The utilization of thin film transistor liquid crystal display waste glass as a pozzolanic material.

This investigation elucidates the pozzolanic behavior of waste glass blended cement (WGBC) paste used in thin film transistor liquid crystal displays (TFT-LCD). X-ray diffraction (XRD) results demonstrate that the TFT-LCD waste glass was entirely non-crystalline. The leaching concentrations of the clay and TFT-LCD waste glass all met the current regulatory thresholds of the Taiwan EPA. The pozzolanic strength activity indices of TFT-LCD waste glass at 28 days and 56 days were 89% and 92%, respectively. Accordingly, this material can be regarded as a good pozzolanic material. The amount of TFT-LCD waste glass that is mixed into WGBC pastes affects the strength of the pastes. The strength of the paste clearly declined as the amount of TFT-LCD waste glass increased. XRD patterns indicated that the major difference was the presence of hydrates of calcium silicate (CSH, 2 theta=32.1 degrees), aluminate and aluminosilicate, which was present in WGBC pastes. Portland cement may have increased the alkalinity of the solution and induced the decomposition of the glass phase network. WGBC pastes that contained 40% TFT-LCD waste glass have markedly lower gel/space ratios and exhibit less degree of hydration than ordinary Portland cement (OPC) pastes. The most satisfactory characteristics of the strength were observed when the mixing ratio of the TFT-LCD waste glass was 10%.

A nucleus-localization-deficient mutant serves as a dominant-negative inhibitor of gut-enriched Krüppel-like factor function.

Cancer cells differ from normal cells in many aspects, including loss of differentiation and uninhibited cell proliferation. Recent studies have suggested that gut-enriched Krüppel-like factor (GKLF) played an important role in the regulation of cell growth in the colon. Studies from this laboratory have shown that GKLF protein predominantly expressed in the cytoplasm but not the nucleus of colon cancer cells, suggesting that impaired nuclear translocation of GKLF might contribute to cancer formation. In this report, a region containing putative nuclear localization signal (NLS) of GKLF (PKRGRR; amino acids 385-390) was investigated. Mutation of KR to WT had no effect on the inhibitory properties of GKLF on cyclin D1 promoter activity and [(3)H]thymidine uptake in HT-29 cells, whereas mutation of RR to GL abolished GKLF function completely. Additional mutation analyses demonstrated that Arg(390) is the most critical moiety within this region that mediated GKLF function and its nucleus localization. Cotransfection of Arg(390) mutant (RR/RS) completely inhibited wild-type GKLF function, and GFP-RR/RS GKLF fusion proteins failed to translocate to the nucleus. The results from this study demonstrate that Arg(390) confers the NLS of GKLF and that the nucleus-localization-deficient mutant serves as dominant-negative inhibitor of GKLF function.

Liquid products from oxidative thermal treatment of oil sludge with different oxygen concentrations of air.

Oxidative thermal treatment of oil sludge with different oxygen concentrations of air by using a dynamic thermogravimetric (TG) reaction system is investigated. The experimental conditions employed are: gas flow rate of 50 cm3/min (value at 298 K) for 300 mg dry waste, a constant heating rate of 5.2 K/min, the oxygen concentrations in air of 1.09, 8.62 and 20.95 vol. % O2, and the temperature (T) range of 378-873 K. From the experimental results, the residual mass fractions (M) are about 78.95, 28.49, 8.77 and 4.13 wt. % at the oxidative T of 563, 713, 763 and 873 K for the case with 20.95 vol. % O2, respectively. The values of M with 8.62 and 1.09 vol. % O2 at T of 873 K are 4.87 and 9.44 wt. %, respectively. The distillation characteristics of the oil portion of liquid products (condensates of gas at 298 K) from the oxidative thermal treatment of oil sludge with 20.95 vol. % O2 at T of 378-873 K is close to those of commercial gasoline. Nevertheless, the liquid product contains a large amount of water. The distillation characteristics of the oil portions of liquid products with 8.62 and 1.09 vol. % O2 at T of 378-873 K are close to those of diesel and fuel oils, respectively. The oil quality with 8.62 vol. % O2 is better than that with 1.09 vol. % O2. However, the liquid product with 8.62 vol. % O2 still contains a large amount of water; nonetheless, that with 1.09 vol. % O2 is with negligible water. Compared with the oil product of nitrogen pyrolysis, the oil quality with 1.09 vol. % O2 is better. Certainly, low oxygen conditions (i.e. 1.09 vol. % O2) not only accelerate the thermal reaction of oil sludge, but also at the same time avoid or reduce the production of water. Further, from the analysis of benzene (B), ethylbenzene (E), toluene (T) and iso-xylene (X) concentrations of the oil portion of liquid products, the BETX concentrations of oil with 20.95 vol. % O2 are higher than those with 8.62 and 1.09 vol. % O2. The yields of liquid products with 20.95, 8.62 and 1.09 vol. % O2 at T of 378-873 K are 31.96, 34.42 and 37.3 wt. %, respectively. From the experimental results, the improvement effects of oxygen on the qualities of the oil portion of liquid products are obvious. The above technique not only formats good quality gasoline and diesel oils but also reduces large amount of oil sludge. If the oil exists with water, it may be obtained by further separation or collected by fractional condensation.

