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| 1 | Silver Nanowire Electrodes: Conductivity Improvement Without Post-treatment and Application in Capacitive Pressure Sensors显示文摘Transparent electrode based on silver nanowires(Ag NWs) emerges as an outstanding alternative of indium tin oxide film especially for flexible electronics. However, the conductivity of Ag NWs transparent electrode is still dramatically limited by the contact resistance between nanowires at high transmittance. Polyvinylpyrrolidone(PVP) layer adsorbed on the nanowire surface acts as an electrically insulating barrier at wire–wire junctions, and some devastating post-treatment methods are proposed to reduce or eliminate PVP layer, which usually limit the application of the substrates susceptible to heat or pressure and burden the fabrication with high-cost, time-consuming, or inefficient processes. In this work, a simple and rapid pre-treatment washing method was proposed to reduce the thickness of PVP layer from 13.19 to0.96 nm and improve the contact between wires. Ag NW electrodes with sheet resistances of 15.6 and 204 X sq-1have been achieved at transmittances of 90 and 97.5 %, respectively. This method avoided any post-treatments and popularized the application of high-performance Ag NW transparent electrode on more substrates. The improved Ag NWs were successfully employed in a capacitive pressure sensor with high transparency, sensitivity, and reproducibility. | Jun Wang Jinting Jiu Teppei Araki Masaya Nogi Tohru Sugahara Shijo Nagao Hirotaka Koga Peng He Katsuaki Suganuma | 2015 | Nano-Micro Letters2015，7，1： | 9 |
| 2 | Activin A prevents neuron-like PC12 cell apoptosis after oxygen-glucose deprivation显示文摘In this study, PC12 cells were induced to differentiate into neuron-like cells using nerve growth facto and were subjected to oxygen-glucose deprivation. Cells were treated with 0, 10, 20, 30, 50, 100 ng/mL exogenous Activin A. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay and Hoechst 33324 staining showed that the survival percentage of PC12 cells significantly decreased and the rate of apoptosis significantly increased after oxygen-glucose deprivation. Exogenous Activin A significantly increased the survival percentage of PC12 cells in a dose-dependent manner. Reverse transcription-PCR results revealed a significant increase in Activin receptor IIA, Smad3 and Smad4 mRNA levels, which are key sites in the Activin A/Smads signaling pathway, in neuron-like cells subjected to oxygen-glucose deprivation, while mRNA expression of the apoptosis-regulation gene caspase-3 decreased. Our experimental findings indicate that exogenous Activin A plays an anti-apoptotic role and protects neurons by means of activating the Activin A/Smads signaling pathway. | Guihua Xu Jinting He Hongliang Guo Chunli Mei Jiaoqi Wang Zhongshu Li Han Chen Jing Mang Hong Yang Zhongxin Xu | 2013 | Neural Regeneration Research2013，8，11： | 5 |
| 3 | Changes of hypoxia-inducible factor-1 signaling and the effect of cilostazol in chronic cerebral ischemia显示文摘Hypoxia-inducible factor-1 and its specific target gene heme oxygenase-1, are involved in acute cerebral ischemia. However, very few studies have examined in detail the changes in the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway in chronic cerebral ischemia. In this study, a rat model of chronic cerebral ischemia was established by permanent bilateral common carotid artery occlusion, and these rats were treated with intragastric cilostazol (30 mg/kg) for 9 weeks. Morris water maze results showed that cognitive impairment gradually worsened as the cerebral ischemia proceeded. Immunohistochemistry, semi-quantitative PCR and western blot analysis showed that hypoxia-inducible factor-1α and heme oxygenase-1 expression levels increased after chronic cerebral ischemia, with hypoxia-inducible factor-1α expression peaking at 3 weeks and heme oxygenase-1 expression peaking at 6 weeks. These results suggest that the elevated levels of hypoxia-inducible factor-1α may upregulate heme oxygenase-1 expression following chronic cerebral ischemia and that the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway is involved in the development of cognitive impairment induced by chronic cerebral ischemia. Cilostazol treatment alleviated the cognitive impairment in rats with chronic cerebral ischemia, decreased hypoxia-inducible factor-1α and heme oxygenase-1 expression levels, and reduced apoptosis in the frontal cortex. These findings demonstrate that cilostazol can protect against cognitive impairment induced by chronic cerebral ischemic injury through an anti-apoptotic mechanism. | Han Chen Aixuan Wei Jinting He Ming Yu Jing Mang Zhongxin Xu | 2013 | Neural Regeneration Research2013，8，19： | 5 |
| 4 | Preparation of an anti-diethylstilbestrol monoclonal antibody and development of an indirect competitive ELISA to detect diethylstilbestrol in biological samples显示文摘Based on the preparation of an anti-diethylstilbestrol(DES) monoclonal antibody,a simple and convenient indirect competitive enzyme-linked immunosorbent assay(ELISA) method for DES detection has been developed.The monoclonal antibody demonstrated high sensitivity to DES with an IC50 value of 275 pg mL-1 and detection limit(LOD) of 90 pg mL-1.The specificity of the assay was studied by measuring cross-reactivity of the antibody with structurally related compounds of ethinyl estradiol(<7%),estrone(<0.1%),estriol(<0.1%),and diethylstilbestrol benzoate(<0.1%).Chicken,fish,shrimp,urine and bile spiked with different concentration of DES were detected by the developed method,and the recovery rates were greater than 79.5%.Intra-and inter-assay variations were about 6%.This method exhibited high stability with a coefficient of variation less than 10% in buffer and in real samples.The LODs in fish/shrimp,liver,feed and urine spiked with DES were 600,600,4800 and 600 pg mL-1,respectively.These results confirmed that the antibody to DES was successfully produced and could be used to establish ELISA methods for DES detection in food producing animals. | LI WeiHua MENG Meng HE FangYang WAN YuPing XUE HuYin LIU Wei YIN WeiWei XU Jing FENG CaiWei WANG ShanLiang LU Xiao LIU JinTing XI RiMo | 2011 | Chinese Science Bulletin2011，56，8： | 4 |
