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Now showing items 1 - 16 of 357

  • Two Novel Guaiane Sesquiterpenes from the Whole Plant of Youngia japonica

    Lee, Ji   Cha, Mi-Ran   Kim, Mi   Lee, Kwangho   Choi, Sang-Un   Ryu, Shi  

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  • Robust Pedestrian Detection by Combining Visible and Thermal Infrared Cameras

    Lee, Ji   Choi, Jong-Suk   Jeon, Eun   Kim, Yeong   Le, Toan   Shin, Kwang   Lee, Hyeon   Park, Kang  

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  • Osteogenic effects of Phlomis umbrosa via up‑regulation of Runx2 in osteoporosis

    Lee, Ji   Lee, Haesu   Kim, Mi   Yang, Woong  

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  • The Pharmacokinetics of Intradialytic Administration of Eculizumab in an Infant

    Lee, Ji   Imani, Peace   Geer, Jessica   Braun, Michael   Srivaths, Poyyapakkam   Orjuela, Alvaro  

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  • Collision Avoidance from Multiple Passive Agents with Partially Predictable Behavior

    Zuhaib, Khalil   Khan, Abdul   Iqbal, Junaid   Ali, Mian   Usman, Muhammad   Ali, Ahmad   Yaqub, Sheraz   Lee, Ji   Han, Changsoo  

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  • A Novel Gaze Tracking Method Based on the Generation of Virtual Calibration Points

    Lee, Ji   Heo, Hwan   Park, Kang  

    Most conventional gaze-tracking systems require that users look at many points during the initial calibration stage, which is inconvenient for them. To avoid this requirement, we propose a new gaze-tracking method with four important characteristics. First, our gaze-tracking system uses a large screen located at a distance from the user, who wears a lightweight device. Second, our system requires that users look at only four calibration points during the initial calibration stage, during which four pupil centers are noted. Third, five additional points (virtual pupil centers) are generated with a multilayer perceptron using the four actual points (detected pupil centers) as inputs. Fourth, when a user gazes at a large screen, the shape defined by the positions of the four pupil centers is a distorted quadrangle because of the nonlinear movement of the human eyeball. The gaze-detection accuracy is reduced if we map the pupil movement area onto the screen area using a single transform function. We overcame this problem by calculating the gaze position based on multi-geometric transforms using the five virtual points and the four actual points. Experiment results show that the accuracy of the proposed method is better than that of other methods.
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  • The NO TRAIL to YES TRAIL in cancer therapy (Review)

    Lee, Ji   Huerta-Yepez, Sara   Vega, Mario   Baritaki, Stavroula   Spandidos, Demetrios   Bonavida, Benjamin  

    Treatment of cancer patients with conventional therapies (chemotherapy, hormonal therapy, immunotherapy and radiation) respond initially well and experience prolonged tumor-free survival. However, in many patients tumor recurrences and relapses occur and such tumors exhibit the resistant phenotype i.e. cross-resistance to various cytotoxic and apoptotic agents. Therefore, new therapeutic strategies are currently being explored and are based on a better understanding of the underlying biochemical and molecular mechanisms of tumor cell resistance. Hence, novel sensitizing agents that can modify the tumor dysregulated apoptotic gene products can reverse resistance when used in combination with subtoxic doses of cytotoxic reagents. Targeted antitumor therapies are the current choice in the treatment of resistant tumors. One such targeted therapy is the application of TRAIL or TRAIL agonist monoclonal antibodies (mAbs) (anti-DR4 and anti-DR5) because, unlike Fas ligand and TNF-alpha, they are not cytotoxic to normal tissues. TRAIL as monotherapy will only be effective against TRAIL sensitive tumors, however, most tumors are resistant to TRAIL and their sensitization can restore their sensitivity to TRAIL apoptosis. We present, herein, one potential novel sensitizing agent, namely, nitric oxide (NO) that has been shown to sensitize TRAIL-resistant tumor cells to TRAIL apoptosis via its inhibitory effect on the transcription factors NF-kappa B and Yin Yang 1 (YY1), concomitantly with upregulation of DR5. We propose the therapeutic application of NO donors as sensitizing agents used in combination with TRAIL/DR4 or DR5 mAbs in the treatment of TRAIL-resistant tumors.
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  • Treatment of pediatric hyperkalemia with sodium polystyrene sulfonate

    Lee, Ji   Moffett, Brady S.  

