When droplets are placed on hydrophobic textured surfaces, different wetting states Cassie−Baxter (CB) state or Wenzel (W) state may occur depending on materials and structures of surfaces, types and sizes of droplets, thermal fluctuations, and external stimuli. The wetting transition from the CB to the W state and the opposite process have attracted a great deal of attention because of their primary importance for designing and fabricating textured surfaces. In this work, molecular dynamics (MD) simulations are employed to understand the mechanism behind the CB-to-W transition for a nanoscale water film placed on a surface decorated with a single nanogroove when an external electric field is applied. The free energy variation during the transition process is computed on the basis of the restrained MD simulations. Water intrusion into the groove is observed by simulation snapshots, which provides direct evidence for the electric fieldinduced CB-to-W transition. In the previous experiments, however, only a sharp reduction in the apparent contact angle is employed to judge whether the transition takes place. The free energy curves reveal that there are two energy barriers separating the CB and W states (ΔE 1 ) as well as separating the W and CB states (ΔE 2 ). Owing to the presence of ΔE 1 , although the CB state has a higher free energy than the W state, it cannot spontaneously convert to the W state. When the external energy input exceeds ΔE 1 , the CB-to-W transition can be triggered, otherwise the transition will stop, and the water film will return to the CB state. Moreover, it is found that the maximum of free energy always occurs after the film touches the groove bottom. Thus, the requirement that the film should touch the groove bottom is responsible for the presence of the energy barrier ΔE 1 . Finally, the dependence of the two energy barriers on the electric field strength, groove aspect ratio, and intrinsic contact angle of the groove is also discussed.

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Impact dynamics of nanodroplets has recently gained extensive attention because of its potential applications in nanoscale inkjet printing, nanodroplet spray cooling, and nanocoating. In this study, a nanodroplet impacting unheated, flat, smooth, and hydrophobic surfaces is investigated via molecular dynamics simulations. The emphasis is placed on spreading and retraction kinetics, i.e., time-dependent wetting radius or r–τ relation, where r and τ are the normalized wetting radius and time. On the basis of an energy conservation approach, an analytical model of r–τ kinetics is developed for impacting nanodroplets. Hypotheses of cylinder droplet and extensional flow are employed to calculate the transient kinetic energy and viscous dissipation rate, which are found to be the most appropriate for impacting nanodroplets. The model is tested in a range of Weber numbers from We = 15 to 60, Reynolds numbers from Re = 11.07 to 22.19, and surface wettability θ0 = 105° and 125°. The tests show that the mean relative deviation ranges from 2.22% to 5.47%, and hence, the developed model captures the spreading and retraction kinetics of a nanodroplet impacting hydrophobic surfaces with satisfactory accuracy. Furthermore, it is found that the model can also be extended to predict the retraction kinetics of nanodroplets on hydrophilic surfaces for high Weber numbers.

BackgroundThe resistance to EGF receptor (EGFR) tyrosine kinase inhibitors (TKI) is a major challenge in the treatment of non-small cell lung cancer (NSCLC). Understanding the molecular mechanisms behind resistance is therefore an important issue. Here we assessed the role of EGFR pathway substrate 8 (EPS8) and Forkhead box O 3a (FoxO3a) as potentially valuable targets in the resistance of NSCLC .MethodsThe expression levels of EPS8 and FoxO3a in patients with NSCLC (n = 75) were examined by immunohistochemistry staining, while in cells were detected by qPCR and western blot. The effects of EPS8 and FoxO3a on resistance, migration and invasion, cell cycle arrest were detected by MTT, transwell and flow cytometry, respectively. Chromatin immunoprecipitation and luciferase reporter assays were performed to determine the mechanisms of EPS8 expression and FoxO3a regulation.FindingsWe observed that the expression of EPS8 inversely correlated with FoxO3a in NSCLC cell lines and NSCLC patients. FoxO3a levels were significantly decreased in tumor tissues compared with para-carcinoma tissues, while EPS8 is opposite. Besides, they play reverse roles in the resistance to gefitinib, the migration and invasion abilities, the cell cycle arrest in vitro and the tumor growth in vivo. Mechanistically, FoxO3a inhibits EPS8 levels by directly binding its gene promoter and they form a negative loop in EGFR pathway.InterpretationTargeting FoxO3a and EPS8 in EGFR signaling pathway prevents the progression of NSCLC, which implied that the negative loop they formed could served as a therapeutic target for overcoming resistance in NSCLC.FundsNational Natural Science Foundation of China, Science and Technology Project of Henan, Outstanding Young Talent Research Fund of Zhengzhou University and the National Scholarship Fund.