Diesel exhaust particles (DEPs) can induce and trigger airway hyperresponsiveness (AHR) and inflammation. The aim of this study was to investigate the effect of long-term DEP exposure on AHR, inflammation, lung fibrosis, and goblet cell hyperplasia in a mouse model. METHODS: BALB/c mice were exposed to DEPs 1 hour a day for 5 days a week for 3 months in a closed-system chamber attached to a ultrasonic nebulizer (low dose: 100 microg/m3 DEPs, high dose: 3 mg/m3 DEPs). The control group was exposed to saline. Enhanced pause was measured as an indicator of AHR. Animals were subjected to whole-body plethysmography and then sacrificed to determine the performance of bronchoalveolar lavage and histology. RESULTS: AHR was higher in the DEP group than in the control group, and higher in the high-dose DEP than in the low-dose DEP groups at 4, 8, and 12 weeks. The numbers of neutrophils and lymphocytes were higher in the high-dose DEP group than in the low-dose DEP group and control group at 4, 8, and 12 weeks. The levels of interleukin (IL)-5, IL-13, and interferon-gamma were higher in the low-dose DEP group than in the control group at 12 weeks. The level of IL-10 was higher in the high-dose DEP group than in the control group at 12 weeks. The level of vascular endothelial growth factor was higher in the low-dose and high-dose DEP groups than in the control group at 12 weeks. The level of IL-6 was higher in the low-dose DEP group than in the control group at 12 weeks. The level of transforming growth factor-beta was higher in the high-dose DEP group than in the control group at 4, 8, and 12 weeks. The collagen content and lung fibrosis in lung tissue was higher in the high-dose DEP group at 8 and 12 weeks. CONCLUSIONS: These results suggest that long-term DEP exposure may increase AHR, inflammation, lung fibrosis, and goblet cell hyperplasia in a mouse model.
Airway Remodeling
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Animals
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Bronchoalveolar Lavage
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Collagen
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Fibrosis
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Goblet Cells
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Hyperplasia
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Inflammation*
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Interferon-gamma
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Interleukin-10
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Interleukin-13
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Interleukin-6
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Interleukins
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Lung
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Lymphocytes
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Mice*
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Nebulizers and Vaporizers
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Neutrophils
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Plethysmography
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Pneumonia
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Ultrasonics
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Vascular Endothelial Growth Factor A
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Vehicle Emissions*