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Shin-Horng Chen,Pei-Chang Wen 기술경영경제학회 2016 ASIAN JOURNAL OF TECHNOLOGY INNOVATION Vol.24 No.-
This paper sets out to examine a key issue: how a latecomer like Taiwan may develop itsindustry in a post catch-up manner. We make intensive inquiries into this issue via casestudies on two sectors in Taiwan, namely the bicycle industry and the electric vehicle (EV)industry. Our conceptual framework gives special account to fuzzy front-end at theindustrial level and how market cultivation and innovative business models come to play animportant role in shaping the innovation path for post catch-up. For leading players inTaiwan’s bicycle industry, a key issue they faced was how to transform themselves andlocal setting in Taiwan to become a leader in high-end bicycles to fend off escalatedinternational competition. In the emerging EV industry, the Taiwanese players try toovercome its structural weaknesses in the mainstream automotive industry to explore thepossibility of levelling the playing field with the forerunners in the advanced countries. Ourcase studies suggest that technological catch-up is not necessarily a prelude to post catch-up,depending on the nature of new innovation trajectory and entry modes of the emergingindustry. Our analyses also lend support to the importance of product servicising as a meansof post catch-up, especially from the perspective of market cultivation.
Monacolin K affects lipid metabolism through SIRT1/AMPK pathway in HepG2 cells
Chia-Hsin Huang,Shin-Mau Shiu,Min-Tze Wu,Wei-Lu Chen,Shyang-Guang Wang,Horng-Mo Lee 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.12
Monacolin K is the secondary metabolite isolatedfrom Monascus spp. It is the natural form of lovastatin,which is clinically used to reduce the synthesis of cholesterolby inhibiting 3-hydroxy-3-methylglutaryl coenzyme Areductase. In the present study, monacolin K increased proteinexpression of SIRT1 and phosphorylation level of AMPactivatedprotein kinase (AMPK) in HepG2 cells. Throughactivation of SIRT1/AMPK pathway, monacolin Kincreased phosphorylation of acetyl CoA carboxylase andcaused nuclear translocation of forkhead box O1. The westernblotting results showed that monacolin K increasedexpression of adipose triglyceride lipase but decreasedabundances of fatty acid synthase (FAS) and sterol regulatory element-binding protein 1 (SREBP1). MonacolinK also decreased the intracellular accumulation of lipids asdemonstrated by Oil Red O staining. In addition, theimmunostaining showed that monacolin K prevented thenuclear translocation of SREBP1, indicating the associationwith down-regulation of FAS. All the demonstrated effectsof monacolin K were counteracted by nicotinamide orcompound C, the inhibitors of SIRT1 orAMPK. In summary,monacolin K reduces the lipid content through SIRT1/AMPK pathway in HepG2 cells, which promotes catabolismand inhibits anabolism of lipid.