Revealing thermally-activated nucleation pathways of diffusionless solid-to-solid transition
Solid-to-solid transitions usually occur via athermal nucleation pathways on pre-existing defects due to immense strain energy. However, the extent to which athermal nucleation persists under low strain energy comparable to the interface energy, and whether thermally-activated nucleation is still po...
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Veröffentlicht in: | Nature communications 2021-06, Vol.12 (1), p.4042-4042, Article 4042 |
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Sprache: | eng |
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Zusammenfassung: | Solid-to-solid transitions usually occur via athermal nucleation pathways on pre-existing defects due to immense strain energy. However, the extent to which athermal nucleation persists under low strain energy comparable to the interface energy, and whether thermally-activated nucleation is still possible are mostly unknown. To address these questions, the microscopic observation of the transformation dynamics is a prerequisite. Using a charged colloidal system that allows the triggering of an fcc-to-bcc transition while enabling in-situ single-particle-level observation, we experimentally find both athermal and thermally-activated pathways controlled by the softness of the parent crystal. In particular, we reveal three new transition pathways: ingrain homogeneous nucleation driven by spontaneous dislocation generation, heterogeneous nucleation assisted by premelting grain boundaries, and wall-assisted growth. Our findings reveal the physical principles behind the system-dependent pathway selection and shed light on the control of solid-to-solid transitions through the parent phase’s softness and defect landscape.
Normally the diffusionless solid-to-solid transition between phases are driven by athermal processes, due to strain being overwhelmingly dominant. Here, the authors present a unique series of in-situ particle level observations of the solid-to-solid transition in colloidal particles suspended in a solvent, revealing new transition pathways. |
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ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/s41467-021-24256-9 |