11 research outputs found

    Training Effectiveness at PT XYZ Using Kirkpatrick Model and Return on Investment of Training (ROI-Training)

    Full text link
    The goal of the research was to evaluate the effectiveness of Kirkpatrick model and Return on Investment of Training at PT XYZ. Observation was applied to this research. The result has shown several facts such as trainee\u27s feedback score was 4,62 above 4,10 as required by the company in terms of reaction, the average final exam score was 3,66 above 3,00 as required by the company in terms of learning, the trainees\u27 superiors\u27 feedback score was 3,53 above 3,00 as required by the company and Return on Investment of Training (ROI-Training) was 58,88% above 15% as required by the company. With these results, the company can conclude that the program is effective in nurturing its supervisory leaders

    The kinetics of each specific substrate glucuronidation in pooled commercial, adjacent normal and HBV-positive HCC human liver microsomes.

    No full text
    <p>(A) Metabolism kinetics of genistein in commercial, adjacent normaland HBV-positive HCC HLMs (n = 5). (B) Metabolism kinetics of zidovudine in commercial, adjacent normal and HBV-positive HCC HLMs (n = 5). (C) Metabolism kinetics of tamoxifen in commercial, adjacent normal and HBV-positive HCCHLMs (n = 5). (D) Metabolism kinetics of propofol in commercial, adjacent normal and HBV-positive HCC HLMs (n = 5). (E) Metabolism kinetics of SN-38 in commercial, adjacent normal and HBV-positive HCC HLMs (n = 5). Each data point represents the average of three determinations. Representative data from three independent experiments are shown as the mean ± S.D.</p

    The pairwise correlation of UGT1As and UGT2B7 among metabolic activity reduction ratio, protein expression reduction ratio and mRNA expression reduction ratio.

    No full text
    <p><sup>a</sup>Pearson Correlation</p><p><sup>b</sup>Spearman's rho</p><p>Bold represents a significant difference.</p><p>The pairwise correlation of UGT1As and UGT2B7 among metabolic activity reduction ratio, protein expression reduction ratio and mRNA expression reduction ratio.</p

    Clinical characteristics of human liver tissue donors.

    No full text
    <p><sup>a</sup> Histological; HCC, Hepatocellular carcinoma</p><p><sup>b</sup> TNM classification</p><p><sup>c</sup> AFP, Alpha-fetoprotein</p><p><sup>d</sup> Tumor volume was determined by two-dimensional Volume*(cm<sup>3</sup>) using the formula: length*width<sup>2</sup>/2, length and width of tumor were diagnosed by US or CT</p><p>Clinical characteristics of human liver tissue donors.</p

    Image_2_Evodiamine, a Novel NOTCH3 Methylation Stimulator, Significantly Suppresses Lung Carcinogenesis in Vitro and in Vivo.TIF

    No full text
    <p>Lung cancer is a leading cause of cancer-related deaths worldwide. NOTCH3 signaling is mainly expressed in non-small cell lung carcinoma (NSCLC), and has been proposed as a therapeutic target of NSCLC. While, few agents for preventing or treating NSCLC via targeting NOTCH3 signaling are used in modern clinical practice. Evodiamine (EVO), an alkaloid derived from Euodiae Fructus, possesses low toxicity and has long been shown to exert anti-lung cancer activity. However, the underlying anti-lung cancer mechanisms of EVO are not yet fully understood. In this study, we explored the involvement of NOTCH3 signaling in the anti-lung cancer effects of EVO. Urethane-induced lung cancer mouse model and two NSCLC cell models, A549 and H1299, were used to evaluate the in vivo and in vitro anti-lung cancer action of EVO. A DNA methyltransferase inhibitor was employed to investigate the role of NOTCH3 signaling in the anti-lung cancer effects of EVO. Results showed that EVO potently reduced tumor size and tumor numbers in mice, and inhibited NOTCH3 in the tumors. EVO also dramatically reduced cell viability, induced G2/M cell cycle arrest, inhibited cell migration and reduced stemness in cultured NSCLC cells. Mechanistic studies showed that EVO potently inhibited NOTCH3 signaling by activation of DNMTs-induced NOTCH3 methylation. Importantly, inhibition of NOTCH3 methylation in NSCLC cells diminished EVO’s anti-NSCLC effects. Collectively, EVO, a novel NOTCH3 methylation stimulator, exerted potent anti-lung cancer effects partially by inhibiting NOTCH3 signaling. These findings provide new insight into the EVO’s anti-NSCLC action, and suggest a potential role of EVO in lung cancer prevention and treatment.</p

    Table_1_Evodiamine, a Novel NOTCH3 Methylation Stimulator, Significantly Suppresses Lung Carcinogenesis in Vitro and in Vivo.DOC

