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      • KCI등재

        Ketohexokinase-dependent metabolism of cerebral endogenous fructose in microglia drives diabetes-associated cognitive dysfunction

        Li Yansong,Jiang Tao,Du Mengyu,He Shuxuan,Ning Huang,Cheng Bo,Yan Chaoying,Tang Wenxin,Gao Wei,Guo Hongyan,Li Qiao,Wang Qiang 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

        Dementia, as an advanced diabetes-associated cognitive dysfunction (DACD), has become the second leading cause of death among diabetes patients. Given that little guidance is currently available to address the DACD process, it is imperative to understand the underlying mechanisms and screen out specific therapeutic targets. The excessive endogenous fructose produced under high glucose conditions can lead to metabolic syndrome and peripheral organ damage. Although generated by the brain, the role of endogenous fructose in the exacerbation of cognitive dysfunction is still unclear. Here, we performed a comprehensive study on leptin receptor-deficient T2DM mice and their littermate m/m mice and revealed that 24-week-old db/db mice had cognitive dysfunction and excessive endogenous fructose metabolism in the hippocampus by multiomics analysis and further experimental validation. We found that the rate-limiting enzyme of fructose metabolism, ketohexokinase, is primarily localized in microglia. It is upregulated in the hippocampus of db/db mice, which enhances mitochondrial damage and reactive oxygen species production by promoting nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) expression and mitochondrial translocation. Inhibiting fructose metabolism via ketohexokinase depletion reduces microglial activation, leading to the restoration of mitochondrial homeostasis, recovery of structural synaptic plasticity, improvement of CA1 pyramidal neuron electrophysiology and alleviation of cognitive dysfunction. Our findings demonstrated that enhanced endogenous fructose metabolism in microglia plays a dominant role in diabetes-associated cognitive dysfunction and could become a potential target for DACD.

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        Nanosized Carbon Black Combined with Ni<sub>2</sub>O<sub>3</sub> as “Universal” Catalysts for Synergistically Catalyzing Carbonization of Polyolefin Wastes to Synthesize Carbon Nanotubes and Application for Supercapacitors

        Wen, Xin,Chen, Xuecheng,Tian, Nana,Gong, Jiang,Liu, Jie,Rü,mmeli, Mark H.,Chu, Paul K.,Mijiwska, Ewa,Tang, Tao American Chemical Society 2014 Environmental science & technology Vol.48 No.7

        <P>The catalytic carbonization of polyolefin materials to synthesize carbon nanotubes (CNTs) is a promising strategy for the processing and recycling of plastic wastes, but this approach is generally limited due to the selectivity of catalysts and the difficulties in separating the polyolefin mixture. In this study, the influence of nanosized carbon black (CB) and Ni<SUB>2</SUB>O<SUB>3</SUB> as a novel combined catalyst system on catalyzing carbonization of polypropylene (PP), polyethylene (PE), polystyrene (PS) and their blends was investigated. We showed that this combination was efficient to promote the carbonization of these polymers to produce CNTs with high yields and of good quality. Catalytic pyrolysis and model carbonization experiments indicated that the carbonization mechanism was attributed to the synergistic effect of the combined catalysts rendered by CB and Ni<SUB>2</SUB>O<SUB>3</SUB>: CB catalyzed the degradation of PP, PE, and PS to selectively produce more aromatic compounds, which were subsequently dehydrogenated and reassembled into CNTs via the catalytic action of CB together with Ni particles. Moreover, the performance of the synthesized CNTs as the electrode of supercapacitor was investigated. The supercapacitor displayed a high specific capacitance as compared to supercapacitors using commercial CNTs and CB. This difference was attributed to the relatively larger specific surface areas of our synthetic CNTs and their more oxygen-containing groups.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/esthag/2014/esthag.2014.48.issue-7/es404646e/production/images/medium/es-2013-04646e_0008.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/es404646e'>ACS Electronic Supporting Info</A></P>

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