| 5 | NGF combined with OGD in Juces neural ischemia tolerance in PC12 cells显示文摘 | Chunli Mei Jinting He JingMang | 2011 | AJBR2011，5，10： | 1 |
| 6 | Use of RNAi silencing to target preconditioned glial cell line-derived neurotrophic factor in neuronal apoptosis显示文摘Several studies have suggested that exogenous glial cell line-derived neurotrophic factor may pro-tect neurons from cerebral ischemic injury. However, the mechanisms underlying the neuroprotec-tive effects of endogenous glial cell line-derived neurotrophic factor remain unclear. The present experiments sought to elucidate the influence of various conditioned media on neuronal apoptosis, using a normal culture medium for astrocytes, an astrocyte medium highly expressing glial cell line-derived neurotrophic factor, and an astrocyte medium in which glial cell line-derived neurotro-phic factor expression was silenced using RNAi technology. The results confirmed that the use of RNAi silencing to target pretreated glial cell line-derived neurotrophic factor expression promoted neuronal apoptosis. In addition, oxygen and glucose deprivation preconditioning was found to upregulate glial cell line-derived neurotrophic factor expression, and significantly reduce neuronal apoptosis. | Hongliang Guo Xinhua Li Jing Mang Ying Xing Jinting He Guihua Xu Shijun Yan LifengLiu Chunli Mei Zhongxin Xu | 2011 | Neural Regeneration Research2011，6，7： | 1 |
| 7 | Increased expression of receptor for advanced glycation end-products worsens focal brain ischemia in diabetic rats显示文摘A rat model of diabetes mellitus was induced by a high fat diet,followed by focal brain ischemia induced using the thread method after 0.5 month.Immunohistochemistry showed that expression of receptor for advanced glycation end-products was higher in the ischemic cortex of diabetic rats compared with non-diabetic rats with brain ischemia.Western blot assay revealed increased phosphorylated c-Jun N-terminal kinase expression,and unchanged phosphorylated extracellular signal-regulated protein kinase protein expression in the ischemic cortex of diabetic rats compared with non-diabetic rats with brain ischemia.Additionally,phosphorylated p38 mitogen-activated protein kinase protein was not detected in any rats in the two groups.Severity of limb hemiplegia was worse in diabetic rats with brain ischemia compared with ischemia alone rats.The results suggest that increased expression of receptor for advanced glycation end-products can further activate the c-Jun N-terminal kinase pathway in mitogen-activated protein kinase,thereby worsening brain injury associated with focal brain ischemia in diabetic rats. | Ying Xing Jinting He Weidong Yu Lingling Hou Jiajun Chen | 2012 | Neural Regeneration Research2012，7，13： | 1 |
| 8 | Resilience and functional redundancy of methanogenic digestion microbiome safeguard recovery of methanogenesis activity under the stress induced by microplastics显示文摘Microplastics and nanoplastics are emerging pollutants that substantially influence biological element cycling in natural ecosystems.Plastics are also prevalent in sewage,and they accumulate in waste-activated sludge(WAS).However,the impacts of plastics on the methanogenic digestion of WAS and the underpinning microbiome remain underexplored,particularly during long-term operation.In this study,we found that short-term exposure to individual microplastics and nanoplastics(polyethylene,polyvinyl chloride,polystyrene,and polylactic acid)at a low concentration(10 particles/g sludge)slightly enhanced methanogenesis by 2.1%−9.0%,whereas higher levels(30−200 particles/g sludge)suppressed methanogenesis by 15.2%−30.1%.Notably,the coexistence of multiple plastics,particularly at low concentrations,showed synergistic suppression of methanogenesis.Unexpectedly,methanogenesis activity completely recovered after long-term exposure to plastics,despite obvious suppression of methanogenesis by initial plastic exposure.The inhibition of methanogenesis by plastics could be attributed to the stimulated generation of reactive oxygen species.The stress induced by plastics dramatically decreased the relative abundance of methanogens but showed marginal influence on putative hydrolytic and fermentation populations.Nonetheless,the digestion sludge microbiome exhibited resilience and functional redundancy,contributing to the recovery of methanogenesis during the long-term operation of digesters.Plastics also increased the complexity,modularity,and negative interaction ratios of digestion sludge microbiome networks,but their influence on community assembly varied.Interestingly,a unique plastisphere was observed,the networks and assembly of which were distinct from the sludge microbiome.Collectively,the comprehensive evaluation of the influence of microplastics and nanoplastics on methanogenic digestion,together with the novel ecological insights,contribute to better understanding and manipulating this engineered ecosystem in the face of increasing plastic pollution. | Jinting Liu Guofang Xu Siyan Zhao Jianzhong He | 2023 | mLife2023，2，4： | 0 |
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