• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.156-156
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• 2001

We have previously shown that H-ras, but N-ras, induces an invasiveness and cell motility in human breast epithelial cells (MCFl0A), while both H-ras and N-ras induce transformed phenotype. It has been recently shown that phosphatidylinositol 3-kinase (PI3K) plays an important role on cell migration. In the present study, we wished to investigate the functional role of PI3K in H-ras-induced invasive phenotype in MCF10A cells.(omitted)

• Proceedings of the Korean Powder Metallurgy Institute Conference
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• 2006.09a
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• pp.680.2-680.2
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• 2006

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.142-142
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• 2002

Many studies have identified the phosphatidylinositol 3-kinase (PI3K) as a key regulator for various cellular functions including cell survival, growth and motility. We have previously shown that H-ras, but not N-ras, induces invasiveness and motility in human breast epithelial cells (MCF10A), while both H-ras and N-ras induce transformed phenotype.(omitted)

• Proceedings of the KSRS Conference
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• 2006.03a
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• pp.36-40
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• 2006

The objective of the study is to develop a GIS-based flood map. Hydraulic model (HEC-RAS) is linked with hydrologic model (HEC-HMS) for flood map. Geospatial data processors, HEC-GeoHMS and HEC-GeoRAS, are used for operating HEC-HMS and HEC-RAS. HEC-HMS was calibrated and validated at the Hwa-Ong watershed. HEC-HMS was used for calculating runoff from the Hwa-Ong watershed which consisted of Nam-Yang, Ja-An, U-Eun river sub-watersheds, and HEC-RAS was applied and validated for river flow routing at the Hwa-Ong watershed. The simulated results from HEC-HMS and HEC-RAS were reasonably good compared with the observed data. HEC-RAS and HEC-HMS were applied to simulate flooding from probability rainfall at the Hwa-Ong watershed, and the simulated result was used to develop a flood map. Flood map developed in this study will be used for mitigating and predicting the flood damages.

• Molecules and Cells
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• v.28 no.4
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• pp.315-320
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• 2009

The RAS family of oncoproteins has been studied extensively for almost three decades. While we know that activation of RAS represents a key feature of malignant transformation for many cancers, we are only now beginning to understand the complex underpinnings of RAS biology. Here, we will discuss emerging cancer genome sequencing data in the context of what is currently known about RAS function. Taken together, retrospective studies of primary human tissues and prospective studies of experimental models support the notion that the variable mutation frequencies exhibited by the RAS oncogenes reflect unique functions of the RAS oncoproteins.

• Nuclear Engineering and Technology
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• v.54 no.9
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• pp.3580-3585
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• 2022

The thermal stability of carbohydrazide, hydrazine nitrate, acetohydroxamic acid in nitric acid solutions has been studied at atmospheric pressure and above atmospheric pressure. The volumes of gaseous products of thermolysis and the maximum rate of gas evolution have been determined at atmospheric pressure. It has been shown that, despite the high rate of gas evolution and large volumes of evolved gases, the conditions for the development of autocatalytic oxidation are not created. Exothermic processes are observed in a closed vessel in the temperature range of 50-250 ℃. With an increase in the concentration of nitric acid, the temperatures of the onset of exothermic effects for all mixtures decrease, and the values of the total thermal effects of reactions increase, to the greatest extent for solutions with carbohydrazide.

• Journal of the Institute of Electronics Engineers of Korea CI
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• v.48 no.3
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• pp.54-68
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• 2011

As the prediction accuracy of conditional branch instruction is increased highly, the importance of prediction accuracy for unconditional branch instruction is also increased accordingly. Except the case of RAS(Return Address Stack) overflow, the prediction accuracy of function return address should be 100% theoretically. However, there exist some possibilities of miss-predictions for RAS return addresses, when miss-speculative execution paths are invalidated, in case of modern speculative microprocessor environments. In this paper, we propose the RAS rename technique to prevent RAS pollution, results in the reduction of RAS miss-prediction. We divide a RAS stack into a soft-stack and a hard-stack and we handle the instructions for speculative execution in the soft-stack. When some overwrites happen in the soft-stack, we move the soft-stack data into the hard-stack. In addition, we propose an enhanced version of RAS rename scheme. In simulation results, our solution provide 1/90 reduction of miss-prediction of function return address, results in up to 6.85% IPC improvement, compared to normal RAS method. Furthermore, it reduce miss-prediction ratio as 1/9, compared to previous technique.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.26 no.6
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• pp.581-590
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• 2000

