RESUMO
The ultrafine cellular structure promotes the extraordinary mechanical performance of metals manufactured by laser powder-bed-fusion (L-PBF). An in-depth understanding of the mechanisms governing the thermal stability of such structures is crucial for designing reliable L-PBF components for high-temperature applications. Here, characterizations and 3D discrete dislocation dynamics simulations are performed to comprehensively understand the evolution of cellular structures in 316L stainless steel during annealing. The dominance of screw-type dislocation dipoles in the dislocation cells is reported. However, the majority of dislocations in sub-grain boundaries (SGBs) are geometrically necessary dislocations (GNDs) with varying types. The disparity in dislocation types can be attributed to the variation in local stacking fault energy (SFE) arising from chemical heterogeneity. The presence of screw-type dislocations facilitates the unpinning of dislocations from dislocation cells/SGBs, resulting in a high dislocation mobility. In contrast, the migration of SGBs with dominating edge-type GNDs requires collaborative motion of dislocations, leading to a sluggish migration rate and an enhanced thermal stability. This work emphasizes the significant role of dislocation type in the thermal stability of cellular structures. Furthermore, it sheds light on how to locally tune dislocation structures with desired dislocation types by adjusting local chemistry-dependent SFE and heat treatment.
RESUMO
Stretching elastic materials containing nanoparticle lattices is common in research and industrial settings, yet our knowledge of the deformation process remains limited. Understanding how such lattices reconfigure is critically important, as changes in microstructure lead to significant alterations in their performance. This understanding has been extremely difficult to achieve due to a lack of fundamental rules governing the rearrangements. Our study elucidates the physical processes and underlying mechanisms of three-dimensional lattice transformations in a polymeric photonic crystal from 0% to over 200% strain during uniaxial stretching. Corroborated by comprehensive experimental characterizations, we present analytical models that precisely predict both the three-dimensional lattice structures and the macroscale deformations throughout the stretching process. These models reveal how the nanoparticle lattice and matrix polymer jointly determine the resultant structures, which breaks the original structural symmetry and profoundly changes the dispersion of photonic bandgaps. Stretching induces shifting of the main pseudogap structure out from the 1st Brillouin zone and the merging of different symmetry points. Evolutions of multiple photonic bandgaps reveal potential optical singularities shifting with strain. This work sets a new benchmark for the reconfiguration of soft material structures and may lay the groundwork for the study of stretchable three-dimensional topological photonic crystals.
RESUMO
Endometriosis is a disease characterized by the ectopic growth of endometrial tissue (glands and stroma) outside the confines of the uterus and often involves vital organs such as the intestines and urinary system. Endometriosis is considered a refractory disease owing to its enigmatic etiology, propensity for recurrence following conservative or surgical interventions, and the absence of radical treatment and long-term management. In recent years, the incidence of endometriosis has gradually increased, rendering it a pressing concern among women of childbearing age. A more profound understanding of its pathogenesis can significantly improve prognosis. Recent research endeavors have spotlighted the molecular mechanisms by which microRNAs (miRNAs) regulate the occurrence and progression of endometriosis. Many miRNAs have been reported to be aberrantly expressed in the affected tissues of both patients and animal models. These miRNAs actively participate in the regulation of inflammatory reactions, cellular proliferation, angiogenesis, and tissue remodeling. Their capacity to modulate crucial signaling pathways, such as the Wnt/ß-catenin signaling pathway, reinforces their potential utility as diagnostic markers or therapeutic agents for endometriosis. In this review, we provide the latest insights into the role of miRNAs that interact with the Wnt/ß-catenin pathway to regulate the biological behaviors of endometriosis cells and disease-related symptoms, such as pain and infertility. We hope that this review will provide novel insights and promising targets for innovative therapies addressing endometriosis.
