Research on Fatigue Damage and Affecting Factors of Defected Rock Mass Based on Ultrasonic Wave Velocity

In this paper the fatigue-loading test of defected rock-like specimen has been carried out by electro-hydraulic servo fatigue testing machine. At the same time, the ultrasonic data has been collected and analyzed by the digital ultrasonic instrument. The fatigue damage and influencing factors of the defective rock mass under dynamic load are studied. According to the experimental research and analysis, this paper chooses to define the damage variable by ultrasonic velocity, and the inverse function of the Logistic equation was used to describe the evolution curve of fatigue damage sample. The experimental data fitting results show that the damage model and the experimental data fit well. In addition, this paper analyzes the main influencing factors of fatigue damage in the test. The initial damage represents the damage state before the sample is cyclically loaded. Different initial damages have a significant effect on the fatigue life of the sample. In the case the initial damage is substantially the same, the upper limit stress is larger, the fatigue life of the sample is shorter, and conversely, the fatigue life is longer

Durative sleep fragmentation with or without hypertension suppress rapid eye movement sleep and generate cerebrovascular dysfunction

Either hypertension or chronic insomnia is the risk factor of developing vascular dementia. Durative hypertension can induce vascular remodeling and is used for modeling small vessel disease in rodents. It remains undetermined if the combination of hypertension and sleep disturbance exacerbates vascular dysfunction or pathologies. Previously, we found chronic sleep fragmentation (SF) dampened cognition in young mice without disease predispositions. In the current study, we superimposed SF with hypertension modeling in young mice. Angiotensin II (AngII)-releasing osmotic mini pumps were subcutaneously implanted to generate persistent hypertension, while sham surgeries were performed as controls. Sleep fragmentation with repetitive arousals (10 s every 2 min) during light-on 12 h for consecutive 30 days, while mice undergoing normal sleep (NS) processes were set as controls. Sleep architectures, whisker-stimulated cerebral blood flow (CBF) changes, vascular responsiveness as well as vascular pathologies were compared among normal sleep plus sham (NS + sham), SF plus sham (SF + sham), normal sleep plus AngII (NS + AngII), and SF plus AngII (SF + AngII) groups. SF and hypertension both alter sleep structures, particularly suppressing REM sleep. SF no matter if combined with hypertension strongly suppressed whisker-stimulated CBF increase, suggesting the tight association with cognitive decline. Hypertension modeling sensitizes vascular responsiveness toward a vasoactive agent, Acetylcholine (ACh, 5 mg/ml, 10 μl) delivered via cisterna magna infusion, while SF exhibits a similar but much milder effect. None of the modeling above was sufficient to induce arterial or arteriole vascular remodeling, but SF or SF plus hypertension increased vascular network density constructed by all categories of cerebral vessels. The current study would potentially help understand the pathogenesis of vascular dementia, and the interconnection between sleep and vascular health