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      • KCI등재

        Standardizing and optimizing acupuncture treatment for irritable bowel syndrome: A Delphi expert consensus study

        Xin-Tong Su,Wang Li-Qiong,Zhang Na,Li Jin-Ling,Qi Ling-Yu,Wang Yu,Jing-Wen Yang,Guang-Xia Shi,Cun-Zhi Liu 한국한의학연구원 2021 Integrative Medicine Research Vol.10 No.3

        Background: Acupuncture has been widely utilized for irritable bowel syndrome (IBS). However, heterogeneity is large among therapeutic strategies and protocols. The aim of this study was to propose some down-to-earth recommendations and establish an optimized protocol for acupuncture practice in IBS. Methods: A panel of 74 traditional Chinese medicine (TCM) acupuncturists participated in clinical issue investigation. Subsequently, systematic reviews concerning acupuncture for IBS were screened within 3 databases. An initial consensus questionnaire was formed from the results of clinical issue investigation and literature review. Ultimately, a Delphi vote was carried out to determine these issues. 30 authoritative experts with extensive experience were requested to respond with agreement, neutrality, or disagreement for the items. Consensus achievement on a given item was defined as greater than 80% agreement. Results: Following a 2-round Delphi survey, there were 19 items reaching consensus; of which 5 items (26.32%) achieved thorough consensus, and significant agreement was reached for the other 14 items. These items can be classified into the 3 major domains: 1) clinical outcomes that acupuncture can bring for favorable intervention population (5 items), 2) suitable therapeutic principles and parameters of acupuncture (13 items), 3) possible adverse events in the treatment (1 item). Conclusion: Without any ready-made guidelines and lacking of homogeneity in the published literatures, such expert consensus could be valuable for TCM acupuncturists in daily practice and patients with IBS to obtain appropriate and standardized acupuncture treatment. In addition, it also points out the clinical focus which need to be further explored in future trials.

      • KCI등재

        ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells

        Lei Wang,Qiu-Tong Wang,Yu-Peng Liu,Qing-Qing Dong,Hai-Jie Hu,Zhi Miao,Shuang Li,Yong Liu,Hao Zhou,Tong-Cun Zhang,Wen-Jian Ma,Xuegang Luo 대한위암학회 2017 Journal of gastric cancer Vol.17 No.4

        Purpose: We previously found that the histone methyltransferase suppressor of variegation, enhancer of zeste, trithorax and myeloid-nervy-deformed epidermal autoregulatory factor-1 domain-containing protein 3 (SMYD3) is a potential independent predictive factor or prognostic factor for overall survival in gastric cancer patients, but its roles seem to differ from those in other cancers. Therefore, in this study, the detailed functions of SMYD3 in cell proliferation and migration in gastric cancer were examined. Materials and Methods: SMYD3 was overexpressed or suppressed by transfection with an expression plasmid or siRNA, and a wound healing migration assay and Transwell assay were performed to detect the migration and invasion ability of gastric cancer cells. Additionally, an MTT assay and clonogenic assay were performed to evaluate cell proliferation, and a cell cycle analysis was performed by propidium iodide staining. Furthermore, the expression of genes implicated in the ataxia telangiectasia mutated (ATM) pathway and proteins involved in cell cycle regulation were detected by polymerase chain reaction and western blot analyses. Results: Compared with control cells, gastric cancer cells transfected with si-SMYD3 showed lower migration and invasion abilities (P<0.05), and the absence of SMYD3 halted cells in G2/M phase and activated the ATM pathway. Furthermore, the opposite patterns were observed when SMYD3 was elevated in normal gastric cells. Conclusions: To the best of our knowledge, this study provides the first evidence that the absence of SMYD3 could inhibit the migration, invasion, and proliferation of gastric cancer cells and halt cells in G2/M phase via the ATM-CHK2/p53-Cdc25C pathway. These findings indicated that SMYD3 plays crucial roles in the proliferation, migration, and invasion of gastric cancer cells and may be a useful therapeutic target in human gastric carcinomas.

