| 1. |
- Cui, Luqing, et al.
(author)
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New insights into the anisotropic ductility of additively manufactured Inconel 718
- 2023
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In: International journal of plasticity. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0749-6419 .- 1879-2154. ; 169
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Journal article (peer-reviewed)abstract
- Anisotropic ductility in additively manufactured (AM) alloys, namely better ductility along the building direction (BD) has been extensively studied and traditionally attributed to the crystallographic texture. However, recent studies have shown significant ductility anisotropy in weakly or non-textured AM alloys, indicating that other factors may also play critical roles. To explore this, AM Inconel 718 with weak crystallographic texture was selected as the model material, and the in-situ high-energy X-ray diffraction tests together with multiscale microstructural characterization techniques were performed to explore the deformation micromechanisms. The results of this study, for the first time, revealed that the better ductility in the vertical specimen (loading parallel to BD) was partially due to the negative stress triaxiality factor (TF) of the {220} grains during plastic deformation, which results in the shrinkage or even healing of the microvoids. Furthermore, the & delta;-phase alignment in conjunction with grain boundary orientation were also proved to have a pronounced impact on the anisotropic ductility of AM alloys. On the other hand, though in the overall weak-textured microstructure, the proportion of 101 grains were marginally over other grains. Thus, the positive effect of {220} grains on ductility was stronger than the negative effect of {200} and {311} grains, contributing to the excellent failure elongation exceeding 12% for both samples. The findings of this study shed new light on the mechanisms underlying the anisotropic ductility of AM alloys and provide insight into strategies for enhancing their performance.
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| 2. |
- Wang, Xiaohua, et al.
(author)
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Tacrolimus Causes Hypertension by Increasing Vascular Contractility via RhoA (Ras Homolog Family Member A)/ROCK (Rho-Associated Protein Kinase) Pathway in Mice
- 2022
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In: Hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0194-911X .- 1524-4563. ; 79:10, s. 2228-2238
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Journal article (peer-reviewed)abstract
- Background: To provide tacrolimus is first-line treatment after liver and kidney transplantation. However, hypertension and nephrotoxicity are common tacrolimus side effects that limit its use. Although tacrolimus-related hypertension is well known, the underlying mechanisms are not. Here, we test whether tacrolimus-induced hypertension involves the RhoA (Ras homolog family member A)/ROCK (Rho-associated protein kinase) pathway in male C57Bl/6 mice. methods: Intra-arterial blood pressure was measured under anesthesia. The reactivity of renal afferent arterioles and mesenteric arteries were assessed in vitro using microperfusion and wire myography, respectively. Results: Tacrolimus induced a transient rise in systolic arterial pressure that was blocked by the RhoA/ROCK inhibitor Fasudil (12.0 +/- 0.9 versus 3.2 +/- 0.7; P<0.001). Moreover, tacrolimus reduced the glomerular filtration rate, which was also prevented by Fasudil (187 +/- 20 versus 281 +/- 8.5; P<0.001). Interestingly, tacrolimus enhanced the sensitivity of afferent arterioles and mesenteric arteries to Ang II (angiotensin II), likely due to increased intracellular Ca2+ mobilization and sensitization. Fasudil prevented increased Ang II-sensitivity and blocked Ca2+ mobilization and sensitization. Preincubation of mouse aortic vascular smooth muscle cells with tacrolimus activated the RhoA/ROCK/MYPT-1 (myosin phosphatase targeting subunit 1) pathway. Further, tacrolimus increased cytoplasmic reactive oxygen species generation in afferent arterioles (107 +/- 5.9 versus 163 +/- 6.4; P<0.001) and in cultured mouse aortic vascular smooth muscle cells (100 +/- 7.5 versus 160 +/- 23.2; P<0.01). Finally, the reactive oxygen species scavenger Tempol inhibited tacrolimus-induced Ang II hypersensitivity in afferent arterioles and mesenteric arteries. Conclusions: The RhoA/ROCK pathway may play an important role in tacrolimus-induced hypertension by enhancing Ang II-specific vasoconstriction, and reactive oxygen species may participate in this process by activating the RhoA/ROCK pathway.
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