Controlling the final grain size in a uniform and controlled manner in powder metallurgy nickel-based superalloys is important since many mechanical properties are closely related to it. However, it has been widely documented that powder metallurgy superalloys are prone to suffer from growth of abnormally large grains (ALGs) during supersolvus heat treatment, which is harmful to in-service mechanical performance. The underlying mechanisms behind the formation of ALGs are not yet fully understood. In this research, ALGs were intentionally created using spherical indentation applied to a polycrystalline nickel-based superalloy at room temperature, establishing a deformation gradient underneath the indentation impression, which was quantitatively determined using finite element modelling, electron backscatter diffraction (EBSD) and synchrotron diffraction. Subsequent supersolvus heat treatment leads to the formation of ALGs in a narrow strain range, which also coincides with the contour of residual plastic strain in a range of about 2% to 10%. The formation mechanisms can be attributed to: (1) nucleation sites available for recrystallization are limited, (2) gradient distribution of stored energy across grain boundary. The proposed mechanisms were validated by the phase-field simulation. This research provides a deeper insight in understanding the formation of ALGs in polycrystalline nickel-based superalloy components during heat treatment, when subsurface plastic deformation caused by (mis)handling before super-solvus heat treatment occurs. The practical relevance of looking at small strains at room temperature this research is to understand what happens when turbine disks undergo small dents and scratches during (mis) handling before heat treatment.

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Osteosarcoma (OS) is an aggressive malignant tumor with a high rate of lung metastasis and a lack of therapeutic targets. Although the anomalous expression of long non-coding RNA (lncRNA) has been extensively documented in human cancer, its contribution to OS metastasis remains poorly understood. In this study, we found that MIR205 host gene (MIR205HG) was significantly elevated in human OS tissues, especially in metastatic OS tissues. Stable knockdown of MIR205HG inhibited OS cell invasion and lung metastatic foci formation, but did not affect cell viability. The vast majority of MIR205HG was situated in the cytosol, and served as a competing endogenous RNA (ceRNA) that directly bound to microRNA 2114-3p (miR-2114-3p), resulting in increased twist family bHLH transcription factor 2 (TWIST2) level. Pre-clinically, high MIR205HG was linked with dismal overall and relapse-free survival. Functionally, the attenuated cell invasion caused by MIR205HG knockdown was effectively rescued by miR-2114-3p silencing or TWIST2 overexpression. Overall, our findings suggest that the previously uncharacterized regulatory axis of MIR205HG/miR-2114-3p/TWIST2 plays a critical role in promoting OS metastasis, which implies a potential therapeutic target in OS patients with metastasis.

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