60년대 초반 중국 조선족 장편소설에 나타난 민족의식의 내면화

이해영(Li Hai-ying) 국어국문학회 2011 국어국문학 Vol.- No.157

This paper focuses on the internalization of the national spirit in Tiger Cliff written by Li Genquan who was the representative Chinese Ethnic Korean writer of the first generation appeared in the 1950s. Compared with Jin Xuetie who appeared at the same time but was evaluated as the master of the Chinese Ethnic Koreans' literature, although Li Genquan was active in the creation and left a lot of works, he couldn't draw the attention of the Ethnic Korean academics. The main reason was that as an influential local leader of the Communist Party of China, Li Genquan not only faithfully enforced the various politics and culture policy but also strove for incorporating the literary works with the mainstream of Chinese society, which were reflected from his works. The criticism and the indifference from the Ethnic Korean academics were the results of his consciousness of "Party Centralism" which was out of tune with the national consciousness. However, this paper indicates that standing on the Chinese political reality and Yanbian's situation in the early 1960s, considering about Li Genquan's political experience and his novels which drew materials from the Ethnic Koreans' history, the one-sidedness of the above evaluation can be found. The major theme of the novel Tiger Cluff written by Li Genquan in the early 1960's was that under the leadership of the Communist Party of China, Ethnic Koreans highly united to defeat the reactionary of Nationalist Party and finally got the thorough liberation, which definitely adhered to the "Party Centralism" and "Directivity of China", but the works at the same internalized Ethnic Koreans' history of their struggles even the history of Ethnic Koreans in China. In the early 60s, national problems were prohibited in political reality of Yanbian area. So Li Genquan's courage could only be explained by his national consciousness and his subject consciousness. Spreading out the national history under the leadership of Party and establishing the position in the big frame of country were probably called "internalization" of national consciousness. This kind internalization of national consciousness was the way of living which chose the Chinese Ethnic Koreans including Li Genquan, meanwhile chosen by them after National Independence. This paper discusses the way of "internalization" of national consciousness and national consciousness with this kind of "internalization" embodied in the Li Genquan's novel Tiger Cliff. Li Genquan's novel Tiger Cliff published in the early 60s did not simply express the policy of Party and the education of national history but finally pointed to the establishment of Ethnic Koreans' national rights.

Protective Effect of Magnolol on TBHP-Induced Injury in H460 Cells Partially via a p53 Dependent Mechanism

Hai-bo Li,Jian-mei Gao,Xi-xiang Ying,Shu-Peng Wang,Jian-chun Li 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.7

The aim is to investigate the effect of Magnolol preserved H460 cells from an oxidative agent tert-butylhydroperoxide (TBHP)-induced cell death. Magnolol augmented cell survival ratio after TBHP challenged. The protective action of this drug was more efficacious than that of Nacetylcysteine (NAC) which is a putative antioxidant. DNA damage, detected by the comet assay, was diminished after treatment of Magnolol. The cells viability decreased after treatment with 0.15 mM TBHP for 24 h, accompanied by inducing apoptotic death of the cells. Cytotoxicity and apoptosis induced by TBHP were significantly inhibited or attenuated after pretreatment with 20 µM Magnolol. Magnolol contributes to the cells survival through downregulated the p53 phosphorylation and PTEN expression, and upregulated Akt phosphorylation. Taken together, Magnolol was effective against DNA single strand breaks (SSB) formation, cytotoxicity and lipid peroxidation induced by TBHP, and its effects on p53 phosphorylation, PTEN and Akt phosphorylation were due to its antioxidative function, and partially via a p53 dependent mechanism in this protective effects.

