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The safety requirements demanded from rail traffic have risen above all in view of the rapid development of modern high-speed trains. Railway fastener is the important part of rail line. The normal state of the fastener is the guarantee of the rail transportation security. The missing or broken fastener may be the tremendous threaten to the security, or even cause the serious traffic accidents. This paper presents a new fully automatic and configurable wireless sensor network system able to detect the absence of the fastening bolts that fix the rails to the sleepers. The experement indicated that the system by using sensor networks and LabVIEW can guarantee a high accurate detection for the missing or broken fastening elements in combination with the strain measurement of the rubber pad under rail.

Objectives: Chronic hyperglycemia is considered as an important factor to promote the neurodegenerative process of brain, and the synaptic plasticity as well as heterogeneity of hippocampal cells are thought to be associated with cognitive dysfunction in the early process of neurodegeneration. To date, fibronectin type III domain‐containing protein 5 (FNDC5) has been highlighted its protective role in multiple neurodegenerative diseases. However, the potential molecular and cellular mechanisms of FNDC5 on synaptic plasticity regulation in cognitive impairment (CI) induced by diabetics are still need to known. Methods/Design: To investigate the heterogeneity and synaptic plasticity of hippocampus in animals with CI state induced by hyperglycemia, and explore the potential role of FNDC5 involved in this process. Firstly, the single cell sequencing was performed based on the hippocampal tissue from db diabetic mice induced CI and normal health control mice by ex vivo experiments; and then the integrated analysis and observations validation using Quantitative Real‐time PCR, western blot as well as other in vitro studies. Results: We observed and clarified the sub‐cluster of type IC spiral ganglion neurons expressed marker genes as Trmp3 and sub‐cluster of astrocytes with marker gene as Atp1a2 in hippocampal cells from diabetic animals induced CI and the effect of those on neuron‐glial communication. We also found that FNDC5\BDNF‐Trk axis was involved in the synaptic plasticity regulation of hippocampus. In high glucose induced brain injury model in vitro, we investigated that FNDC5 significantly regulates BDNF expression and that over‐expression of FNDC5 up‐regulated BDNF expression (p < 0.05) and can also significantly increase the expression of synapsin‐1 (p < 0.05), which is related to synaptic plasticity, In addition, the unbalanced methylation level between H3K4 and H3K9 in Fndc5 gene promoter correlated with significantly down‐regulated expression of FNDC5 (p < 0.05) in the hyperglycemia state. Conclusion: The current study revealed that the synaptic plasticity of hippocampal cells in hyperglycemia might be regulated by FNDC5\BDNF‐Trk axis, playing the protective role in the process of CI induced by hyperglycemia and providing a target for the early treatment of hyperglycemia induced cognitive dysfunction in clinic. Key points: The heterogeneity and synaptic plasticity of hippocampus between the db−/− diabetic mice with cognitive dysfunction and control groups were profiled by the single cell sequencing.FNDC5\BDNF‐Trk axis was involved in the synaptic plasticity regulation of hippocampus.Over‐expression of FNDC5 up‐regulated BDNF expression and can also increase the expression of synapsin‐1, which is related to synaptic plasticity.The unbalanced methylation level between H3K4 and H3K9 in Fndc5 gene promoter correlated with significantly down‐regulated expression of FNDC5 in the hyperglycemia state. [ABSTRACT FROM AUTHOR]