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Lihua Xu,Biao Li,Xiaoxiao Ding,Yin Chi,Changning Li,Biao Huang,Yuchuan Shi 한국콘크리트학회 2018 International Journal of Concrete Structures and M Vol.12 No.7
This paper presents an experimental investigation on the stress–strain behavior and the damage mechanism of polypropylene fiber reinforced concrete (PFRC) under monotonic and cyclic compression. Fifty-four specimens for different fiber volume fractions and aspect ratios were tested. Acoustic emission (AE) technique was used to monitor the damage progression. The damage mechanism of concrete was analyzed based on the AE parametric analysis. The results show that the incorporation of polypropylene fiber (PF) has a positive effect on the monotonic and cyclic behaviors of concrete, especially for the post-cracking branch. The toughness and ultimate strain are enhanced and the performance degradation in terms of elastic stiffness and strength is alleviated by the addition of PF. However, PF has little influences on the plastic strain, and the damage process of concrete is mainly driven by the envelope strain. The effect of fiber volume fraction on the cyclic behavior of concrete shows more pronounced than that of aspect ratio. In addition, it is found from AE results that the damage, closely related to AE events, has a quick evolution just after the peak stress, with the AE hits having a concentrated release. The total amount of AE hits increases with increasing fiber volume fraction due to fiber pullout and sliding, while the concrete with fiber aspect ratio of 280 reaches the largest amount. Meanwhile, as substantiated by AE, the failure of PFRC shows an obvious shear mode, with shear cracks dominating the damage progression. Finally, a damage elasto-plastic model is developed to predict the monotonic and cyclic responses of PFRC and the prediction yields a fairly close estimation with experimental results.
Immunosuppression and Neuroinflammation in Stroke Pathobiology
Qian Jiang,Christopher R. Stone,Kenneth Elkin,Xiaokun Geng,Yuchuan Ding 한국뇌신경과학회 2021 Experimental Neurobiology Vol.30 No.2
Over the preceding decades, there have been substantial advances in our knowledge of the pathophysiology of stroke. One such advance has been an increased understanding of the multifarious crosstalk in which the nervous and immune systems engage in order to maintain homeostasis. By interrupting the immune-nervous nexus, it is thought that stroke induces change in both systems. Additionally, it has been found that both innate and adaptive immunosuppression play protective roles against the effects of stroke. The release of danger-/damage-associated molecular patterns (DAMPs) activates Toll-like receptors (TLRs), contributing to the harmful inflammatory effects of ischemia/reperfusion injury after stroke; the Tyro3, Axl, and MerTK (TAM)/Gas6 system, however, has been shown to suppress inflammation via downstream signaling molecules that inhibit TLR signaling. Anti-inflammatory cytokines have also been found to promote neuroprotection following stroke. Additionally, adaptive immunosuppression merits further consideration as a potential endogenous protective mechanism. In this review, we highlight recent studies regarding the effects and mechanism of immunosuppression on the pathophysiology of stroke, with the hope that a better understanding of the function of both of innate and adaptive immunity in this setting will facilitate the development of effective therapies for post-stroke inflammation.