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      • KCI등재

        Role of microRNA-520h in 20(R)-ginsenoside-Rg3-mediated angiosuppression

        Man-Hong Keung,Lai-Sheung Chan,Hoi-Hin Kwok,Ricky Ngok-Shun Wong,Patrick Ying-Kit Yue 고려인삼학회 2016 Journal of Ginseng Research Vol.40 No.2

        Background: Ginsenoside-Rg3, the pharmacologically active component of red ginseng, has been found to inhibit tumor growth, invasion, metastasis, and angiogenesis in various cancer models. Previously, we found that 20(R)-ginsenoside-Rg3 (Rg3) could inhibit angiogenesis. Since microRNAs (miRNAs) have been shown to affect many biological processes, they might play an important role in ginsenosidemediated angiomodulation. Methods: In this study, we examined the underlying mechanisms of Rg3-induced angiosuppression through modulating the miRNA expression. In the miRNA-expression profiling analysis, six miRNAs and three miRNAs were found to be up- or down-regulated in vascular-endothelial-growth-factor-induced human-umbilical-vein endothelial cells (HUVECs) after Rg3 treatment, respectively. Results: A computational prediction suggested that mature hsa-miR-520h (miR-520h) targets ephrin receptor (Eph) B2 and EphB4, and hence, affecting angiogenesis. The up-regulation of miR-520h after Rg3 treatment was validated by quantitative real-time polymerase chain reaction, while the protein expressions of EphB2 and EphB4 were found to decrease, respectively. The mimics and inhibitors of miR- 520h were transfected into HUVECs and injected into zebra-fish embryos. The results showed that overexpression of miR-520h could significantly suppress the EphB2 and EphB4 protein expression, proliferation, and tubulogenesis of HUVECs, and the subintestinal-vessel formation of the zebra fish. Conclusion: These results might provide further information on the mechanism of Rg3-induced angiosuppression and the involvement of miRNAs in angiogenesis.

      • SCIESCOPUSKCI등재

        Role of microRNA-520h in 20(R)-ginsenoside-Rg3-mediated angiosuppression

        Keung, Man-Hong,Chan, Lai-Sheung,Kwok, Hoi-Hin,Wong, Ricky Ngok-Shun,Yue, Patrick Ying-Kit The Korean Society of Ginseng 2016 Journal of Ginseng Research Vol.40 No.2

        Background: Ginsenoside-Rg3, the pharmacologically active component of red ginseng, has been found to inhibit tumor growth, invasion, metastasis, and angiogenesis in various cancer models. Previously, we found that 20(R)-ginsenoside-Rg3 (Rg3) could inhibit angiogenesis. Since microRNAs (miRNAs) have been shown to affect many biological processes, they might play an important role in ginsenoside-mediated angiomodulation. Methods: In this study, we examined the underlying mechanisms of Rg3-induced angiosuppression through modulating the miRNA expression. In the miRNA-expression profiling analysis, six miRNAs and three miRNAs were found to be up- or down-regulated in vascular-endothelial-growth-factor-induced human-umbilical-vein endothelial cells (HUVECs) after Rg3 treatment, respectively. Results: A computational prediction suggested that mature hsa-miR-520h (miR-520h) targets ephrin receptor (Eph) B2 and EphB4, and hence, affecting angiogenesis. The up-regulation of miR-520h after Rg3 treatment was validated by quantitative real-time polymerase chain reaction, while the protein expressions of EphB2 and EphB4 were found to decrease, respectively. The mimics and inhibitors of miR- 520h were transfected into HUVECs and injected into zebra-fish embryos. The results showed that overexpression of miR-520h could significantly suppress the EphB2 and EphB4 protein expression, proliferation, and tubulogenesis of HUVECs, and the subintestinal-vessel formation of the zebra fish. Conclusion: These results might provide further information on the mechanism of Rg3-induced angiosuppression and the involvement of miRNAs in angiogenesis.

      • KCI등재

        Impact of CO2 Laser Pretreatment on the Thermal Endurance of Bragg Gratings

        Dinusha Serandi Gunawardena,Man-Hong Lai,Kok-Sing Lim,Harith Ahmad 한국광학회 2016 Current Optics and Photonics Vol.20 No.5

        The thermal endurance of fiber Bragg gratings (FBGs), written with the aid of 193-nm ArF excimerlaser irradiation on H2-loaded Ge/B codoped silica fiber, and pretreated with a CO2 laser and a subsequentslow cooling process, is investigated. These treated gratings show relatively less degradation of gratingstrength during the thermal annealing procedure. The thermal decay characteristics of treated and untreatedfiber, recorded over a time period of 9 hours, have been compared. The effect on the Bragg transmissiondepth (BTD) and the center-wavelength shift, as well as the growth of refractive-index change during thegrating inscription process for both treated and untreated fiber, are analyzed.

