ABSTRACT
We perform molecular dynamics simulations to investigate the energy dissipation of the resonant oscillation for the group IV monolayers of puckered configuration, in which the oscillation is driven with different actuation velocities. We find that, in the moderate actuation velocity regime, the nonlinear coupling between the resonant oscillation mode and other high-frequency modes will lead to the non-resonant motion of the system. For the larger actuation velocity, the effective strain generated during the resonant oscillating causes a structural transition from the puckered configuration into the planar configuration, which is a characteristic energy dissipation mechanism for the resonant oscillation of these group IV puckered monolayers. Our findings shed light on mechanical applications of the group IV monolayers in the nanomechanical resonator field.
ABSTRACT
Two-dimensional (2D) layered crystals are prone to bending and folding owing to their ultra-low bending stiffness. Folds are traditionally viewed as defects that degrade the material performance. Here, we demonstrate that folds and cohesive forces in 2D layered crystals like graphene and MoS2 can be exploited to collect and clean up interlayer impurities, wherein multiple separated impurities agglomerate into a single, large cluster. We combine classical molecular dynamics simulations and an analytical model to elucidate the competing roles of membrane bending and impurity-membrane cohesive energies in the self-cleaning process. Our findings shed light on the mechanisms by which the forces that are present in 2D layered crystals can positively impact, through the possibility of intrinsic cleaning and defect engineering, the synthesis of van der Waals homo- and heterostructures with improved reliability and functionalities.
ABSTRACT
OBJECTIVE: To investigate the effects of nanogold in inhibition of angiogenesis and growth of liver cancer cells. METHODS: Nanogold was co-incubated with VEGF165 and VDGF121 respectively. Atomic force microscopy (AFM) was used to observe the changes of the form of the particles. Human umbilical vascular endothelial cells (HUVEC) were serum-starved for 24 hours, then co-cultured with VEGF165 + nanogold or VEGF121 + nanogold for 24 h. ATM was used to observe the ultrastructure of the cells. Another HUVEC were serum-starved for 24 hours and then cultured with VEGF165 (10 microg/L) 100 microl + nanogold 125, 250, and 500 nmol/L 100 microl respectively for 5 min. Then Western blotting was used to detect the phosphorylation protein of phospholipase C (PLC)-gamma1 on VEGFR-2. Hepatocellular cancer cells of the line H22 were injected subcutaneously into the right armpit of 20 Balb/c nude mice. When the size of transplanted tumor reached about 8 mm, the mice were divided into 2 equal groups: experimental group undergoing injection of nanogold into the tumor once a day for 8 days, and control group injected with normal saline. On day 14 the mice were sacrificed with the liver tumors taken out to measure the size and weight. The microvascular density (MVD) of tumor was determined by immunohistochemical staining. RESULTS: ATM showed that acted with VEGF165, the size of nanogold became over 30 nm. Treated with VEGF165 the HUVEC became larger with obvious pseudopodium. However, such changes were obviously milder in those HUVEC treated with nanogold + VEGF165. The PLC-gamma1 phosphorylation level VEGF receptor-2 was decreased along with the increase of the concentration of nanogold. The MVD of liver cancer tissue in the experimental group was 14.27 +/- 1.08, significantly lower than that of the control group [(23.52 +/- 1.36), P < 0.01]. The mean weight and volume of tumor of the experimental group were (1.39 +/- 0.08) g and (1.37 +/- 0.34) cm(3) respectively, both significantly lower than those of the control group [(2.47 +/- 0.15) g and (2.49 +/- 0.78) cm(3) respectively, both P < 0.05] with a tumor growth inhibition rate of 43.72%. CONCLUSION: Nanogold significantly inhibits the angiogenesis and growth of liver cancer cells with the possible mechanism that nanogold inhibits the VEGF165-induced signaling.
