• Journal of the Korean GEO-environmental Society
• /
• v.15 no.12
• /
• pp.117-128
• /
• 2014

Generally, when constructing a tunnel close to existing structures, the tunnel must be built at a constant distance from the structures that is more than width of tunnel to minimize the impact of interference between an existing structures and new tunnel. Spacing of these closed tunnels should be designed considering soil state, size of tunnel and reinforcement method. Particularly when the ground is soft, a care should be taken with the tunnel plans because the closer the tunnel is to the existing structures, the greater the deformation becomes. As methods of reviewing the effect of cavities on the stability of a tunnel, field measurement, numerical analysis and scaled model test can be considered. In the methods, the scaled model test can reproduce the engineering characteristics of a rock in a field condition and the shape of structures using the scale factor even not all conditions cannot be considered. In this study, when construction of a tunnel close to existing structures, the method and considering factors of the scaled model test were studied to predict the actual tunnel behavior in planning stage. Furthermore, model test results were compared with the numerical analysis results for verifying the proposed model test procedure. Also, practical results were derived to verify the stability of a tunnel vis-a-vis cavities through the scaled model test, which assumed spacing distances of 0.25 D, 0.50 D, and 1.00 D between the cavities and tunnel as well as the network state distribution. The spacing distances of 1.0 D is evaluated as the critical distance by the results of model test and numerical analysis.

• Journal of Microbiology and Biotechnology
• /
• v.25 no.10
• /
• pp.1751-1760
• /
• 2015

Mucin2 (MUC2), an important regulatory factor in the immune system, plays an important role in the host defense system against bacterial translocation. Probiotics known to regulate MUC2 gene expression have been widely studied, but the interactions among probiotic, pathogens, and mucin gene are still not fully understood. The aim of this study was to investigate the role of MUC2 in blocking effects of probiotics on meningitic E. coli-induced pathogenicities. In this study, live combined probiotic tablets containing living Bifidobacterium, Lactobacillus bulgaricus, and Streptococcus thermophilus were used. MUC2 expression was knocked down in Caco-2 cells by RNA interference. 5-Aza-2'-deoxycytidine (5-Aza-CdR), which enhances mucin-promoted probiotic effects through inducing production of Sadenosyl-L-methionine (SAMe), was used to up-regulate MUC2 expression in Caco-2 cells. The adhesion to and invasion of meningitic E. coli were detected by competition assays. Our studies showed that probiotic agents could block E. coli-caused intestinal colonization, bacteremia, and meningitis in a neonatal sepsis and meningitis rat model. MUC2 gene expression in the neonatal rats given probiotic agents was obviously higher than that of the infected and uninfected control groups without probiotic treatment. The prohibitive effects of probiotic agents on MUC2-knockdown Caco-2 cells infected with E44 were significantly reduced compared with nontransfected Caco-2 cells. Moreover, the results also showed that 5-Aza-CdR, a drug enhancing the production of SAMe that is a protective agent of probiotics, was able to significantly suppress adhesion and invasion of E44 to Caco-2 cells by upregulation of MUC2 expression. Taken together, our data suggest that probiotic agents can efficiently block meningitic E. coli-induced pathogenicities in a manner dependent on MUC2.

• Journal of Life Science
• /
• v.19 no.8
• /
• pp.1073-1080
• /
• 2009

A number of studies have demonstrated that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risks of colorectal, oesophageal and lung cancers. NSAIDs have been shown to exert their anti-cancer effects through inducing apoptosis in cancer cells. The susceptibility of tumor cells to anti-tumor drug-induced apoptosis appears to depend on the balance between pro-apoptotic and anti-apoptotic programs such as nuclear factor kB (NF-kB), phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) and MEK1/2-ERK1/2 pathways. We examined the effects of pro-survival PI3K and ERK1/2 signal pathways on cell cycle arrest and apoptosis in response to NSAIDs including sulindac sulfide and NS398. We show that simultaneous inhibition of the Akt/PKB and ERK1/2 signal cascades could synergistically enhance the potential pro-apoptotic activities of sulindac sulfide and NS398. Similar enhancement was observed in cells treated with sulindac sulfide or NS398 and 100 ${\mu}$M genistein, an inhibitor of receptor tyrosine kinases (RTKs) that are upstream of PI3K and MEK1/2 signaling. We further demonstrate that NAG-1 is induced and plays a critical role(s) in apoptosis by NSAIDs-based combined treatment. In sum, our results show that combinatorialtreatment of sulindac sulfide or NS398 and genistein results in a highlysynergistic induction of apoptotic cell death to increase the chemopreventive effects of the NSAIDs, sulindac sulfide and NS398.