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Controllable tuning of the electronic transport in pre-designed graphene nanoribbon
Hui Zeng,Jun Zhao,Jianwei Wei,Dahai Xu,J.-P. Leburton 한국물리학회 2012 Current Applied Physics Vol.12 No.6
We make use of ab initio density functional theory calculation to explore the electronic and transport properties of zigzag-edged graphene nanoribbon (ZGNR) with peculiar designed electronic transport channels by tailoring the atomic configuration of the nanostructure. Tailoring the atomic structure has significant influences on the electronic transport of the defective nanostructure, and eventually the metal-semiconducting transition are identified with the increasing number of missing atoms. Our results demonstrate that pre-designed graphene nanoribbon by selective tailoring with high precision is expected to be served as the basic component for nanoelectronic device.
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Chu Zhe,Liu Zuolong,Li Wei,Xu Dahai,Pang Li 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.2
Background Carbon monoxide (CO) poisoning is a leading cause of morbidity and mortality worldwide. The delayed encephalopathy occurs a period after poisoning in patients without effective treatment. Simvastatin (Sim), a lipid-lowering drug, was reported to exert endothelial protective effects and inhibit inflammatory response. This research focused on the effects of Sim on delayed encephalopathy caused by CO poisoning. Objective The acute CO poisoning model was established by exposing rats to 2500 ppm CO gas for 40 min, then 3000 ppm for 30 min or until they lost consciousness. Rats in the treatment group were given Sim (20 mg/kg/day, ig.). The behavioral tests included the Morris water maze test and shuttle box. The pathological changes were evaluated by H and E staining. The inflammatory mediators were analyzed by ELISA. The expression levels of eNOS, iNOS and the NF-κB-related proteins were analyzed by Western blot. Results The results showed that Sim could alleviate CO-induced behavioral disorders and the hippocampal nerve cells apoptosis. Sim administration reversed the effects of CO on oxidative stress-related molecules. Sim could also inhibit the production of the inflammatory mediators induced by CO. The level of eNOS was decreased after CO exposure, while iNOS was increased. Sim could significantly inhibit the effects of CO. Furthermore, Sim inhibited the phosphorylation of IκBα (an NF-κB inhibitory protein), i.e., the activation of NF-κB, which indicated that Simvastatin reduced the inflammatory response induced by CO poisoning partially through inhibiting the activation of NF-κB signaling pathway. Conclusion To sum up, our research indicated that Sim could attenuate the delayed encephalopathy induced by CO poisoning via regulating oxidative stress, inflammation and NF-κB pathway. Background Carbon monoxide (CO) poisoning is a leading cause of morbidity and mortality worldwide. The delayed encephalopathy occurs a period after poisoning in patients without effective treatment. Simvastatin (Sim), a lipid-lowering drug, was reported to exert endothelial protective effects and inhibit inflammatory response. This research focused on the effects of Sim on delayed encephalopathy caused by CO poisoning. Objective The acute CO poisoning model was established by exposing rats to 2500 ppm CO gas for 40 min, then 3000 ppm for 30 min or until they lost consciousness. Rats in the treatment group were given Sim (20 mg/kg/day, ig.). The behavioral tests included the Morris water maze test and shuttle box. The pathological changes were evaluated by H and E staining. The inflammatory mediators were analyzed by ELISA. The expression levels of eNOS, iNOS and the NF-κB-related proteins were analyzed by Western blot. Results The results showed that Sim could alleviate CO-induced behavioral disorders and the hippocampal nerve cells apoptosis. Sim administration reversed the effects of CO on oxidative stress-related molecules. Sim could also inhibit the production of the inflammatory mediators induced by CO. The level of eNOS was decreased after CO exposure, while iNOS was increased. Sim could significantly inhibit the effects of CO. Furthermore, Sim inhibited the phosphorylation of IκBα (an NF-κB inhibitory protein), i.e., the activation of NF-κB, which indicated that Simvastatin reduced the inflammatory response induced by CO poisoning partially through inhibiting the activation of NF-κB signaling pathway. Conclusion To sum up, our research indicated that Sim could attenuate the delayed encephalopathy induced by CO poisoning via regulating oxidative stress, inflammation and NF-κB pathway.
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