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Gene expression analysis of “green tide” alga Ulva prolifera (Chlorophyta) in China
Shangang Jia,Xumin Wang,Guiming Liu,Dan Luo,Jing Zhang,Yan Liu,Xiangzhi Lin,Tao Liu 한국유전학회 2011 Genes & Genomics Vol.33 No.2
Ulva prolifera (Ulvophyceae, Chlorophyta) is the causative species of the annual “green tides” in the Bohai Gulf of Northern China. In order to gain some more insight into the transcriptome of this fast-growing species of algae, we acquired 6,203 high-quality expressed-sequence-tags (ESTs),which were clustered into 4,080 unique sequences (UniSeqs). Functional classification revealed that most of the acquired transcripts were related to metabolic and biosynthetic processes,nucleotide binding, and cell part that might contribute to the organism’s rapid growth. Using 39 EST pools, 28 mitochondria genomes, and 18 chloroplast genomes from algae and land plants, we constructed three phylogenetic trees. These trees provided evidence that U. prolifera was in a sister position to Ulva linza, and shared a similar chloroplast origin with Pseudendoclonium akinetum. The findings of this study will improve our knowledge of the transcriptome and taxonomic position of U. prolifera.
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Wen Liu,Zhonghan Zhou,Dahai Dong,Lijiang Sun,Guiming Zhang 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.2
Purpose: This study aimed to evaluate the prognostic impact of lymphovascular invasion (LVI) in patients treated with radicalnephroureterectomy (RNU) for upper urinary tract urothelial carcinoma (UTUC). Materials and Methods: We collected data from 180 patients who were treated with RNU from 2005 to 2013 at our institution. TheKaplan-Meier method with log-rank test and Cox proportional hazards regression models were used for univariate and multivariateanalyses. Results: LVI was present in 28 patients (15.6%), which was associated with higher pathological tumor stage (p<0.001), tumor necrosis(p=0.012), lymph node metastasis (p=0.017) and multifocality (p=0.012). On multivariate analysis, LVI was an independentprognostic factor of recurrence-free survival [RFS: hazard ratio (HR)=2.954; 95% confidence interval (CI)=1.539–5.671; p=0.001]and cancer-specific survival (CSS: HR=3.530; 95% CI=1.701–7.325; p=0.001) in all patients. In patients with node-negative UTUC,LVI was also a significant predictor of RFS (HR=3.732; 95% CI 1.866–7.464; p<0.001) and CSS (HR=3.825; 95% CI=1.777–8.234;p=0.001). Conclusion: LVI status was an independent predictor in patients with UTUC who underwent RNU. The estimate of LVI couldhelp physicians identify high-risk patients and make a better medication regimen of adjuvant chemotherapy.
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Chen Liang,Liu Yuting,Wang Zheyu,Zhang Leiyang,Xu Yi,Li Yinan,Zhang Lan,Wang Guiming,Yang Shuofei,Xue Guanhua 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Neutrophil extracellular traps (NETs) play an important role in abdominal aortic aneurysm (AAA) formation; however, the underlying molecular mechanisms remain unclear. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) may exert therapeutic effects on AAA through their immunomodulatory and regenerative abilities. This study aimed to examine the role and mechanism of MSC-EVs in regulating the development of NET-mediated AAA. Excessive release of NETs was observed in patients with AAA, and the levels of NET components were associated with the clinical outcomes of the patients. Datasets from the Gene Expression Omnibus database were analyzed and revealed that the PI3K/AKT pathway and ferroptosis were strongly associated with NETosis during AAA formation. Further experiments verified that NETs promoted AAA formation by inducing ferroptosis in smooth muscle cells (SMCs) by inhibiting the PI3K/AKT pathway. The PI3K agonist 740 Y-P, the ferroptosis inhibitor ferrostatin-1, and Padi4 deficiency significantly prevented AAA formation. MSC-EVs attenuated AAA formation by reducing NET release in an angiotensin II-induced AAA mouse model. In vitro experiments revealed that MSC-EVs reduced the release of NETs by shifting NETosis to apoptosis. Our study indicates an important role for NET-induced SMC ferroptosis in AAA formation and provides several potential targets for AAA treatment
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Yun Li,Jinping Liu,Rong Luo,Yong You,Guiming Chen 한국생물공학회 2022 Biotechnology and Bioprocess Engineering Vol.27 No.4
Gefitinib has been widely used as a firstgeneration epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for non-small-cell lung cancer (NSCLC) patients with EGFR mutation. In this study, we explored the key molecules responsible for acquired Gefitinib resistance in NSCLC cells. 3-(4,5-Dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay was performed to analyze the Gefitinib resistance and proliferation ability of NSCLC cells. Cell proliferation was also assessed by colony formation assay. Flow cytometry was performed to analyze cell apoptosis. Wound healing assay and transwell invasion assay were performed to the migration and invasion abilities of NSCLC cells, respectively. The target relationship between microRNA-409-3p (miR-409-3p) and circular RNA mannosidase alpha class 1A member 2 (circ- MAN1A2) or twist family bHLH transcription factor 1 (TWIST1) was verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Circ-MAN1A2 level was markedly elevated in Gefitinib-resistant NSCLC cell lines and tissues. Circ-MAN1A2 interference sensitized Gefitinib-resistant NSCLC cells to Gefitinib. Furthermore, circ-MAN1A2 interference suppressed the proliferation, migration and invasion and promoted the apoptosis of Gefitinib-resistant NSCLC cells. Circ-MAN1A2 overexpression negatively regulated miR-409-3p level by directly binding to it. miR-409-3p silencing partly counteracted circ-MAN1A2 silencing-mediated anti-tumor effects in Gefitinib-resistant NSCLC cells. TWIST1 was a target of miR-409-3p, and miR-409-3p overexpression-induced antitumor effects in Gefitinib-resistant NSCLC cells were partly reversed by TWIST1 overexpression. Circ-MAN1A2 silencing aggravated Gefitinib-mediated inhibition of tumor growth in vivo. In conclusion, circ-MAN1A2 facilitated the acquired resistance of Gefitinib and other malignant behaviors of NSCLC cells through mediating miR-409-3p/ TWIST1 axis.
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