Numerous studies have focused on designing functional surfaces that delay frost formation or reduce ice adhesion. However, solutions to the scientific challenges of developing antiicing surfaces remain elusive because of degradation such as mechanical wearing. Inspired by the discontinuous frost pattern on natural leaves, here we report findings on the condensation frosting process on surfaces with serrated structures on the millimeter scale, which is distinct from that on a conventional planar surface with microscale/nanoscale textures. Dropwise condensation, during the first stage of frosting, is enhanced on the peaks and suppressed in the valleys, causing frost to initiate from the peaks, regardless of surface chemistry. The condensed droplets in the valley are then evaporated due to the lower vapor pressure of ice compared with water, resulting in a frost-free zone in the valley, which resists frost propagation even on superhydrophilic surfaces. The dependence of the frost-free areal fraction on the geometric parameters and the ambient conditions is elucidated by both numerical simulations based on steady-state diffusion and an analytical method with an understanding of boundary conditions independent of surface chemistry. We envision that this study would provide a unified framework to design surfaces that can spatially control frost formation, crystal growth, diffusion-controlled growth of biominerals, and material deposition over a broad range of applications.
The build-up of ice on aircraft, bridges, oil rigs, wind turbines, electrical lines, and other surfaces exposed to cold environments diminishes their safe and effective operation. To engineer robust surfaces that reduce ice adhesion, it is necessary to understand the physics of what makes a surface icephobic (“ice-hating”) as well as the relationship between icephobicity and ice adhesion. Here we elucidate the molecular origin of icephobicity based on ice-surface interactions and characterize the correlation between material icephobicity and liquid wettability. This fundamental understanding of icephobic characteristics enables us to propose a robust design for topologically textured, icephobic surfaces. The design identifies the critical confinement length scale to sustain liquid water (as opposed to ice) in between roughness features and can reduce the strength of ice adhesion by over a factor of twenty-seven compared to traditional hydrophobic surfaces. The reduction in ice adhesion is due to the metastability of liquid water; as ambient ice cleaves from the textured surface, liquid water leaves confinement and freezes – a process which takes the system from a local energy minimum to a global energy minimum. This phase transition generates a detachment force that actively propels ambient ice from the surface.
The coronavirus severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) remains an extant threat against public health on a global scale. Cell infection begins when the spike protein of SARS‐CoV‐2 binds with the human cell receptor, angiotensin‐converting enzyme 2 (ACE2). Here, we address the role of tetracycline as an inhibitor for the receptor‐binding domain (RBD) of the spike protein. Targeted molecular investigation show that tetracycline binds more favorably to the RBD (−9.40 kcal/mol) compared to doxycycline (−8.08 kcal/mol), chloroquine (−6.31 kcal/mol), or gentamicin (−4.83 kcal/mol) while inhibiting attachment to ACE2 to a greater degree (binding efficiency of 2.98 kcal/(mol nm 2 ) for tetracycline–RBD, 5.16 kcal/(mol nm 2 ) for doxycycline–RBD, 5.59 kcal/(mol nm 2 ) for chloroquine–RBD, and 7.02 kcal/(mol nm 2 ) for gentamicin–RBD. Stronger inhibition by tetracycline is verified with nonequilibrium PMF calculations, for which the tetracycline–RBD complex exhibits the lowest free energy profile along the dissociation pathway from ACE2. Tetracycline binds to tyrosine and glycine residues on the viral contact interface that are known to modulate molecular recognition and bonding affinity. These RBD residues also engage in significant hydrogen bonding with the human receptor ACE2. The ability to preclude cell infection complements the anti‐inflammatory and cytokine suppressing capability of tetracycline; this may reduce the duration of ICU stays and mechanical ventilation induced by the coronavirus SARS‐CoV‐2.
The Leidenfrost layer is characterized by an insulating vapor film between a heated surface and an ambient liquid. The collapse of this film has been canonically theorized to occur from an interfacial instability between the liquid and vapor phases. The interfacial instability alone, however, is insufficient to explain the known influence of the surface on the film collapse process. In this work, we provide visual evidence for two key mechanisms governing the film collapse: the interfacial instability, and the nucleation of vapor upon multiple non-terminal liquid-solid contacts. These results were obtained by implementing high-speed X-ray imaging of the film collapse on a heated sphere submerged in liquid-water. The X-ray images were synchronized with a second high-speed visible light camera and two thermocouples to provide insight into the film formation and film collapse processes. Lastly, the dynamic film thickness was quantified by analysis of the X-ray images. This helped assess the influence of surface roughness on the disruption of the film. The results of this work encourage further investigation into non-linear stability theory to consolidate the role of the surface on the liquid-vapor interface during the film collapse process.
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