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      • Prognostic Significance of Desmoglein 2 and Desmoglein 3 in Esophageal Squamous Cell Carcinoma

        Fang, Wang-Kai,Gu, Wei,Liao, Lian-Di,Chen, Bo,Wu, Zhi-Yong,Wu, Jian-Yi,Shen, Jian,Xu, Li-Yan,Li, En-Min Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.2

        Objective: Desmogleins (DSGs) are major members among the desmosomal cadherins critically involved in cell-cell adhesion and the maintenance of normal tissue architecture in epithelia. Reports exploring links of DSG family member expression with cancers are few and vary. The aim of this study was to investigate the ratio of DSG2 and DSG3 mRNA expression in esophageal squamous cell carcinoma (ESCC) tissue to normal tissue (T/N ratio) and evaluate correlations with clinical parameters. Methods: The mRNA expression of DSGs, as well as ${\gamma}$-catenin and desmoplakin, was detected by real-time quantitative RT-PCR in 85 cases of ESCC tissue specimens. Results: The expression level of DSG3 mRNA was significantly higher than that of DSG2 in ESCC specimens (p=0.000). DSG3 mRNA expression highly correlated with histological grade (p=0.009), whereas that of DSG2 did not significantly relate to any clinicopathologic parameter. Kaplan-Meier survival analysis showed that only DSG3 expression had an impact on the survival curve, with negative DSG3 expression indicating worse survival (p=0.038). Multivariate Cox regression analysis demonstrated DSG3 to be an independent prognostic factor for survival. Furthermore, correlation analysis demonstrated the mRNA level of DSG3 to highly correlate with those of ${\gamma}$-catenin and desmoplakin in ESCC samples (p=0.000), implying that the expression of desmosomal components might be regulated by the same upstream regulatory molecules. Conclusions: Our findings suggest that DSG3 may be involved in the progression of ESCC and serve as a prognostic marker, while expression of DSG2 cannot be used as a predictor of ESCC patient outcome.

      • KCI등재

        Tranexamic Acid Ameliorates Skin Hyperpigmentation by Downregulating Endothelin-1 Expression in Dermal Microvascular Endothelial Cells

        Liu Lin-Xia,Liao Zhi-Kai,Dong Bing-Qi,Jiang Shan,Lei Tie-Chi 대한피부과학회 2024 Annals of Dermatology Vol.36 No.3

        Background: Although reports suggest that tranexamic acid (TXA) has clinical benefits for melasma patients by oral, intralesional and topical treatment, the optimal route of TXA therapy and the underlying mechanism involved remain poorly defined. Objective: To compare the skin lightening effect between oral TXA and topical TXA and to dissect the molecular mechanisms using ultraviolet B (UVB)-induced hyperpigmentation mouse model, ex vivo cultured human skin explant, and cultured melanocytes (MCs) and endothelial cells. Methods: Melanin content and cluster of differentiation 31 (CD31)-positive cell numbers were measured in tail skins from UVB-irradiated mice treated by intragastral or topical TXA using immunofluorescent and Fontana-Masson staining. The conditioned medium (CM) was har vested from human umbilical vein endothelial cells treated with or without 3 mM TXA and was used to treat MCs for 48 hours. mRNA and protein levels of tyrosinase and microphthalmia-associated transcription factor were measured using quantitative real-time reverse transcription polymerase chain reaction and western blotting assays. HMB45- and CD31-positive cell numbers as well as melanin content were also examined in ex vivo cultured human skin explants. Results: The hyperpigmented phenotype were significantly mitigated in UVB-irradiated tail skin plus intragastral TXA-treated mice compared with mice treated with UVB only or with UVB plus topical TXA. CD31-positive cell numbers correlated with the anti-melanogenic activity of TXA ther- apy. The data from cultured cells and skin tissues showed that suppression of endothelin-1 (ET-1) in vascular endothelial cells by TXA reduced melanogenesis and MC proliferation. Conclusion: Oral TXA outperforms topical TXA treatment in skin lightening, which contributes to suppression of ET-1 in dermal microvascular endothelial cells by TXA.