Alterations in the cellular genome affecting the expression or function of genes controlling cell growth and differentiation are considered to be the main cause of cancer. Over 30 oncogenes can be activated by insertional mutagenesis, single point mutations, chromosomal translocations and gene amplification. The ras oncogenes have been detected in $15{\sim}20%$ of human tumors that include some of the most common forms of human neoplasia and are known to acquire their transforming properties by single point mutations in two domains of their coding sequences, most commonly in codons 12 and 61. The ras gene family consists of three functional genes, N-ras, K-ras and H-ras which encode highly similar proteins of 188 or 189 amino acid residues generically known as P21. ras proteins have been shown to bind GTP and GTP, and possess intrinsic GTPase activity. Experimental study was performed to observe the mutational change of the ras gene family and apply the results to the clinical activity. 36 Golden Syrian Hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek (control side) was treated with mineral oil as the same manner of the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were completely dissected by microdissection and DNA from both tissue were isolated by proteinase K/phenol/chloroform extraction. Segments of the K-ras and H-ras gene were amplified by PCR using the oligonucleotide primers corresponding to the homologous region (codon 12 and 61) of the hamster gene, and then confirmational change of ras genes was observed by SSCP and autosequencing analysis. The results were as follows : 1. Malignant lesion could be found in the experimental side from the experimental six weeks. 2. One hamster among six showed point mutation of the H-ras codon 12($G{\rightarrow}A$ transition) at the experimental 10 and 14 weeks. 3. One of six at 6 weeks, two of six at 8 weeks and one of six at 12 weeks revealed the confirmational change of the H-ras codon 61($A{\rightarrow}T$ transversion). 4. The incidence of point mutation of H-ras codon 12 and 61 were 5.5%(2 of 36) and 11%(4 of 36) respectively. 5. Point mutation of the K-ras could not be seen during the whole experimental period. Form the above results, these findings strongly support the concept that H-ras oncogenes may have the influence of the DMBA induced carcinoma of hamster buccal pouch.

• BMB Reports
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• v.40 no.5
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• pp.825-831
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• 2007

Tumor cell invasion and metastasis are often associated with matrix metalloproteinases (MMPs), among which MMP-2 and MMP-9 are of central importance. We previously showed that H-Ras, but not N-Ras, induced invasion of MCF10A human breast epithelial cells in which the enhanced expression of MMP-2 was involved. MMP-2 is produced as a latent pro-MMP-2 (72 kDa) to be activated resulting the 62 kDa active MMP-2. The present study investigated if H-Ras and/or N-Ras induces pro-MMP-2 activation of MCF10A cells when cultured in two-dimensional gel of type I collagen. Type I collagen induced activation of pro-MMP-2 only in H-Ras MCF10A cells but not in N-Ras MCF10A cells. Induction of active MMP-2 by type I collagen was suppressed by blocking integrin ${\alpha}2$, indicating the involvement of integrin signaling in pro-MMP-2 activation. Membrane-type (MT)1-MMP and tissue inhibitor of metalloproteinase (TIMP)-2 were up-regulated by H-Ras but not by N-Ras in the type I collagen-coated gel, suggesting that H-Ras-specific up-regulation of MT1-MMP and TIMP-2 may lead to the activation of pro-MMP-2. Since acquisition of pro-MMP-2 activation can be associated with increased malignant progression, these results may help understanding the mechanisms for the cell surface matrix-degrading potential which will be crucial to the prognosis and therapy of breast cancer metastasis.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6517-6521
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• 2012

To analyze the growth, proliferation, apoptosis, invasiveness and chemotherapy sensitivity of EC9706 cells after K-Ras gene silencing, an expression carrier pSilencer-siK-Ras was constructed, and the EC9706 cell line was transfected using a liposome technique. Six groups were established: Control, siRNA NC (transfected with empty vector pSilencer2.1); Ras siRNA (transfected with pSilencer-siK-Ras2); Paclitaxel; Paclitaxel + siRNA NC; and Ras siRNA + Paclitaxel. After the treatment, RT-PCR, Western blotting, MTT assay, flow cytometry and the Transwell technique were used to assess expression of K-Ras mRNA and protein in EC9706 cells, as well as cell growth, proliferation, apoptosis and invasiveness. The effect of Paclitaxel chemotherapy was also tested. pSilencer-siK-Ras2 effectively down-regulated expression of K-Ras mRNA and protein in EC9706 cells, growth being significantly inhibited. Flow cytometry indicated obvious apoptosis of cells in the experimental group, with arrest in the G1 phase; cell migration ability was also reduced. After pSilencer-siK-Ras2 transfection or the addition of Paclitaxel, EC9706 cells were suppressed to different extents; the suppressive effect was strengthened by combined treatment. The results suggested that RNAi-induced K-Ras gene silencing could enhance chemotherapy sensitivity of esophageal cancer.