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Objective:In order to efficiently remove TMAH from the wastewater generated by the TFT-LCD manufacturing process, the oxidation of TMAH was tested by applying an UV/persulfate. The optimum reaction conditions for high concentration TMAH oxidation were investigated by evaluating and comparing the removal efficiency according to the factors affecting TMAH oxidative degradation. Methods:In this study, TMAH was decomposed by sulfate radical (SO4-∙) and hydroxyl radical (OH∙) generated from persulfate activated by UV. Factors affecting on the treatment efficiency were try to be optimized by comparing and evaluating the removal efficiency depending on the initial pH, oxidant concentration, and initial TMAH concentration. Results and Discussion:Depending on initial pH (2, 7, 12), persulfate addition (0, 50, 100, 150, 200 mM), initial TMAH concentration (100, 300, 500, 700 mg/L) degradation rates of TMAH were compared. When UV/persulfate was applied, the removal efficiency of TMAH was close to 90% regardless of the initial pH and, at initial pH 12, was the highest with 89%. It was confirmed that the generation pattern of intermediate formed were different depending on the initial pH. When the oxidizing agent was not added, there was little change in TMAH concentration. The removal efficiency was highest when 100 mM persulfate was added. However the efficiency was rather low when 150 mM persulfate was added. When the initial TMAH concentration was 100 mg/L, it was decreased within 150 minutes. As the initial concentration increased, the removal efficiency and reaction rate constant decreased. Conclusions:As a results, during the oxidation of 750 mg/L TMAH by using UV/persulfate, the removal efficiency was highest with initial pH 12 and 100 mM of persulfate addition.

Background: Previous studies have shown that lung cancer stem cells express CD133 and that certain cancer stem cells express cancer germline antigens (CGAs). The transcriptional regulation of CD133 is complicated and poorly understood. We investigated CD133 and CGA expression in a non-small cell lung cancer cell line. Methods: The expression levels of CD133 and CGAs (MAGE-6, GAGE, SSX, and TRAG-3) were measured in an NCI-H292 lung cancer cell line. The methylation status of the CD133 gene promoter region was analyzed. The expression levels and promoter methylation statuses of CD133 and CGAs were confirmed by treatment with the demethylating agent 5-aza-2'-deoxycytidine (ADC). Results: After treatment with ADC, CD133 expression was no longer detected. MAGE-6 and TRAG-3 were detected before ADC treatment, while GAGE and SSX were not detected. ADC treatment upregulated MAGE-6 and TRAG-3 expression, while GAGE expression was still undetected after treatment, and only weak SSX expression was observed. GAGE expression was not correlated with expression of CD133, while the levels of expression of MAGE-6, TRAG-3, and SSX were inversely correlated with CD133 expression. Conclusion: These results showed that CD133 expression can be regulated by methylation. Thus, the demethylation of the CD133 promoter may compromise the treatment of lung cancer by inactivating cancer stem cells and/or activating CGAs.