Magnolol-Induced H460 Cells Death via Autophagy but Not Apoptosis

Hai-bo Li,Xin Yi,Jian-mei Gao,Xi-xiang Ying,Hong-quan Guan,Jian-chun Li 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.12

We have reported that the protective effect of Magnolol on TBHP-induced injury in human nonsmall lung cancer H460 cells is partially via a p53 dependent mechanism. In this study, we found that Magnolol displayed a stimulatory effect at low concentrations (≤20 µM) whilst inhibitory effect at high concentrations (≥40 µM) in H460 cells. To investigate the mechanism of inducing the biphasic effect in H460 cells with Magnolol, we showed that Magnolol stimulated DNA synthesis at low concentrations and displayed an inhibition effect at high concentrations in H460 cells. More importantly, the inhibition of DNA synthesis was accompanied by the S phase cell cycle arrest and the appearance of intense intracytoplasmic vacuoles. These vacuoles can be labeled by autophagic marker monodansylcadaverin (MDC), 3-methyladenine (3- MA), an inhibitor of autophagy, was able to inhibit the occurrence of autophagy. The results of the LDH activity assay and TUNEL assay also showed that Magnolol at high concentrations inhibiting H460 cell growth was not via apoptotic pathway. Furthermore, accompanied by the occurrence of autophagy, the expression of phospho-Akt was down-regulated but PTEN significantly was up-regulated. In conclusion, Magnolol induces H460 cells death by autophagy but not apoptotic pathway. Blockade of PI3K/PTEN/Akt pathway is maybe related to Magnololinduced autophagy. Autophagic cells death induction by Magnolol underlines the potential utility of its induction as a new cancer treatment modality.

Eugenol Inhibits ATP-induced P2X Currents in Trigeminal Ganglion Neurons

Li, Hai Ying,Lee, Byung-Ky,Kim, Joong-Soo,Jung, Sung-Jun,Oh, Seog-Bae The Korean Society of Pharmacology 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.6

Eugenol is widely used in dentistry to relieve pain. We have recently demonstrated voltage-gated $Na^+$ and $Ca^{2+}$ channels as molecular targets for its analgesic effects, and hypothesized that eugenol acts on $P2X_3$, another pain receptor expressed in trigeminal ganglion (TG), and tested the effects of eugenol by whole-cell patch clamp and $Ca^{2+}$ imaging techniques. In the present study, we investigated whether eugenol would modulate 5'-triphosphate (ATP)-induced currents in rat TG neurons and $P2X_3$-expressing human embryonic kidney (HEK) 293 cells. ATP-induced currents in TG neurons exhibited electrophysiological properties similar to those in HEK293 cells, and both ATP- and $\alpha$, $\beta$-meATP-induced currents in TG neurons were effectively blocked by TNP-ATP, suggesting that $P2X_3$ mediates the majority of ATP-induced currents in TG neurons. Eugenol inhibited ATP-induced currents in both capsaicin-sensitive and capsaicin-insensitive TG neurons with similar extent, and most ATP-responsive neurons were IB4-positive. Eugenol inhibited not only $Ca^{2+}$ transients evoked by $\alpha$, $\beta$-meATP, the selective $P2X_3$ agonist, in capsaicin-insensitive TG neurons, but also ATP-induced currents in $P2X_3$-expressing HEK293 cells without co-expression of transient receptor potential vanilloid 1 (TRPV1). We suggest, therefore, that eugenol inhibits $P2X_3$ currents in a TRPV1-independent manner, which contributes to its analgesic effect.

Upregulation of PITX2 Promotes Letrozole Resistance Via Transcriptional Activation of IFITM1 Signaling in Breast Cancer Cells

Ying-ying Xu,Hai-ru Yu,Jia-yi Sun,Zhao Zhao,Shuang Li,Xin-feng Zhang,Zhi-xuan Liao,Ming-ke Cui,Juan Li,Chan Li,Qiang Zhang 대한암학회 2019 Cancer Research and Treatment Vol.51 No.2