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        Differential Impacts on Bacterial Composition and Abundance in Rhizosphere Compartments between Al-Tolerant and Al-Sensitive Soybean Genotypes in Acidic Soil

        Wen Zhong-Ling,Yang Min-Kai,Fazal Aliya,Liao Yong-Hui,Cheng Lin-Run,Hua Xiao-Mei,Hu Dong-Qing,Shi Ji-Sen,Yang Rong-Wu,Lu Gui-Hua,Qi Jin-Liang,Zhi Hong,Qian Qiu-Ping,Yang Yong-Hua 한국미생물·생명공학회 2020 Journal of microbiology and biotechnology Vol.30 No.8

        In this study, two soybean genotypes, i.e., aluminum-tolerant Baxi 10 (BX10) and aluminumsensitive Bendi 2 (BD2), were used as plant materials and acidic red soil was used as growth medium. The soil layers from the inside to the outside of the root are: rhizospheric soil after washing (WRH), rhizospheric soil after brushing (BRH) and rhizospheric soil at two sides (SRH), respectively. The rhizosphere bacterial communities were analyzed by high-throughput sequencing of V4 hypervariable regions of 16S rRNA gene amplicons via Illumina MiSeq. The results of alpha diversity analysis showed that the BRH and SRH of BX10 were significantly lower in community richness than that of BD2, while the WRH exhibited no significant difference between BX10 and BD2. Among the three sampling compartments of the same soybean genotype, WRH had the lowest community richness and diversity while showing the highest coverage. Beta diversity analysis results displayed no significant difference for any compartment between the two genotypes, or among the three different sampling compartments for any same soybean genotype. However, the relative abundance of major bacterial taxa, specifically nitrogen-fixing and/or aluminum-tolerant bacteria, was significantly different in the compartments of the BRH and/or SRH at phylum and genus levels, indicating genotype-dependent variations in rhizosphere bacterial communities. Strikingly, as compared with BRH and SRH, the WRH within the same genotype (BX10 or BD2) always had an enrichment effect on rhizosphere bacteria associated with nitrogen fixation

      • KCI등재

        Impact of NR1I2, adenosine triphosphateebinding cassette transporters genetic polymorphisms on the pharmacokinetics of ginsenoside compound K in healthy Chinese volunteers

        Luping Zhou,Lulu Chen,Yaqin Wang,Jie Huang,Guo Ping Yang,Zhi-Rong Tang,Yicheng Wang,Jianwei Liao,Gan Zhou,Kai-hua Wei,Zhenyu Li,Dongsheng Ouyang 고려인삼학회 2019 Journal of Ginseng Research Vol.43 No.3

        Background: Ginsenoside compound K (CK) is a promising drug candidate for rheumatoid arthritis. Thisstudy examined the impact of polymorphisms in NR1I2, adenosine triphosphateebinding cassette (ABC)transporter genes on the pharmacokinetics of CK in healthy Chinese individuals. Methods: Forty-two targeted variants in seven genes were genotyped in 54 participants using SequenomMassARRAY system to investigate their association with major pharmacokinetic parameters of CK and itsmetabolite 20(S)-protopanaxadiol (PPD). Subsequently, molecular docking was simulated using theAutoDock Vina program. Results: ABCC4 rs1751034 TT and rs1189437 TT were associated with increased exposure of CK anddecreased exposure of 20(S)-PPD, whereas CFTR rs4148688 heterozygous carriers had the lowestmaximum concentration (Cmax) of CK. The area under the curve from zero to the time of the lastquantifiable concentration (AUClast) of CK was decreased in NR1I2 rs1464602 and rs2472682 homozygouscarriers, while Cmax was significantly reduced only in rs2472682. ABCC4 rs1151471 and CFTR rs2283054influenced the pharmacokinetics of 20(S)-PPD. In addition, several variations in ABCC2, ABCC4, CFTR, andNR1I2 had minor effects on the pharmacokinetics of CK. Quality of the best homology model of multidrugresistance protein 4 (MRP4) was assessed, and the ligand interaction plot showed the mode of interactionof CK with different MRP4 residues. Conlusion: ABCC4 rs1751034 and rs1189437 affected the pharmacokinetics of both CK and 20(S)-PPD. NR1I2 rs1464602 and rs2472682 were only associated with the pharmacokinetics of CK. Thus, thesehereditary variances could partly explain the interindividual differences in the pharmacokinetics of CK.

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