      • HBV : PO-01 ; Declination of hepatitis B surface antigen (HBsAg) levels with the treatment of entecavir (ETV) in HBeAg-positive nucleoside naive chronic hepatitis B patients-results from phase III study ETV-022

        ( Robert G Gish ),( Ting Tsung Chang ),( Ching Lung Lai ),( Robert A De Man ),( Adrian Gadano ),( Song Yu ),( Cyril Llamoso ),( Hong Tang ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-

        Background: Entecavir (ETV) 0.5 mg demonstrated superior virologic, histologic, and biochemical benefit compared to lamivudine in phase III study ETV-022. Through 96 weeks of treatment and 24 weeks post-treatment follow-up, 5% of the patients achieved HBsAg loss. We present the changes in quantitative HBsAg levels in patients with HBeAg-positive nucleoside naive chronic hepatitis B patients treated with ETV in study ETV-022. Methods: The nucleoside-naive HBeAg-positive patients received ETV 0.5mg daily in study ETV-022. HBsAg levels were assessed qualitatively and quantitatively every 12 weeks. The quantitative HBsAg levels were measured with the Abbott Architect Assay. Mean HBsAg levels were calculated at baseline, week 12, 24, 36 and 48 for the overall cohort and cohorts with HBeAg loss or HBsAg loss. Results: A total of 95 ETV-treated patients from study ETV-022 had available blood samples and were analyzed for quantitative HBsAg levels. Baseline characteristics of patients include mean age 38 years old, mean HBV DNA 9.64 log10 copies/mL and ALT 156.65 U/L. The quantitative HBsAg levels over time in different patient groups are listed below: Conclusion: Quantitative HBsAg levels decreased overtime during the first 48 weeks of ETV therapy in HBeAg-positive nucleoside naive patients. A greater declination in quantitative HBsAg value was observed among subjects who had HBeAg loss or HBsAg loss.

      • HBV : PO-01 ; Declination of hepatitis B surface antigen (HBsAg) levels with the treatment of entecavir (ETV) in HBeAg-positive nucleoside naive chronic hepatitis B patients-results from phase III study ETV-022

        ( Robert G Gish ),( Ting Tsung Chang ),( Ching Lung Lai ),( Robert A De Man ),( Adrian Gadano ),( Song Yu ),( Cyril Llamoso ),( Hong Tang ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.1

        Background: Entecavir (ETV) 0.5 mg demonstrated superior virologic, histologic, and biochemical benefit compared to lamivudine in phase III study ETV-022. Through 96 weeks of treatment and 24 weeks post-treatment follow-up, 5% of the patients achieved HBsAg loss. We present the changes in quantitative HBsAg levels in patients with HBeAg-positive nucleoside naive chronic hepatitis B patients treated with ETV in study ETV-022. Methods: The nucleoside-naive HBeAg-positive patients received ETV 0.5mg daily in study ETV-022. HBsAg levels were assessed qualitatively and quantitatively every 12 weeks. The quantitative HBsAg levels were measured with the Abbott Architect Assay. Mean HBsAg levels were calculated at baseline, week 12, 24, 36 and 48 for the overall cohort and cohorts with HBeAg loss or HBsAg loss. Results: A total of 95 ETV-treated patients from study ETV-022 had available blood samples and were analyzed for quantitative HBsAg levels. Baseline characteristics of patients include mean age 38 years old, mean HBV DNA 9.64 log10 copies/mL and ALT 156.65 U/L. The quantitative HBsAg levels over time in different patient groups are listed below Conclusion: Quantitative HBsAg levels decreased overtime during the first 48 weeks of ETV therapy in HBeAg-positive nucleoside naive patients. A greater declination in quantitative HBsAg value was observed among subjects who had HBeAg loss or HBsAg loss.

      • KCI등재

        Antioxidative and Hepatoprotective Effects of Magnolol on Acetaminophen-induced Liver Damage in Rats

        Yung-Hsiang Chen,Feng-Yen Lin,Po-Len Liu,Yi-Tsau Huang,Jen-Hwey Chiu,Yi-Chun Chang,Kee-Ming Man,Chuang-Ye Hong,Yen-Yi Ho,Ming-Tsung Lai 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.2

        Acute liver failure (ALF), an often fatal condition characterized by massive hepatocyte necrosis, is frequently caused by drug poisoning, particularly with acetaminophen (N-acetyl-p-aminophenol/APAP). Hepatocyte necrosis is consecutive to glutathione (GSH) depletion and mitochondrial damage caused by reactive oxygen species (ROS) overproduction. Magnolol, one major phenolic constituent of Magnolia officinalis, have been known to exhibit potent antioxidative activity. In this study, the anti-hepatotoxic activity of magnolol on APAP-induced toxicity in the Sprague-Dawley rat liver was examined. After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 μg/kg). Histological changes around the hepatic central vein, lipid peroxidation (thiobarbituric acid-reactive substance/TBARS), and GSH depletion in liver tissue induced by APAP were also recovered by magnolol treatment. The data show that oxidative stress followed by lipid peroxidation may play a very important role in the pathogenesis of APAP-induced hepatic injury; treatment with lipid-soluble antioxidant, magnolol, exerts anti-hepatotoxic activity. Our study points out the potential interest of magnolol in the treatment of toxic ALF.

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