The high cycle fatigue of aero-engine blades is mainly vibration bending fatigue. To study the high-frequency vibration characteristics of the blade under actual working conditions, the high-frequency vibration characteristics test of the blade under ultrasonic excitation was carried out by using the horn-blade ultrasonic excitation laser vibrometry system and analyzing the blade high-frequency vibration characteristics. The results show that the ultrasonic generator can produce stable 20k Hz ultrasonic vibration, and the laser vibration measurement system can accurately measure the high-frequency vibration. Due to the structure shape of the complex blade, there is energy dissipation, which results in the blade amplitude being much smaller than the excitation source amplitude. Under the same excitation position and ultrasonic excitation conditions, the smaller the blade mass can cause the larger the amplitude, the higher the number of high harmonics, the lower the fundamental frequency, and the more complex the vibration waveform. The research provides a test method for the analysis of the blade high-frequency vibration characteristics and has a certain guiding significance for the research on the blade ultra-high cycle fatigue.

This article through the establishment of quantitative model and the corresponding prediction model orientation of network information mining, through the database to adjust some of this information and integration, the database of the directivity classification work, can according to the requirements in terms of system analysis of data at the same time, through the data to forecast its trend, get the best prediction model and the prediction results. In this paper, a data set is established based on the stage new information indicators of database information and the corresponding rise and fall trend broken line graph, and a quantitative Model and trend prediction system based on two-brain Strategy Model are established to predict and evaluate the situation of directional information. And then to predict the trend of fluctuations is relatively accurate prediction results quantitative optimization model is established, the grid strategy and hedge strategy is adopted to improve the decision-making and judgment, decision variable coding as operands, can converge to the optimal solution with large probability, data analysis and forecast the dynamic change of process, with different weights allocation scheme to give corresponding risk prediction.

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Background: Brain-derived neurotrophic factor/tyrosine kinase receptor B (BDNF/TrkB) pathway dysregulation may be induced by hypoxia and inflammation, and play pivotal roles during the development of neurological disorders. Propofol is an anesthetic agent with neuro-protective properties. We aimed to verify whether propofol affected BDNF/TrkB pathway in neurons and astrocytes exposed to hypoxia and inflammation.Methods: Primary rat hippocampal neurons and astrocytes were cultured and exposed to propofol followed by hypoxia or TNF-α treatment. The production of BDNF and the expression/truncation/phosphorylation of TrkB were measured. The underlying mechanisms such as ERK, CREB, p35 and Cdk5 were investigated.Results: In hippocampal neurons and astrocytes, hypoxia and TNF-α reduced the production of BDNF. Pretreatment of hippocampal neurons with 25μM propofol reversed the inhibitory effect of hypoxia or TNF-α on BDNF production. However, even 100μM propofol had no such effect in astrocytes. Further, we found that in hippocampal neurons hypoxia and TNF-α increased the phosphorylation of ERK (p-ERK) and CREB at Ser142 (p-CREB Ser142), while reduced the phosphorylation of CREB at Ser133 (p-CREB Ser133), which were all reversed by 25μM propofol and 10μM ERK inhibitor. In addition, we reported that hypoxia- and TNF-α-mediated reduction of BDNF was mitigated by 10μM ERK inhibitor, and the beneficial effect of propofol was abolished by 10μM ERK activator. We also found neither hypoxia nor TNF-α affected TrkB expression, truncation or phosphorylation in hippocampal neurons and astrocytes. However 50μM propofol induced TrkB phosphorylation without affecting its expression and truncation only in hippocampal neurons. Furthermore, we detected that in hippocampal neurons, 50μM propofol induced p35 expression and Cdk5 activation, and blockade of p35 or Cdk5 mitigated propofol-induced TrkB phosphorylation.Conclusions: Propofol, via ERK/CREB and p35/Cdk5, may modulate BDNF/TrkB pathway in hippocampal neurons that were exposed to hypoxia or TNF-α.

Background: BDNF/TrkB pathway dysregulation may be induced by hypoxia and inflammation, and play pivotal roles during the development of neurological disorders. Propofol is an anesthetic agent with neuro-protective properties. We aimed to verify whether propofol affected BDNF/TrkB pathway in neurons exposed to hypoxia or TNF-α.Methods: Primary rat hippocampal neurons and astrocytes were cultured and exposed to propofol followed by hypoxia or TNF-α treatment. The production of BDNF and the expression/truncation/phosphorylation of TrkB were measured. The underlying mechanisms such as ERK, CREB, p35 and Cdk5 were investigated.Results: In hippocampal neurons and astrocytes, hypoxia and TNF-α reduced the production of BDNF. Pretreatment of hippocampal neurons with 25μM propofol reversed the inhibitory effect of hypoxia or TNF-α on BDNF production. However, even 100μM propofol had no such effect in astrocytes. Further, we found that in hippocampal neurons hypoxia and TNF-α increased the phosphorylaion of ERK (p-ERK) and CREB at Ser142 (p-CREBSer142), while reduced the phosphorylation of CREB at Ser133 (p-CREBSer133), which were all reversed by 25μM propofol and 10μM ERK inhibitor. In addition, neither hypoxia nor TNF-α affected TrkB expression, truncation or phosphorylation in hippocampal neurons and astrocytes. However 50μM propofol induced TrkB phosphorylation without affecting its expression and truncation only in hippocampal neurons. Furthermore, we detected that in hippocampal neurons, 50μM propofol induced p35 expression and Cdk5 activation, and blockade of p35 or Cdk5 mitigated propofol-induced TrkB phosphorylation.Conclusions: Propofol, via ERK/CREB and p35/Cdk5, may modulate BDNF/TrkB pathway in hippocampal neurons that were exposed to hypoxia or TNF-α.