허가(虛假)소송(訴訟)지(之)식별(識別)

모소원 ( Xiao Yuan Mou ) 제주대학교 법과정책연구원 2015 국제법무 Vol.7 No.2

Recently, false litigation whereby litigants attempt to obtain illegal benefits from litigations has been increasing. Those litigants, who utilise the legal loophole in civil litigation procedure and maliciously collude so as to obtain legal documents from courts and arbitral tribunals, gain illegal proceeds. As a result, a third parties`` interests may be at risk and unable to be legally protected. To curb this illegal activity, the Chinese Civil Procedure was amended in August 2012 to insert a provision for a third -party with draw al procedure. This paper investigates the characteristics of false litigations and discusse show to identify/detect a false a litigation. Further, it an alyses the difficulties and responses relating to false litigation in order to beable to prevent and penalise such illegal activities.

Cancer-Associated Fibroblasts Promote the Chemo-resistance in Gastric Cancer through Secreting IL-11 Targeting JAK/STAT3/Bcl2 Pathway

Jun Ma,Xiao Song,Xiaowu Xu,Yiping Mou 대한암학회 2019 Cancer Research and Treatment Vol.51 No.1

Purpose Our aim was to detect the potential role of interleukin 11 (IL-11) in the development of chemo-resistance in gastric cancer and to reveal the mechanism involved in the process. Materials and Methods Here, we used flow cytometry to examine the percentage of cancer-associated-fibroblasts in tumor samples from chemo-resistant and -sensitive gastric cancer patients. Using MTT assay, we detected the cell viability under different conditions. Using quantitative real-time polymerase chain reaction and Western blotting, we determined the target expressions in mRNA and protein levels. We also performed immunohistochemistry and immunofluorescence to detect the target proteins under different conditions. Animal models were constructed to verify the potential role of IL-11 in chemo-resistant develop in vivo. Results Herein, we observed enriched cancer associated fibroblasts in drug resistant tumor tissues from gastric patients. Those fibroblasts facilitate the chemotherapeutic drugs resistance development through the secretion of IL-11, which activates the IL-11/IL-11R/gp130/ JAK/STAT3 anti-apoptosis signaling pathway in gastric cancer cells. We found that the combination of chemotherapeutic drugs and JAK inhibitor overcomes the resistance and increases the survival of mice with gastric cancer xenografts. Conclusion Our results demonstrated that IL-11 contributed to the obtain of resistance to chemotherapy drugs through gp130/JAK/STAT3/Bcl2 pathway, and targeting the IL-11 signaling pathway induced by fibroblasts might be a promising strategy to overcome the multi-drugs resistant cancer in clinic.

<i>Roseivivax</i> <i>roseus</i> sp. nov., an alphaproteobacterium isolated from a solar saltern soil sample

Zhang, Yu-Qin,Lee, Jae-Chan,Park, Dong-Jin,Lu, Xin-Xin,Mou, Xiao-Zhen,Kim, Chang-Jin International Union of Microbiological Societies 2014 International journal of systematic and evolutiona Vol.64 No.5

<P>A pink, Gram-stain-negative, motile, halotolerant bacterium with subpolar flagellum, designated strain BH87090<SUP>T</SUP>, was isolated from a saline soil sample collected from the south-west coastal area of South Korea (125° 58′ 58.08″ E 34° 45′ 37.32″ N). The isolate formed opaque pink to red colonies on marine agar plates at 30 °C. The polar lipid profile consisted of diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, sulfoquinovosyl diacylglycerol, phosphatidylcholine and one unidentified phospholipid. The sole respiratory quinone was ubiquinone-10 (Q-10). The major cellular fatty acids were C<SUB>18 : 1</SUB>ω7<I>c</I>, C<SUB>19 : 0</SUB> cyclo ω8<I>c</I>, C<SUB>16 : 0</SUB> and 11-methyl C<SUB>18 : 1</SUB>ω7<I>c</I>. The genomic DNA G+C content was 61.8 mol%. These chemotaxonomic characteristics were all consistent with specific properties of the genus <I>Roseivivax</I>. Phylogenetic analysis based on 16S rRNA gene sequences showed that the isolate affiliated to the cluster with members of the genus <I>Roseivivax</I> in the <I>Roseobacter</I> clade, which suggested that the strain belonged to the genus <I>Roseivivax</I>. However, the low 16S rRNA gene similarities (93.5–95.3 %) of strain BH87090<SUP>T</SUP> with all the members of the genus <I>Roseivivax</I> indicated that it represented a novel species of the genus <I>Roseivivax</I>. On the basis of phenotypic and genotypic data, strain BH87090<SUP>T</SUP> should be classified as a novel species of the genus <I>Roseivivax</I>. The name <I>Roseivivax roseus</I> sp. nov. is proposed, with strain BH87090<SUP>T</SUP> ( = DSM 23042<SUP>T</SUP> = KCTC 22650<SUP>T</SUP>) as the type strain.</P>