Purpose Although the interferon  (IFN) signaling and the paired-like homeodomain transcription factor 2 (PITX2) have both been implicated in the progression of breast cancer (BCa), it remains obscure whether these two pathways act in a coordinated manner. We therefore aimed to elucidate the expression and function of PITX2 during the pathogenesis of endocrine resistance in BCa. Materials and Methods PITX2 expression was assessed in BCa tissues using quantitative reverse transcription polymerase chain reaction (RT-qPCR) and immunohistochemistry and in experimentally induced letrozole-resistant BCa cells using RT-qPCR and immunoblotting. Effects of PITX2 deregulation on BCa progression was determined by assessing MTT, apoptosis and xenograft model. Finally, using multiple assays, the transcriptional regulation of interferon-inducible transmembrane protein 1 (IFITM1) by PITX2 was studied at both molecular and functional levels. Results PITX2 expression was induced in letrozole-resistant BCa tissues and cells, and PITX2 induction by IFN signaling powerfully protected BCa cells against letrozole insult and potentiated letrozole-resistance. Mechanistically, PITX2 enhanced IFN-induced AKT activation by transactivating the transcription of IFITM1, thus rendering BCa cells unresponsive to letrozoleelicited cell death. Additionally, ablation of IFITM1 expression using siRNA substantially abolished IFN-elicited AKT phosphorylation, even in the presence of PITX2 overexpression, thus sensitizing BCa cells to letrozole treatment. Conclusion These results demonstrate that constitutive upregulation of PITX2/IFITM1 cascade is an intrinsic adaptive mechanism during the pathogenesis of letrozole-resistance, and modulation of PITX2/IFITM1 level using different genetic and pharmacological means would thus have a novel therapeutic potential against letrozole resistance in BCa.

Web-Development ; A Comparison of Price and Price Dispersion of Online Retailers in Different Internet Maturity Stage

Hai Ying Li,Gee Woo Bock,Sang Yong Tom Lee 한국경영정보학회 2005 한국경영정보학회 학술대회논문집 Vol.2005 No.-

L-carnitine treatment attenuates renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction

( Hai Yan Zhao ),( Hui Ying Li ),( Jian Jin ),( Ji Zhe Jin ),( Long Ye Zhang ),( Mei Ying Xuan ),( Xue Mei Jin ),( Yu Ji Jiang ),( Hai Lan Zheng ),( Ying Shun Jin ),( Yong Jie Jin ),( Bum Soon Choi ) 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.0

Background/Aims: Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. Methods: Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H₂O₂-exposed human kidney cells (HK-2) were treated with LC. Results: LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H₂O₂-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. Conclusions: LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.

Eugenol Inhibits ATP-induced P2X Currents in Trigeminal Ganglion Neurons

Hai Ying Li,Byung Ky Lee,Joong Soo Kim,Sung Jun Jung,Seog Bae Oh 대한생리학회-대한약리학회 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.6

Eugenol is widely used in dentistry to relieve pain. We have recently demonstrated voltage-gated Na⁺ and Ca²⁺ channels as molecular targets for its analgesic effects, and hypothesized that eugenol acts on P2X₃, another pain receptor expressed in trigeminal ganglion (TG), and tested the effects of eugenol by whole-cell patch clamp and Ca²⁺ imaging techniques. In the present study, we investigated whether eugenol would modulate 5 -triphosphate (ATP)-induced currents in rat TG neurons and P2X₃-expressing human embryonic kidney (HEK) 293 cells. ATP-induced currents in TG neurons exhibited electrophysiological properties similar to those in HEK293 cells, and both ATP- and Ձ,Ղ-meATP-induced currents in TG neurons were effectively blocked by TNP-ATP, suggesting that P2X₃ mediates the majority of ATP-induced currents in TG neurons. Eugenol inhibited ATP-induced currents in both capsaicin-sensitive and capsaicin-insensitive TG neurons with similar extent, and most ATP-responsive neurons were IB4-positive. Eugenol inhibited not only Ca²⁺ transients evoked by Ձ,Ղ-meATP, the selective P2X₃ agonist, in capsaicin-insensitive TG neurons, but also ATP-induced currents in P2X₃-expressing HEK293 cells without co-expression of transient receptor potential vanilloid 1 (TRPV1). We suggest, therefore, that eugenol inhibits P2X₃ currents in a TRPV1-independent manner, which contributes to its analgesic effect.

