In order to improve the quality of Hunyuan inferior Ca-based bentonite （Ca-Bent）, semidry process was used to modify Ca-Bent into superior Na-based bentonite （Na-Bent）. The factors affecting sodium-modification we...In order to improve the quality of Hunyuan inferior Ca-based bentonite （Ca-Bent）, semidry process was used to modify Ca-Bent into superior Na-based bentonite （Na-Bent）. The factors affecting sodium-modification were investigated. The optimized experimental parameters are obtained as follows： Na2CO3 dosage 4.0%, ageing time 25 d, briquetting pressure 25 MPa and briquetting moisture 20%. Under the optimization conditions, the modified Na-Bent has a colloid value of 73.6 mL/（3g）, dilation of 38 mL/g and water absorption in 2 h （2HWA） of 465%, respectively. The bailing results indicate that the modified Na-Bent pellets have higher drop strength and compression strength than the Ca-Bent pellets.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Project(50725416) supported by the National Science Fund for Distinguished Young Scholars Project(50804059) supported by the National Natural Science Foundation of China+1 种基金 Project(2008BAB32B06) supported by the Key Project in the National Science and Technology Pillar Program during the 11th Five-Year Plan PeriodProject(200805331080) supported by the Specialized Research Fund for the Doctoral Program of Higher Education
文摘In order to improve the quality of Hunyuan inferior Ca-based bentonite （Ca-Bent）, semidry process was used to modify Ca-Bent into superior Na-based bentonite （Na-Bent）. The factors affecting sodium-modification were investigated. The optimized experimental parameters are obtained as follows： Na2CO3 dosage 4.0%, ageing time 25 d, briquetting pressure 25 MPa and briquetting moisture 20%. Under the optimization conditions, the modified Na-Bent has a colloid value of 73.6 mL/（3g）, dilation of 38 mL/g and water absorption in 2 h （2HWA） of 465%, respectively. The bailing results indicate that the modified Na-Bent pellets have higher drop strength and compression strength than the Ca-Bent pellets.
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.