Autophagy inhibition contributes to epigallocatechin-3-gallate-mediated apoptosis in papillary thyroid cancer cells

Bu Ling,Zheng Tingting,Mao Chaoming,Fei Wu,Mou Xiao,Xu Chengcheng,Luo Xuan,Lu Qingyan,Dong Liyang,Wang Xuefeng 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4

Background Epigallocatechin-3-gallate is a natural polyphenolic compound that induces apoptosis in papillary thyroid cancer cells. However, its underlying molecular mechanism was not completely clarified. Objectives The present study demonstrated the role of apoptosis and autophagy in EGCG-treated papillary thyroid cancer cells and the relationship between these processes. Results EGCG significantly suppressed the viability of TPC-1 papillary thyroid cancer cells at an IC50 of 17.2 μM. EGCG induced TPC-1 cell apoptosis and cell cycle arrest at S phase and downregulated the protein expression of cyclin A and cyclin-dependent kinase-2. EGCG decreased reactive oxygen species levels, upregulated Bax expression, downregulated Bcl-2 expression and increased cytochrome C levels in the cytosol. Treatment with EGCG also increased the levels of cleaved caspase 3, cleaved caspase 9 and cleaved poly(ADP-ribose) polymerase. EGCG induced an autophagic response via the upregulation of the autophagy-related protein LC3-II and suppression of the AKT/mTOR signalling pathway. Autophagy inhibition further enhanced EGCG-induced cell apoptosis and ROS suppression, which indicated that autophagy played a cytoprotective role in EGCG-treated TPC-1 cells. Conclusion Taken together, these results demonstrated that autophagy inhibition was beneficial to EGCG–mediated apoptosis in papillary thyroid cancer cells. Background Epigallocatechin-3-gallate is a natural polyphenolic compound that induces apoptosis in papillary thyroid cancer cells. However, its underlying molecular mechanism was not completely clarified. Objectives The present study demonstrated the role of apoptosis and autophagy in EGCG-treated papillary thyroid cancer cells and the relationship between these processes. Results EGCG significantly suppressed the viability of TPC-1 papillary thyroid cancer cells at an IC50 of 17.2 μM. EGCG induced TPC-1 cell apoptosis and cell cycle arrest at S phase and downregulated the protein expression of cyclin A and cyclin-dependent kinase-2. EGCG decreased reactive oxygen species levels, upregulated Bax expression, downregulated Bcl-2 expression and increased cytochrome C levels in the cytosol. Treatment with EGCG also increased the levels of cleaved caspase 3, cleaved caspase 9 and cleaved poly(ADP-ribose) polymerase. EGCG induced an autophagic response via the upregulation of the autophagy-related protein LC3-II and suppression of the AKT/mTOR signalling pathway. Autophagy inhibition further enhanced EGCG-induced cell apoptosis and ROS suppression, which indicated that autophagy played a cytoprotective role in EGCG-treated TPC-1 cells. Conclusion Taken together, these results demonstrated that autophagy inhibition was beneficial to EGCG–mediated apoptosis in papillary thyroid cancer cells.