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  • Efficient Conversion of Acetate to 3-Hydroxypropionic Acid by Engineered Escherichia coli

    Lee, Ji   Cha, Sanghak   Kang, Chae   Lee, Geon   Lim, Hyun   Jung, Gyoo  

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  • N-Terminal Domain Mediated Regulation of RORα1 Inhibits Invasive Growth in Prostate Cancer

    Park, Su   Park, Il-Geun   Kim, Hyunkyung   Lee, Ji  

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  • The Analgesic Effect of Venlafaxine and Its Mechanism on Oxaliplatin-Induced Neuropathic Pain in Mice

    Li, Daxian   Lee, Ji   Choi, Chang   Kim, Jaihwan   Kim, Sun   Kim, Woojin  

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  • Inhibitory effects of PGE2on K+currents and Ca2+oscillations in rat pancreatic acinar cells

    Lee, Ji   Kim, Jun   Choi, So-Jung   Han, Tae-Hee   Uhm, Dae-Yong   Kim, Sung  

    Prostaglandin E2 (PGE2) inhibits pancreatic enzyme secretion and shows a protective action against pancreatitis. In this study, we tested the effects of PGE2 on the slowly activating voltage-dependent K+ channel current (IKs) and cholecystokinin (CCK)-induced oscillations of cytosolic (Ca2+) ((Ca2+)i) in rat pancreatic acini (RPA). IKs in RPA is reportedly augmented by both Ca2+- and cAMP-mediated secretagogues. PGE2 (10-7 M) decreased the amplitude of IKs, an effect that was more prominent following prior stimulation with secretin. The application of the membrane-permeable cAMP analogue 8-Br-cAMP prevented the effect of PGE2 on IKs. The Ca2+-mediated augmentation of IKs by ACh was unaffected by pretreatment with PGE2. Using fura-2 fluorescence ratiometry to assess (Ca2+)i, CCK (ltoreq10-10 M)-induced Ca2+ oscillations were observed in RPAs. The amplitude of the Ca2+ oscillations was decreased by PGE2, irrespective of the presence of 8-Br-cAMP. RT-PCR analysis showed that RPAs express predominantly the EP3 subtype of the PGE2 receptor and its splice variants. Enzyme-immunoassay showed that the secretin-induced production of cAMP in RPAs was inhibited by treatment with PGE2. In summary, PGE2 acts on the EP3 receptors to antagonize the cAMP-generating effect of secretin, resulting in the decrease of IKs. In addition, PGE2 suppresses CCK-induced Ca2+ oscillations in a cAMP-independent manner. These effects of PGE2 may explain the inhibitory action mechanism of PGE2 in the exocrine pancreas.
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  • Tunable Electronic Properties of Nitrogen and Sulfur Doped Graphene: Density Functional Theory Approach

    Lee, Ji   Kwon, Sung   Kwon, Soonchul   Cho, Min   Kim, Kwang   Han, Tae   Lee, Seung  

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  • Regulatory Circuit of Human MicroRNA Biogenesis

    Lee, Ji   Li, Zhihua   Brower-Sinning, Rachel   John, Bino  

    miRNAs (microRNAs) are a class of endogenous small RNAs that are thought to negatively regulate protein production. Aberrant expression of many miRNAs is linked to cancer and other diseases. Little is known about the factors that regulate the expression of miRNAs. We have identified numerous regulatory elements upstream of miRNA genes that are likely to be essential to the transcriptional and posttranscriptional regulation of miRNAs. Newly identified regulatory motifs occur frequently and in multiple copies upstream of miRNAs. The motifs are highly enriched in G and C nucleotides, in comparison with the nucleotide composition of miRNA upstream sequences. Although the motifs were predicted using sequences that are upstream of miRNAs, we find that 99% of the top-predicted motifs preferentially occur within the first 500 nucleotides upstream of the transcription start sites of protein-coding genes; the observed preference in location underscores the validity and importance of the motifs identified in this study. Our study also raises the possibility that a considerable number of well-characterized, disease-associated transcription factors (TFs) of protein-coding genes contribute to the abnormal miRNA expression in diseases such as cancer. Further analysis of predicted miRNA-protein interactions lead us to hypothesize that TFs that include c-Myb, NF-Y, Sp-1, MTF-1, and AP-2 alpha are master-regulators of miRNA expression. Our predictions are a solid starting point for the systematic elucidation of the causative basis for aberrant expression patterns of disease-related (e.g., cancer) miRNAs. Thus, we point out that focused studies of the TFs that regulate miRNAs will be paramount in developing cures for miRNA-related diseases. The identification of the miRNA regulatory motifs was facilitated by a new computational method, K-Factor. K-Factor predicts regulatory motifs in a set of functionally related sequences, without relying on evolutionary conservation.
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  • Cyclohexene Oxidation with H2O2 over Metal-Organic Framework MIL-125(Ti): The Effect of Protons on Reactivity

    Maksimchuk, Nataliya   Lee, Ji   Ayupov, Artem   Chang, Jong-San   Kholdeeva, Oxana  

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  • Simvastatin enhances the radiosensitivity of p53‑deficient cells via inhibition of mouse double minute 2 homolog

    Lee, Ji   Kim, Mi-Sook   Ju, Jae   Lee, Mi   Chung, Namhyun   Jeong, Youn  

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