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Multiwavelength switchable SOA-fibre ring laser using digital micromirrors
Yu, B.-A.,Shin, W.,Lee, Y.L.,Eom, T.J.,Noh, Y.-C.,Lee, J.,Ko, D.-K. Inst. of Eng. and Technol 2006 Electronics letters Vol.42 No.13
A novel multiwavelength switchable SOA-fibre ring laser incorporating digital micromirrors is demonstrated. By controlling the states of micromirrors, the flexible allocation of the wavelength channels and the multiwavelength switching operations is achieved. Up to 12 wavelength channels with 0.8 nm spacing at room temperature are generated.
Inhibition of Dermatitis Development by Sopungsan in Nc/Nga Mice
Yuba Raj Pokharel,Sung Chul Lim,Sang Chan Kim,Hoo Kyun Choi,Keon Wook Kang 한국독성학회 2008 Toxicological Research Vol.24 No.1
Sopungsan (SS) is a traditional Korean decoction used for the treatment of dermatitis. The aim of this study is to confirm whether or not SS has a preventive effect on the development of atopic dermatitis in dinitrochlorobenzene-applied Nc/Nga mice. SS was administered orally to Nc/Nga mice, which led to the remarkable suppression of the development of dermatitis, as determined by a histological examination and the serum IgE levels. Moreover, SS inhibited the production of thymus- and activation-regulated chemokine (TARC) and its mRNA expression in a keratinocyte cell line, HaCaT, which had been stimulated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). Activation of the nuclear factor-κB (NF-κB) or activator protein-1 (AP-1) is one of key steps in the signaling pathways mediating induction of TARC. In this study, SS selectively suppressed NF-κB activation which may be essential for TARC expression in TNF-α/IFN-γ treated keratinocytes. The inhibitory effect of SS on NF-κB activation and TARC production might be associated with the anti-dermatitic effects of SS.
Screening of potential chemopreventive compounds from Poncirus trifoliata Raf.
Pokharel, Yuba Raj,Jeong, Ji-Eun,Oh, Soo Jin,Kim, Sang Kyum,Woo, Eun-Rhan,Kang, Keon Wook GOVI VERLAG GMBH 2006 PHARMAZIE Vol.61 No.9
<P>Chemopreventive agents induce a battery of genes whose protein products can protect cells from chemical-induced carcinogenesis. In this study, we isolated three different coumarins compounds (1; poncimarin, 2; heraclenol 3'-methyl ester and 3; oxypeucedanin methanolate) from Poncirus trifoliata Raf., and studied whether these compounds increase glutathione S-transferase (GST) expression and activity in the H4IIE cell-line (a rat hepatocyte cell line). CDNB (1-chloro-2,4-dinitrobenzene; GST subtype-nonspecific) and NBD (7-chloro-4-nitrobenzo-2-oxa-1,3-diazole; GSTalpha-type-specific) assays revealed that compound 1 most potently increased GST enzyme activities. Western blot analysis using subtype-specific antibodies confirmed that these three coumarins also selectively increased GSTalpha-protein expression, and that compound 1 most actively induced GSTalpha. In contrast, the expressions of the GSTmu and GSTmu subtypes were not altered by these three coumarins. Reporter gene analysis using an antioxidant response element (ARE) containing construct and subcellular fractionation assays, revealed that GSTalpha-induction by compound 1 might be associated with Nrf2/ARE activation. These results suggest that these three coumarin compounds from Poncirus trifoliata Raf possess phase II enzyme inducible functions, and in particular, that poncimarin has chemopreventive potential.</P>
Inhibition of Dermatitis Development by Sopungsan in Nc/Nga Mice
Pokhare, Yuba Raj,Lim, Sung-Chul,Kim, Sang-Chan,Choi, Hoo-Kyun,Kang, Keon-Wook Korean Society of ToxicologyKorea Environmental Mu 2008 Toxicological Research Vol. No.
Sopungsan (SS) is a traditional Korean decoction used for the treatment of dermatitis. The aim of this study is to confirm whether or not SS has a preventive effect on the development of atopic dermatitis in dinitrochlorobenzene-applied Nc/Nga mice. SS was administered orally to Nc/Nga mice, which led to the remarkable suppression of the development of dermatitis, as determined by a histological examination and the serum IgE levels. Moreover, SS inhibited the production of thymus- and activation-regulated chemokine (TARC) and its mRNA expression in a keratinocyte cell line, HaCaT, which had been stimulated with tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interferon-${\gamma}$ (IFN-${\gamma}$). Activation of the nuclear factor-${\kappa}B$ (NF-${\kappa}B$) or activator protein-1 (AP-1) is one of key steps in the signaling pathways mediating induction of TARC. In this study, SS selectively suppressed NF-${\kappa}B$ activation which may be essential for TARC expression in $TNF-{\alpha}/IFN-{\gamma}$ treated keratinocytes. The inhibitory effect of SS on NF-${\kappa}B$ activation and TARC production might be associated with the anti-dermatitic effects of SS.