Role of gut-enriched Krüppel-like factor in colonic cell growth and differentiation.

Cancer cells differ from normal cells in many aspects, including hyperproliferation and loss of differentiation. Recent research has focused on the role of transcription factors in regulating abnormal cell growth. Gut-enriched Krüppel-like factor (GKLF) is a newly identified eukaryotic zinc finger protein expressed extensively in the gastrointestinal tract. In the current study, we demonstrated that GKLF mRNA levels were significantly decreased in the dysplastic epithelium of the colon, including adenomatous polyp and cancer. GKLF immunostains in the normal colon were higher at the surface epithelium and gradually decreased toward the crypt, but this gradient was not present in the adenomatous and cancerous mucosa. Constitutive overexpression of GKLF DNA in a human colonic adenocarcinoma cell line (HT-29) decreased [(3)H]thymidine incorporation, whereas suppression of GKLF gene increased DNA synthesis, indicating that downregulation of the GKLF gene might contribute to cellular hyperproliferation. Cyclin D1 (CD1) protein level and CD1-associated kinase activity were decreased in HT-29 cell overexpressed GKLF cDNA, and CD1 promoter activity was profoundly suppressed by GKLF. When HT-29 cells were cultured in the presence of sodium butyrate, GKLF mRNA levels increased as cells acquired more differentiated phenotypes. These results suggest that GKLF plays an important role in regulating cell growth and differentiation in the colonic epithelium and that downregulation of GKLF expression may cause colonic cells to become hyperproliferative. Furthermore, GKLF appears to be a transcriptional repressor of the CD1 gene.

Gut-enriched Krüppel-like factor represses cyclin D1 promoter activity through Sp1 motif.

Cancer cells differ from normal cells in many characteristics including loss of differentiation and uninhibited cell proliferation. Recent studies have focused on the identification of factors contributing to cell growth and differentiation. Gut-enriched Krüppel-like factor (GKLF or KLF4) is a newly identified eukaryotic transcription factor and has been shown to play a role in regulating growth arrest. We have previously shown that GKLF mRNA levels were significantly decreased in colon cancer tissues, and that over-expression of GKLF in colonic adenocarcinoma cells (HT-29) resulted in reduction of cyclin D1 (CD1) mRNA and protein levels. The current study was undertaken to determine the mechanisms by which GKLF inhibited CD1 expression. In a transient transfection system, GKLF suppressed CD1 promoter activity by 55%. Sequential deletion and site-directed mutation analysis of the CD1 promoter have identified the sequence between -141 and -66, a region containing an Sp1 response element, to be essential for GKLF function. By electrophoretic mobility gel shift assay, recombinant GKLF and nuclear extracts from HT-29 cells were found to bind to the Sp1 motif on the CD1 promoter. The inhibitory effect of GKLF on the CD1 promoter activity was completely abolished by excessive amount of Sp1 DNA and GKLF significantly reduced the stimulatory function of Sp1 suggesting that GKLF and Sp1 may compete for the same binding site on the CD1 promoter. These results indicate that GKLF is a transcriptional repressor of the CD1 gene and that the inhibitory effect of GKLF is, in part, mediated by interaction with the Sp1 binding domain on its promoter.