      • SCOPUSKCI등재

        ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells

        Wang, Lei,Wang, Qiu-Tong,Liu, Yu-Peng,Dong, Qing-Qing,Hu, Hai-Jie,Miao, Zhi,Li, Shuang,Liu, Yong,Zhou, Hao,Zhang, Tong-Cun,Ma, Wen-Jian,Luo, Xue-Gang The Korean Gastric Cancer Association 2017 Journal of gastric cancer Vol.17 No.4

        Purpose: We previously found that the histone methyltransferase suppressor of variegation, enhancer of zeste, trithorax and myeloid-nervy-deformed epidermal autoregulatory factor-1 domain-containing protein 3 (SMYD3) is a potential independent predictive factor or prognostic factor for overall survival in gastric cancer patients, but its roles seem to differ from those in other cancers. Therefore, in this study, the detailed functions of SMYD3 in cell proliferation and migration in gastric cancer were examined. Materials and Methods: SMYD3 was overexpressed or suppressed by transfection with an expression plasmid or siRNA, and a wound healing migration assay and Transwell assay were performed to detect the migration and invasion ability of gastric cancer cells. Additionally, an MTT assay and clonogenic assay were performed to evaluate cell proliferation, and a cell cycle analysis was performed by propidium iodide staining. Furthermore, the expression of genes implicated in the ataxia telangiectasia mutated (ATM) pathway and proteins involved in cell cycle regulation were detected by polymerase chain reaction and western blot analyses. Results: Compared with control cells, gastric cancer cells transfected with si-SMYD3 showed lower migration and invasion abilities (P<0.05), and the absence of SMYD3 halted cells in G2/M phase and activated the ATM pathway. Furthermore, the opposite patterns were observed when SMYD3 was elevated in normal gastric cells. Conclusions: To the best of our knowledge, this study provides the first evidence that the absence of SMYD3 could inhibit the migration, invasion, and proliferation of gastric cancer cells and halt cells in G2/M phase via the ATM-CHK2/p53-Cdc25C pathway. These findings indicated that SMYD3 plays crucial roles in the proliferation, migration, and invasion of gastric cancer cells and may be a useful therapeutic target in human gastric carcinomas.

      • KCI등재

        SMYD3-associated pathway is involved in the anti-tumor effects of sulforaphane on gastric carcinoma cells

        Qing-Qing Dong,Qiu-Tong Wang,Lei Wang,Ya-Xin Jiang,Mei-Ling Liu,Hai-Jie Hu,Yong Liu,Hao Zhou,Hong-Peng He,Tong-Cun Zhang,Xuegang Luo 한국식품과학회 2018 Food Science and Biotechnology Vol.27 No.4

        Sulforaphane (SFN), a natural compound derived from cruciferous vegetables, has been proved to possess potent anti-cancer activity. SMYD3 is a histone methyltransferase which is closely related to the proliferation and migration of cancer cells. This study showed that SFN could dose-dependently induce cell cycle arrest, stimulate apoptosis, and inhibit proliferation and migration of gastric carcinoma cells. Accompanied with these anticancer effects, SMYD3 and its downstream genes, myosin regulatory light chain 9, and cysteine-rich angiogenic inducer 61, was downregulated by SFN. Furthermore, overexpression of SMYD3 via transfection could abolish the effects of SFN, suggesting that SMYD3 might be an important mediator of SFN. To the best of our knowledge, this is the first report describing the role of SMYD3 in the anti-cancer of SFN. These findings might throw light on the development of novel anti-cancer drugs and functional food using SFN-rich cruciferous vegetables.

