In Situ Atomic-Scale Quantitative Evidence of Plastic Activities Resulting in Reparable Deformation in Ultrasmall-Sized Ag Nanocrystals.

Permanent structural changes in pure metals that are caused by plastic activity are normally irreparable after unloading. Because of the lack of experimental evidence, it is unclear whether the plastic activity can be repaired as the size of the pure metals decreases to several nanometers; it is also unclear how the metals accommodate the plastic deformation. In this study, the in situ atomic-scale loading and unloading of ∼2 nm Ag nanocrystals was investigated, and three modes of plastic deformation were observed: (i) the phase transition from the face-centered cubic (fcc) phase to the hexagonal close-packed (hcp) phase, (ii) stacking faults, and (iii) deformation twin nucleation. We show that all three modes resulted in structural changes that were reparable, and their generation and restoration during loading and unloading were observed in situ. We discovered that the deformation modes of nanosized metals can be predicted from the ratio of the energy barriers of the fcc-hcp phase transition (ΔγH) and the deformation twin nucleation (ΔγT), which differ from those of the theoretical modes of relatively large-sized metals. The proposed ΔγH/ΔγT criterion provides insights into the deformation mechanism of nanometals.

MicroRNA-451 increases vascular permeability and suppresses angiogenesis in pulmonary burn injury in a rat model.

BACKGROUND: Burns are common traumas that cause systemic symptoms by increasing vascular permeability. OBJECTIVES: To investigate the role of miRNA-451 and to clarify the underlying mechanism of the burn process. MATERIAL AND METHODS: We established a heat-induced third-degree burn with acute lung injury (ALI) model in rats. Hematoxylin and eosin (H&E) staining and in situ hybridization were performed. Overexpressed miRNA-451 in human umbilical vascular endothelial cells (HUVEC) were carried out. The migration and proliferation of HUVEC cells were examined. RESULTS: The H&E staining showed that the burn injury caused by heat went through the dermis and damaged deep tissues. Meanwhile, the heat also induced acute lung injury, characterized by inflammatory exudation in the alveoli and significant enlargement of the alveolar septum. In situ hybridization showed that the expression of miRNA-451 increased in the lung endothelial cells. We overexpressed miRNA-451 in human umbilical vascular endothelial cells (HUVEC) and the results showed that miRNA-451 inhibited the migration and proliferation of HUVEC cells, increased HUVEC cell permeability, inhibited cell adhesion, and induced cell apoptosis. Furthermore, the expression of occludin and ZO-1, 2 key protein molecules in forming tight junction between cells, decreased, and the proteins dispersed in the cytoplasm of HUVEC cells. CONCLUSIONS: MiRNA-451 was upregulated in the lung endothelial cells of the rat model, and contributed to increase lung endothelial cell permeability. It suppresses angiogenesis of lung endothelial cells, indicating their potential as a target in the treatment of burn injuries.