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• Fatigue failure mechanism was elucidated for multi-stage centrifugal pump shaft. • Specific technical measures to prevent pump shaft failure were proposed. • Fatigue resistance design is performed for pump shaft structure and coupling. • Feasibility of the new pump shaft system has been verified by experiment. In the operation of multistage centrifugal pump, the pump shaft of 304 stainless steel is subjected to a variety of alternating loads. It is one of the parts prone to failure. The fracture microscopic observation, chemical composition analysis and mechanical property measurement of the fractured pump shaft are carried out. Through the fracture analysis, it is found that the pump shaft failure is caused by fatigue mechanism with characteristic of multi-source crack initiation, and there are many cavities and inclusions at the fracture. From the numerical analysis, it is found that there is significant stress concentration at the fracture, which exceeds the fatigue limit of the material and eventually leads to the fatigue fracture. Besides, the appropriate fillet radius and elastic coupling are designed for the pump shaft, which can effectively reduce the stress concentration and improve the service life of the pump shaft. Finally, the fatigue life of the improved pump shaft was experimentally verified. [ABSTRACT FROM AUTHOR]

Reactor pressure vessel (RPV) is one of the key equipment for nuclear power plant, and long-term exposure to high temperature is an important factor causing its performance deterioration. Under core meltdown conditions, RPV steel experiences high temperature creep due to the In-Vessel Retention (IVR) mitigation measures. This paper aims to investigate high-temperature mechanical properties, especially for the creep behaviors of 16MND5 steel after thermal aging at 650 °C for 2000 h. The results showed that the yield stress and ultimate tensile strength of the 16MND5 steel are decreased, and the creep rupture time is rapidly shortened after thermal aging. The microstructure was analyzed by scanning and transmission electron microscopy (SEM, TEM). 16MND5 steel showed a typical bainitic phase before thermal aging. After 2000 h of thermal aging, the micro-grains were coarsened, and finally changed into a ferritic microstructure. Based on Larson-Miller (LM), Orr-Sherby-Dorn (OSD) parameters methods and Kachanov-Rabotnov (K–R) model to predict uniaxial creep life after thermal aging, the prediction results are satisfactory, and all within the double tolerance band. This work reveals the creep damage mechanism of 16MND5 steel after thermal aging, and provides basic data for the implementation of IVR strategy in nuclear power plants after long-term service. • Characterization of creep behaviors are achieved for 16MND5 steel before and after thermal aging. • Creep failure mechanism of thermal aged 16MND5 steel is explained by microscopic observation. • Influence of thermal aging on macro- and micro-creep failure of 16MND5 steel is understood in depth. • Creep life is well predicted by Larson-Miller and Orr-Sherby-Dorn parameters methods, and validated by experiment. • The K–R model accurately characterizes the three creep stages of thermal aged 16MND5 steel. [ABSTRACT FROM AUTHOR]

Aging is an important risk factor for neurodegenerative diseases. The activation of α7 nicotinic acetylcholine receptor (α7nAChR) is involved in inflammation and cognition, but the specific role it plays in aging remains unknown. This study aimed to investigate the anti-aging effect of the activation of α7nAChR on aging rats and BV2 cells induced by D-galactose, as well as its potential mechanism. D-galactose induced an increase in the SA-β-Gal positive cells, expression of p16 and p21 in vivo and in vitro. α7nAChR selective agonist PNU282987 decreased levels of pro-inflammatory factors, MDA, and Aβ, enhanced SOD activity and levels of anti-inflammatory factor (IL10) in vivo. PNU282987 enhanced the expression of Arg1, decreased the expression of iNOS, IL1β and TNFα in vitro. PNU282987 upregulated the levels of α7nAChR, Nrf2 and HO-1 in vivo and in vitro. The results of Morris water maze and novel object recognition tests showed that PNU282987 improved cognitive impairment in aging rats. Furthermore, α7nAChR selective inhibitor methyllycaconitine (MLA) results were opposite with PNU282987. PNU282987 improves cognitive impairment through inhibiting oxidative stress and neuroinflammation in D-galactose induced aging via regulating the α7nAChR/Nrf2/HO-1 signaling pathway. Therefore, targeting the α7nAChR may be a viable therapeutic approach for anti-inflammaging and neurodegenerative diseases. • D-galactose induces microglial senescence and brain aging. • α7nAChR is downregulated in brain aging and senescent BV2 cells. • The activation of α7nAChR by PNU282987 inhibits oxidative stress and neuroinflammation in vivo and in vitro. • PNU282987 inhibits oxidative stress and neuroinflammation by upregulating the α7nAChR /Nrf2/HO-1 signaling pathway, thereby alleviating cognitive impairment caused by aging. [ABSTRACT FROM AUTHOR]