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Protective mechanism of testosterone on cognitive impairment in a rat model of Alzheimer's disease 被引量:8
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作者 Xu-Sheng Yan Zhan-Jun Yang +5 位作者 Jian-Xin Jia Wei Song Xin Fang zhi-ping cai Dong-Sheng Huo He Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第4期649-657,共9页
Cognitive dysfunction in Alzheimer's disease is strongly associated with a reduction in synaptic plasticity, which may be induced by oxidative stress. Testosterone is beneficial in learning and memory, although th... Cognitive dysfunction in Alzheimer's disease is strongly associated with a reduction in synaptic plasticity, which may be induced by oxidative stress. Testosterone is beneficial in learning and memory, although the underlying protective mechanism of testosterone on cognitive performance remains unclear. This study explored the protective mechanism of a subcutaneous injection of 0.75 mg testosterone on cognitive dysfunction induced by bilateral injections of amyloid beta 1–42 oligomers into the lateral ventricles of male rats. Morris water maze test results demonstrated that testosterone treatment remarkably reduced escape latency and path length in Alzheimer's disease rat models. During probe trials, testosterone administration significantly elevated the percentage of time spent in the target quadrant and the number of platform crossings. However, flutamide, an androgen receptor antagonist, inhibited the protective effect of testosterone on cognitive performance in Alzheimer's disease rat models. Nissl staining, immunohistochemistry, western blot assay, and enzyme-linked immunosorbent assay results showed that the number of intact hippocampal pyramidal cells, the dendritic spine density in the hippocampal CA1 region, the immune response and expression level of postsynaptic density protein 95 in the hippocampus, and the activities of superoxide dismutase and glutathione peroxidase were increased with testosterone treatment. In contrast, testosterone treatment reduced malondialdehyde levels. Flutamide inhibited the effects of testosterone on all of these indicators. Our data showed that the protective effect of testosterone on cognitive dysfunction in Alzheimer's disease is mediated via androgen receptors to scavenge free radicals, thereby enhancing synaptic plasticity. 展开更多
关键词 nerve REGENERATION Alzheimer’s disease TESTOSTERONE cognitive dysfunction synaptic plasticity free radicals MORRIS water maze androgen receptor FLUTAMIDE POSTSYNAPTIC density protein 95 amyloid beta 1–42 NEURODEGENERATIVE change neural REGENERATION
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LLMP: Exploiting LLDP for Latency Measurement in Software-Defined Data Center Networks 被引量:9
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作者 Yang Li zhi-ping cai Hong Xu 《Journal of Computer Science & Technology》 SCIE EI CSCD 2018年第2期277-285,共9页
The administrators of data center networks have to continually monitor path latency to detect network anomaly quickly and ensure the efficient operation of the networks. In this work, we propose Link Layer Measurement... The administrators of data center networks have to continually monitor path latency to detect network anomaly quickly and ensure the efficient operation of the networks. In this work, we propose Link Layer Measurement Protocol (LLMP), a prototype latency measuring framework based on the Link Layer Discovery Protocol (LLDP). LLDP is utilized by the controller to discover network topology dynamically. We insert timestamps into the optional LLDPTLV field in LLDP, so that the controller can estimate latency on any single link. The framework utilizes a reactive measurement approach without injecting any probe packets to the network. Our experiments show that the latency of a link can be measured accurately by LLMP. In relatively complex network conditions, LLMP can still maintain a high accuracy. We store the LLMP measurement results into a latency matrix, which can be used to infer the path latency. 展开更多
关键词 software-defined network (SDN) Link Layer Discovery Protocol (LLDP) latency measurement
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