    No full text
    <p>Lung cancer is a leading cause of cancer-related deaths worldwide. NOTCH3 signaling is mainly expressed in non-small cell lung carcinoma (NSCLC), and has been proposed as a therapeutic target of NSCLC. While, few agents for preventing or treating NSCLC via targeting NOTCH3 signaling are used in modern clinical practice. Evodiamine (EVO), an alkaloid derived from Euodiae Fructus, possesses low toxicity and has long been shown to exert anti-lung cancer activity. However, the underlying anti-lung cancer mechanisms of EVO are not yet fully understood. In this study, we explored the involvement of NOTCH3 signaling in the anti-lung cancer effects of EVO. Urethane-induced lung cancer mouse model and two NSCLC cell models, A549 and H1299, were used to evaluate the in vivo and in vitro anti-lung cancer action of EVO. A DNA methyltransferase inhibitor was employed to investigate the role of NOTCH3 signaling in the anti-lung cancer effects of EVO. Results showed that EVO potently reduced tumor size and tumor numbers in mice, and inhibited NOTCH3 in the tumors. EVO also dramatically reduced cell viability, induced G2/M cell cycle arrest, inhibited cell migration and reduced stemness in cultured NSCLC cells. Mechanistic studies showed that EVO potently inhibited NOTCH3 signaling by activation of DNMTs-induced NOTCH3 methylation. Importantly, inhibition of NOTCH3 methylation in NSCLC cells diminished EVO’s anti-NSCLC effects. Collectively, EVO, a novel NOTCH3 methylation stimulator, exerted potent anti-lung cancer effects partially by inhibiting NOTCH3 signaling. These findings provide new insight into the EVO’s anti-NSCLC action, and suggest a potential role of EVO in lung cancer prevention and treatment.</p

    Image_1_Evodiamine, a Novel NOTCH3 Methylation Stimulator, Significantly Suppresses Lung Carcinogenesis in Vitro and in Vivo.TIF

    No full text
    <p>Lung cancer is a leading cause of cancer-related deaths worldwide. NOTCH3 signaling is mainly expressed in non-small cell lung carcinoma (NSCLC), and has been proposed as a therapeutic target of NSCLC. While, few agents for preventing or treating NSCLC via targeting NOTCH3 signaling are used in modern clinical practice. Evodiamine (EVO), an alkaloid derived from Euodiae Fructus, possesses low toxicity and has long been shown to exert anti-lung cancer activity. However, the underlying anti-lung cancer mechanisms of EVO are not yet fully understood. In this study, we explored the involvement of NOTCH3 signaling in the anti-lung cancer effects of EVO. Urethane-induced lung cancer mouse model and two NSCLC cell models, A549 and H1299, were used to evaluate the in vivo and in vitro anti-lung cancer action of EVO. A DNA methyltransferase inhibitor was employed to investigate the role of NOTCH3 signaling in the anti-lung cancer effects of EVO. Results showed that EVO potently reduced tumor size and tumor numbers in mice, and inhibited NOTCH3 in the tumors. EVO also dramatically reduced cell viability, induced G2/M cell cycle arrest, inhibited cell migration and reduced stemness in cultured NSCLC cells. Mechanistic studies showed that EVO potently inhibited NOTCH3 signaling by activation of DNMTs-induced NOTCH3 methylation. Importantly, inhibition of NOTCH3 methylation in NSCLC cells diminished EVO’s anti-NSCLC effects. Collectively, EVO, a novel NOTCH3 methylation stimulator, exerted potent anti-lung cancer effects partially by inhibiting NOTCH3 signaling. These findings provide new insight into the EVO’s anti-NSCLC action, and suggest a potential role of EVO in lung cancer prevention and treatment.</p

    The pairwise correlation of UGT1Asand UGT2B7 amongmetabolic activities, protein expression ratio and mRNA expression ratio in the adjacent normal tissues or tumor tissues.

    No full text
    <p><sup>a</sup>Pearson Correlation</p><p><sup>b</sup>Spearman's rho</p><p>Bold represents a significant difference.</p><p>The pairwise correlation of UGT1Asand UGT2B7 amongmetabolic activities, protein expression ratio and mRNA expression ratio in the adjacent normal tissues or tumor tissues.</p

    Insight into the Compositional Features of Organic Matter in Xilinguole Lignite through Two Mass Spectrometers

    No full text
    Ethanolysis of lignite is an effective approach for converting organic matter of lignite to liquid coal derivatives. Xilinguole lignite (XL) was reacted with ethanol at 320 °C. Then ethanol and isometric carbon disulfide/acetone mixture were used to extract the reaction mixture in a modified Soxhlet extractor to afford extractable portion 1 (EP1) and extractable portion 2 (EP2), respectively. According to analysis of EP1 with a gas chromatography/mass spectrometer, phenolic compounds made up more than 33% of the compounds detected. This could be ascribed to the ethanolysis of XL; that is, ethanol could selectively break the Calkyl–O bonds in lignite, producing more phenolic compounds. Furthermore, a quadrupole Orbitrap mass spectrometer equipped with an atmospheric pressure chemical ionization source was used for comprehensive analysis of the compositional features of EP1. The analysis indicated that O1–3, N1O0–2, and N2S1O3–6 were predominant class species in EP1. Nitrogen atoms in NO-containing organic compounds may exist in the form of pyridine or amidogen, while oxygen atoms primarily exist in furan, alkoxy, carbonyl, and ester groups. In addition, possible chemical structures of NO-containing organic compounds were speculated

    Metal-Free [3 + 2 + 1]/[2 + 2 + 1] Biscyclization: Stereospecific Construction with Concomitant Functionalization of Indolizin-5(1<i>H</i>)‑one

    No full text
    A metal-free [3 + 2 + 1]/[2 + 2 + 1] biscyclization strategy has been developed for the stereospecific construction with concomitant derivation of biologically significant indolizin-5­(1<i>H</i>)-ones from simple and commercial starting materials. The transformations are notable because they can yield five new σ bonds and six stereocenters including a quaternary carbon center in a single operation
    corecore