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RISS 인기검색어
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- 저자 : Sebastian Bauer (검색결과 4 건)
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A study of preferential flow in heterogeneous media using random walk particle tracking
Chan-Hee Park,Christof Beyer,Sebastian Bauer,Olaf Kolditz 한국지질과학협의회 2008 Geosciences Journal Vol.12 No.3
We investigated the onset of preferential flow in heterogeneous porous media using the random walk particle tracking (RWPT) concept. The RWPT model is first used to analyze empirically the required number of particles to achieve accurate concentration distributions in two-dimensional homogeneous media and under uniform flow conditions. The analysis is then extended to randomly heterogeneous systems. By increasing the variance of log-normal hydraulic conductivity fields, the transition between homogeneous and preferential flows is observed. To analyze the degree of preferential flow in the porous media, we provide a diagram that consists of two dimensionless parameters: normalized travel time and distance. All the heterogeneous media synthetically generated show a linear relation in the diagram. The characteristic travel velocity increases with increasing heterogeneity. We found the diagram is a useful tool to analyze preferential flow.
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Yun, SeongJu,Kim, Won Kyu,Kwon, Yujin,Jang, Mi,Bauer, Sebastian,Kim, Hoguen John Wiley and Sons Inc. 2018 International journal of cancer: Journal internati Vol.142 No.10
<▼1><P>Gain‐of‐function mutations of KIT are pathognomonic in sporadic gastrointestinal stromal tumors (GISTs). Several microRNAs have been shown to be dysregulated in GISTs and impact KIT expression. Little is known though on KIT‐independent targets of KIT‐regulating mRNAs. We sought to investigate how miR‐494 inhibits GIST proliferation and to identify novel target gene. We used microarray‐based gene expression analyses to identify pathways and target genes affected by miR‐494. The expressional relationship between survivin and miR‐494 was determined in 35 GIST tissues. Cell proliferation assay, FACS analysis, colony formation assay, promoter assays and chromatin immunoprecipitation (ChiP) were performed to clarify the roles of survivin in GIST progression. Gene expression microarray analysis revealed that miR‐494 inhibited GISTs by affecting multiple genes in the cell cycle pathway. <I>Survivin (BIRC5)</I> was a key target of miR‐494, and its expression showed an inverse correlation with miR‐494 expression in 35 GIST tissues (Pearson's correlation coefficient, <I>r</I> = −0.418, <I>p</I> = 0.012). Downregulation of survivin inhibited proliferation and colony formation, and resulted in cell cycle alteration. Induced survivin overexpression relieved miR‐494‐mediated inhibition of GIST progression. Targeting PI3K effectively suppressed proliferation of GISTs with downregulation of survivin. Survivin also regulated <I>KIT</I> expression at the transcription level. Immunohistochemical analysis using 113 GISTs revealed that survivin expression was significantly correlated with overall survival of GIST patients (<I>p</I> = 0.004). Our findings indicated that miR‐494 synergistically suppressed GISTs by concomitantly targeting survivin and KIT.</P></▼1><▼2><P><B>What's new?</B></P><P>Gain‐of‐function mutations of KIT are pathognomonic in sporadic gastrointestinal stromal tumors (GISTs). Several microRNAs have also been shown to be dysregulated in GISTs and impact KIT expression. However, still little is known on KIT‐independent targets of KIT‐regulating mRNAs. Here, the authors report that miR‐494 induces alteration of the cell cycle pathways in GISTs by downregulating survivin, which functions as a transcription factor of <I>KIT</I>, accompanying effective blockade of the PI3K pathway that both KIT and survivin belong to. Based on these findings, miR‐494 may play important roles during GIST tumorigenesis and be used as a potent agent to treat GISTs.</P></▼2>
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Kim, Won Kyu,Yun, SeongJu,Park, Cheol Keun,Bauer, Sebastian,Kim, Jiyoon,Lee, Min Goo,Kim, Hoguen American Association for Cancer Research 2017 Clinical Cancer Research Vol.23 No.3
<P><B>Purpose:</B> Tumorigenesis of gastrointestinal stromal tumors (GIST) is driven by gain-of-function mutations in the <I>KIT</I> gene, which result in overexpression of activated mutant KIT proteins (MT-KIT). However, the mechanism of MT-KIT overexpression is poorly understood.</P><P><B>Experimental Design:</B> By protein expression analysis and immunofluorescent microscopic analysis, we determine the stability and localization of MT-KIT in four GIST cell lines with different mutations and HeLa cells transfected with mutant KIT model vectors. We also used 154 human GIST tissues to analyze the relationship between the expression of PKC-θ and MT-KITs, and correlations between PKC-θ overexpression and clinicopathological parameters.</P><P><B>Results:</B> We report that four different MT-KIT proteins are intrinsically less stable than wild-type KIT due to proteasome-mediated degradation and abnormally localized to the endoplasmic reticulum (ER) or the Golgi complex. By screening a MT-KIT-stabilizing factor, we find that PKC-θ is strongly and exclusively expressed in GISTs and interacts with intracellular MT-KIT to promote its stabilization by increased retention in the Golgi complex. In addition, Western blotting analysis using 50 GIST samples shows strong correlation between PKC-θ and MT-KIT expression (correlation coefficient = 0.682, <I>P</I> < 0.000001). Immunohistochemical analysis using 154 GISTs further demonstrates that PKC-θ overexpression significantly correlates with several clinicopathological parameters such as high tumor grade, frequent recurrence/metastasis, and poor patient survival.</P><P><B>Conclusions:</B> Our findings suggest that sustained MT-KIT overexpression through PKC-θ-mediated stabilization in the Golgi contributes to GIST progression and provides a rationale for anti-PKC-θ therapy in GISTs. <I>Clin Cancer Res; 23(3); 845–56. ©2016 AACR</I>.</P>
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