This paper presents a new method of modifying sodium silicate binder with ultra-fine powders. The sodium silicate binder modified by ultra-fine powder A and the organic B can reduce the addition amount of the binder. ...This paper presents a new method of modifying sodium silicate binder with ultra-fine powders. The sodium silicate binder modified by ultra-fine powder A and the organic B can reduce the addition amount of the binder. The results indicate that the 24 h strength has increased by 39.9% at room temperature and the residual strength has decreased by 30.7% at 800℃, compared to the conventional sodium silicate. An available material to improve the moisture resistance was also found by adding about 2% more inorganic C, and it can increase the moist strength by 20%. In the end, the microanalyses are given to explain the modifying machanism, i. e., the ultra-fine powder A can refine the sodium silicate binder to avoid holes in the binder bond, which can increase the 24 h strength at room temperture, and can lead to more cracks in the bond after the molding sand is heated to 800℃. This is because of the stress caused by the new eutectic complex of modified sodium silicate binder.展开更多
AIM: To understand CD133 promoter hypermethyl-ation and expression in 32 colorectal cancer cell lines. METHODS: Nucleic acid was isolated from 32 colorectal cancer cell lines and CD133 expression levels were measured ...AIM: To understand CD133 promoter hypermethyl-ation and expression in 32 colorectal cancer cell lines. METHODS: Nucleic acid was isolated from 32 colorectal cancer cell lines and CD133 expression levels were measured by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. Promoter methylation status of the CD133 gene was analyzed with a methylation-specific PCR after sodium-bisulfi te modification and by clonal sequencing analysis. The correlation between expression and promoter methylation of CD133 gene was confirmed with treatment of 5-aza-2’-deoxycytidine. RESULTS: We measured CD133 expression levels in 32 colorectal cancer cell lines. RT-PCR analysis showed undetectable or low levels of CD133 expression in 34.4%of cell lines. To verify the relation between CD133 expression and methylation status of the CD133 gene promoter in colorectal carcinogenesis, CD133 gene promoter hypermethylation was analyzed in 32 cancer cell lines. Promoter hypermethylation was detected in 13 (40.6%) of the cell lines using methylation specificPCR and confirmed by bisulfite sequencing analysis. Treatment of 11 of the cell lines with the demethylation agent 5-aza-2’-deoxycytidine recovered CD133 expression in most of them. CONCLUSION: Transcriptional repression of CD133 is caused by promoter hypermethylation of the CD133 CpG islands in some of colorectal cancer cell lines. The study may contribute to the understanding of the role of CD133 inactivation in the progression of colorectal cancers.展开更多
基金The subject is supported by National Natural Science Fundof China: 50575085.
文摘This paper presents a new method of modifying sodium silicate binder with ultra-fine powders. The sodium silicate binder modified by ultra-fine powder A and the organic B can reduce the addition amount of the binder. The results indicate that the 24 h strength has increased by 39.9% at room temperature and the residual strength has decreased by 30.7% at 800℃, compared to the conventional sodium silicate. An available material to improve the moisture resistance was also found by adding about 2% more inorganic C, and it can increase the moist strength by 20%. In the end, the microanalyses are given to explain the modifying machanism, i. e., the ultra-fine powder A can refine the sodium silicate binder to avoid holes in the binder bond, which can increase the 24 h strength at room temperture, and can lead to more cracks in the bond after the molding sand is heated to 800℃. This is because of the stress caused by the new eutectic complex of modified sodium silicate binder.
基金Supported by (in part) The Korea Science and Engineering Foundation (KOSEF) funded by the Korean government (MEST R01-2008-000-20108-0)
文摘AIM: To understand CD133 promoter hypermethyl-ation and expression in 32 colorectal cancer cell lines. METHODS: Nucleic acid was isolated from 32 colorectal cancer cell lines and CD133 expression levels were measured by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. Promoter methylation status of the CD133 gene was analyzed with a methylation-specific PCR after sodium-bisulfi te modification and by clonal sequencing analysis. The correlation between expression and promoter methylation of CD133 gene was confirmed with treatment of 5-aza-2’-deoxycytidine. RESULTS: We measured CD133 expression levels in 32 colorectal cancer cell lines. RT-PCR analysis showed undetectable or low levels of CD133 expression in 34.4%of cell lines. To verify the relation between CD133 expression and methylation status of the CD133 gene promoter in colorectal carcinogenesis, CD133 gene promoter hypermethylation was analyzed in 32 cancer cell lines. Promoter hypermethylation was detected in 13 (40.6%) of the cell lines using methylation specificPCR and confirmed by bisulfite sequencing analysis. Treatment of 11 of the cell lines with the demethylation agent 5-aza-2’-deoxycytidine recovered CD133 expression in most of them. CONCLUSION: Transcriptional repression of CD133 is caused by promoter hypermethylation of the CD133 CpG islands in some of colorectal cancer cell lines. The study may contribute to the understanding of the role of CD133 inactivation in the progression of colorectal cancers.
