Crystal plane orientation-dependent surface atom diffusion in sub-10-nm Au nanocrystals.

Surface atom diffusion is a ubiquitous phenomenon in nanostructured metals with ultrahigh surface-to-volume ratios. However, the fundamental atomic mechanism of surface atom diffusion remains elusive. Here, we report in situ atomic-scale observations of surface pressure-driven atom diffusion in gold nanocrystals at room temperature using high-resolution transmission electron microscopy with a high-speed detection camera. The topmost layer of atoms on (001) plane initially diffuse in a column-by-column manner. As diffusion proceeds, the remaining atomic columns collectively inject into adjacent underlayer, accompanied by nucleation of a surface dislocation. In comparison, atoms on (111) plane directly diffuse to the base without collective injection. Quantitative calculations indicate that these crystal plane orientation-dependent atom diffusion behaviors contribute to the larger diffusion coefficient of (111) plane compared to (001) plane in addition to the effect of diffusion activation energy. Our findings provide valuable insights into atomic mechanisms of diffusion-dominant morphology evolution of nanostructured metals and guide the design of nanostructured materials with enhanced structural stability.

Muscle FOXO-Specific Overexpression and Endurance Exercise Protect Skeletal Muscle and Heart from Defects Caused by a High-Fat Diet in Young Drosophila.

BACKGROUND: Obesity appears to significantly reduce physical activity, but it remains unclear whether this is related to obesity-induced damage to skeletal muscle (SM) and heart muscle (HM). Endurance exercise (EE) reduces obesity-induced defects in SM and HM, but its molecular mechanism is poorly understood. METHODS: The UAS/GAL4 system was used to construct the regulation of SM-specific FOXO gene expression in Drosophila, and the transgenic drosophila was subjected to EE and high-fat diet (HFD) intervention. RESULTS: The structure and function of SM and HM were impaired by a HFD and muscle-FOXO-specific RNAi (MFSR), including reduced climbing speed and climbing endurance, reduced fractional shortening of the heart, damaged myofibrils, and reduced mitochondria in HM. Besides, a HFD and MFSR increased triglyceride level and malondialdehyde level, decreased the Sirt1 and FOXO protein level, and reduced carnitine palmityl transferase I, superoxide dismutase, and catalase activity level, and they dow-regulated FOXO and bmm expression level in SM and HM. On the contrary, both muscle FOXO-specific overexpression (MFSO) and EE prevented abnormal changes of SM and HM in function, structure, or physiology caused by HFD and MFSR. Besides, EE also prevented defects of SM and HM induced by MFSR. CONCLUSIONS: Current findings confirmed MFSO and EE protected SM and heart from defects caused by a HFD via enhancing FOXO-realated antioxidant pathways and lipid catabolism. FOXO played a vital role in regulating HFD-induced defects in SM and HM, but FOXO was not a key regulatory gene of EE against damages in SM and HM. The mechanism was related to activity of Sirt1/FOXO/SOD (superoxide dismutase), CAT (catalase) pathways and lipid catabolism in SM and HM.