Dual Anti-oxidative Effects of Fraxetin Isolated from <i>Fraxinus rhinchophylla</i>
Thuong, Phuong Thien,Pokharel, Yuba Raj,Lee, Moo Yeol,Kim, Sang Kyum,Bae, KiHwan,Su, Nguyen Duy,Oh, Won Keun,Kang, Keon Wook Pharmaceutical Society of Japan 2009 Biological & pharmaceutical bulletin Vol.32 No.9
<P>Atherosclerosis is main cause of arteriosclerosis. The pivotal role of low-density lipoprotein (LDL) oxidation in atherogenesis suggests antioxidants may help prevent cardiovascular disease. <I>Fraxinus rhynchophylla</I> D<SMALL>ENCE</SMALL> (Oleaceae) is a traditional medicinal plant from East Asia. During the course of characterizing potential drug candidates from natural products, we isolated two major coumarins, esculetin and fraxetin and found that fraxetin has dual-antioxidative functions. Low concentrations (1—5 μ<SMALL>M</SMALL>) of fraxetin potently inhibited LDL oxidation induced by metal and free radicals. Moreover, treatment of vascular smooth muscle cells (VSMCs) with higher concentrations (above 30 μ<SMALL>M</SMALL>) of fraxetin significantly increased the protein level of heme oxygenase-1 (HO-1), a key enzyme that inhibits vascular proliferation and atherosclerosis. Subcellular fractionation and reporter gene analysis using an antioxidant response element (ARE) construct revealed that fraxetin increased the level of nuclear factor (NF)-E2-related factor 2 (Nrf2) and reporter activity, and these were associated with the induction of antioxidant enzymes, such as HO-1 and glutathione <I>S</I>-transferase-α. In conclusion, fraxetin has direct protective properties against LDL oxidation at lower concentrations, and higher concentrations of fraxetin induce antioxidant enzymes <I>via</I> Nrf2/ARE activation. These effects suggest potential anti-atherosclerosis effects of <I>Fraxinus rhynchophylla</I> D.</P>
Novel role of Pin1 induction in type II collagen-mediated rheumatoid arthritis.
Jeong, Hye Gwang,Pokharel, Yuba Raj,Lim, Sung Chul,Hwang, Yong Pil,Han, Eun Hee,Yoon, Jung-Hoon,Ahn, Sang-Gun,Lee, Kwang Yeol,Kang, Keon Wook Williams Wilkins 2009 JOURNAL OF IMMUNOLOGY Vol.183 No.10
<P>Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation in joints and subsequent destruction of cartilage and bone. Inflammatory mediators such as PGs and proinflammatory cytokines contribute to RA progress. Pin1, a peptidyl prolyl isomerase, plays important pathophysiological roles in several diseases, including cancer and neurodegeneration. We found that both Pin1 and cyclooxygenase-2 (COX-2) were highly expressed in ankle tissues of type II collagen-induced RA mice. HTB-94 cells overexpressing Pin1 and primary cultured human chondrocytes showed increased basal expression of proinflammatory proteins (COX-2, inducible NO synthase, TNF-alpha, and IL-1beta). Site-directed mutagenesis revealed that Pin1-mediated transcriptional activation of COX-2 was coordinately regulated by NF-kappaB, CREB, and C/EBP. Gel shift, reporter gene, and Western blot analyses confirmed that NF-kappaB, CREB, and C/EBP were consistently activated in chondrocytes overexpressing Pin1. Treatment of RA mice with juglone, a chemical inhibitor of Pin1, significantly reduced RA progress and COX-2 expression in the ankle tissues. Moreover, juglone dose dependently decreased the basal COX-2 expression in primary cultured chondrocytes from RA patients. These results demonstrate that Pin1 induction during RA progress stimulates proinflammatory protein expression by activating NF-kappaB, CREB, and C/EBP, and suggest that Pin1 is a potential therapeutic target of RA.</P>