Magnolol-Induced H460 Cells Death via Autophagy but Not Apoptosis

Li, Hai-Bo,Yi, Xin,Gao, Jian-Mei,Ying, Xi-Xiang,Guan, Hong-Quan,Li, Jian-Chun 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.12

We have reported that the protective effect of Magnolol on TBHP-induced injury in human non-small lung cancer H460 cells is partially via a p53 dependent mechanism. In this study, we found that Magnolol displayed a stimulatory effect at low concentrations $(\leq20{\mu}M)$ whilst inhibitory effect at high concentrations $(\geq20{\mu}M)$ in H460 cells. To investigate the mechanism of inducing the biphasic effect in H460 cells with Magnolol, we showed that Magnolol stimulated DNA synthesis at low concentrations and displayed an inhibition effect at high concentrations in H460 cells. More importantly, the inhibition of DNA synthesis was accompanied by the S phase cell cycle arrest and the appearance of intense intracytoplasmic vacuoles. These vacuoles can be labeled by autophagic marker monodansylcadaverin (MDC), 3-methyladenine (3-MA), an inhibitor of autophagy, was able to inhibit the occurrence of autophagy. The results of the LDH activity assay and TUNEL assay also showed that Magnolol at high concentrations inhibiting H460 cell growth was not via apoptotic pathway. Furthermore, accompanied by the occurrence of autophagy, the expression of phospho-Akt was down-regulated but PTEN significantly was up-regulated. In conclusion, Magnolol induces H460 cells death by autophagy but not apoptotic pathway. Blockade of PI3K/PTEN/Akt pathway is maybe related to Magnolol-induced autophagy. Autophagic cells death induction by Magnolol underlines the potential utility of its induction as a new cancer treatment modality.

Clinical Significance of Upregulation of mir-196a-5p in Gastric Cancer and Enriched KEGG Pathway Analysis of Target Genes

Li, Hai-Long,Xie, Shou-Pin,Yang, Ya-Li,Cheng, Ying-Xia,Zhang, Ying,Wang, Jing,Wang, Yong,Liu, Da-Long,Chen, Zhao-Feng,Zhou, Yong-Ning,Wu, Hong-Yan Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5

Background: miRNAs are relatively recently discovered cancer biomarkers which have important implications for cancer early diagnosis, treatment and estimation of prognosis. Here we focussed on expression of mir-196a-5p in gastric cancer tissues and cell lines so as to analyse its significance for clinicopathologic characteristics and generate enriched KEGG pathways clustered by target genes for exploring its potential roles as a biomarker in gastric cancer. Materials and Methods: The expression of mir-196a-5p in poorly, moderate and well differentiated gastric cancer cell lines compared with GES-1 was detected by RT-qPCR, and the expression of mir-196a-5p in gastric cancer tissues comparing with adjacent non cancer tissues of 58 cases were also assessed by RT-qPCR. Subsequently, an analysis of clinical significance of mir-196a-5p in gastric cancer and enriched KEGG pathways was executed based on the miRWalk prediction database combined with bioinformatics tools DAVID 6.7 and Mirfocus 3.0. Results: RT-qPCR showed that mir-196a-5p was up-regulated in 6 poorly and moderate differentiated gastric cancer cell lines SGC-7901, MKN-45, MKN-28, MGC-803, BGC-823, HGC-27 compared with GES-1, but down-regulated in the highly differentiated gastric cancer cell line AGS. Clinical data indicated mir-196a-5p to beup-regulated in gastric cancer tissues (47/58). Overexpression of mir-196a-5p was associated with more extensive degree of lymph node metastasis and clinical stage (P < 0.05; x2 test). Enriched KEGG pathway analyses of predicted and validated targets in miRWalk combined with DAVID 6.7 and Mirfocus 3.0 showed that the targeted genes regulated by mir-196a-5p were involved in malignancy associated biology. Conclusions: Overexpression of mir-196a-5p is associated with lymph node metastasis and clinical stage, and enriched KEGG pathway analyses showed that targeted genes regulated by mir-196a-5p may contribute to tumorgenesis, suggesting roles as an oncogenic miRNA biomarker in gastric cancer.