      • Paris polyphylla Smith Extract Induces Apoptosis and Activates Cancer Suppressor Gene Connexin26 Expression

        Li, Fu-Rong,Jiao, Peng,Yao, Shu-Tong,Sang, Hui,Qin, Shu-Cun,Zhang, Wei,Zhang, Ya-Bin,Gao, Lin-Lin Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.1

        Background: The inhibition of tumor cell growth without toxicity to normal cells is an important target in cancer therapy. One possible way to increase the efficacy of anticancer drugs and to decrease toxicity or side effects is to develop traditional natural products, especially from medicinal plants. Paris polyphylla Smith has shown anti-tumour effects by inhibition of tumor promotion and inducement of tumor cell apoptosis, but mechanisms are still not well understood. The present study was to explore the effect of Paris polyphylla Smith extract (PPSE) on connexin26 and growth control in human esophageal cancer ECA109 cells. Methods: The effects of PPSE on Connexin26 were examined by RT-PCR, western blot and immunofluorescence; cell growth and proliferation were examined by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay. Results: PPSE inhibited the growth and proliferation on esophageal cancer ECA109 cells, while increasing the expression of connexin26 mRNA and protein; conversely, PPSE decreased Bcl-2 and increased Bad. Conclusion: This study firstly shows that PPSE can increase connexin26 expression at mRNA and protein level, exerting anti-tumour effects on esophageal cacner ECA109 cells via inhibiting cell proliferation and inducing cell apoptosis.

      • KCI등재

        Bioconversion of conjugated linoleic acid by Lactobacillus plantarum CGMCC8198 supplemented with Acer truncatum bunge seeds oil

        Dong-Ju Chen,Li-Hua Yan,Qian Li,Cai-jiao Zhang,Chuan-Ling Si,Zhong-Yuan Li,Ya-Jian Song,Hao Zhou,Tong-Cun Zhang,Xuegang Luo 한국식품과학회 2017 Food Science and Biotechnology Vol.26 No.6

        Conjugated linoleic acid (CLA) isomers, c9, t11- CLA and t10, c12-CLA, have been proved to exhibit excellent biomedical properties for potential use in anticancer applications and in reducing obesity. Acer truncatum Bunge (ATB), which is rich in unsaturated fatty acids, including oleic acid, linoleic acid, and nervonic acid, is a new resource for edible oil. In the present study, we developed a new method for producing two CLA isomers from ATB-seed oil by fermentation using Lactobacillus plantarum CGMCC8198 (LP8198), a novel probiotics strain. Polymerase chain reaction results showed that there was a conserved linoleate isomerase (LIase) gene in LP8198, and its transcription could be induced by ATBseed oil. Analyses by gas chromatography–mass spectrometry showed that the concentration of c9, t11-CLA and t10, c12-CLA in ATB-seed oil could be increased by about 9- and 2.25-fold, respectively, after being fermented by LP8198.

      • KCI등재

        Lactobacillus acidophilus Strain Suppresses the Transcription of Proinflammatory-Related Factors in Human HT-29 Cells

        ( Kun Chen ),( Nai Long Liang ),( Xue Gang Luo ),( Tong Cun Zhang ) 한국미생물 · 생명공학회 2013 Journal of microbiology and biotechnology Vol.23 No.1

        Previous studies have shown that lactic acid bacteria can inhibit inflammatory responses, but the mechanisms are very little known. In this study, transaction and expression of three proinflammatory factors, iNOS, PTGS-2, and IL8, which are closely related to the inflammatory response, were investigated by luciferase reporter assay and RTPCR in HT-29 cells treated by Lactobacillus acidophilus. The results showed that the live L. acidophilus sharply down-regulated the transcription of these three genes. Because there was a NF-κB binding site located at -265 bp, -225 bp, and -95 bp upstream of the iNOS, PTGS-2, and IL8 promoters, respectively, we further addressed the effects of NF-κB on transaction of the three promoters by cotransfection. As was expected, NF-κBs remarkably upregulated the activity of the reporter gene and, no effect of NF-κBs on IL-8 promoter transaction was found after NF-κB binding site mutation of the IL8 promoter in HT- 29 cells. In conclusion, the live L. acidophilus decreased the transcriptional activity of NF-κB and, in turn, inhibited the transaction of NF-κB on the three proinflammatory factors mentioned above.

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