Energy dissipation of a contact line moving on a nanotopographical defect.

Understanding the origin of the dissipative mechanisms that control the dynamics of a contact line is a real challenge. In order to study the energy dissipation at the contact line when a moving meniscus encounters topographical defects, we developed atomic force microscopy (AFM) experiments using nanofibers with nanometer scale defects. These experiments realized with three liquids are performed in two AFM modes: the contact mode (C-AFM) is used to measure the energy associated with the contact angle hysteresis in the limit of a static situation, deduced from advancing and receding dipping experiments on an isolated defect; the frequency-modulation mode (FM-AFM) is performed at different amplitudes and then velocities to measure the energy dissipated as the contact line moves over the same defect. Strong dissipation peaks appear above a threshold amplitude characteristic of the liquid and the defect, which is determined by the width of the hysteresis measured in statics. Furthermore, the dissipation energy of the moving contact line measured in dynamics is equal to the hysteresis capillary energy whatever the amplitude and is therefore independent of the contact line velocity. These results point out that the defect contribution to dissipation energy of a moving contact line on real surfaces is only governed by the pinning-depinning energy with no contribution of viscous effects.

Wetting at the Nanoscale: Molecular Mobility Induced by Contact Line Forces.

In this paper, we study the interaction of a contact line with molecules physically adsorbed on a surface. We developed specific atomic force microscopy (AFM) experiments where a nanoneedle attached at the extremity of the cantilever is dipped in a liquid droplet. The motion of the contact line at the extremity of the meniscus formed depends on the presence of topographical and chemical defects at the surface of the nanoneedle. The analysis of the force measured by AFM based on a capillary model allows one to distinguish the effects of topographical and chemical defects and to monitor minute changes of surface properties. Using six different liquids and five tips, we show that the change of the surface properties of one nanoneedle results either from the adsorption of airborne molecules when the tip is left in the air or from their desorption by the moving contact line when the tip is repeatedly dipped in the liquid. The desorption rate is found to depend only on the number of dipping cycles and is not influenced by the velocity or the liquid properties. A model based on the estimation of capillary and adsorption energies confirms a capillary desorption mechanism in agreement with the experimental results. Finally, we demonstrate that three distinct desorption mechanisms may be at play. Interestingly, using a deliberate contamination with large hydrocarbon molecules, we show that the capillary desorption studied in this paper can be used to clean surfaces.

Molecular Desorption by a Moving Contact Line.

The interaction of the contact line with topographical or chemical defects at the nanometer scale sets the macroscopic wetting properties of a liquid on a solid substrate. Based on specific atomic force microscopy (AFM) experiments, we demonstrate that molecules physically sorbed on a surface are removed by a dynamic contact line. The mechanism of molecules desorption is directly determined by the capillary force exerted at the contact line on the molecules. We also emphasize the potential of AFM to clearly decorrelate the effects of topographical and chemical defects and monitor, with a subsecond time resolution, the dynamics of molecules adsorption on a surface.

A computational model for hepatotoxicity by coupling drug transport and acetaminophen metabolism equations.

The spatial distributions of cytochrome P450 (CYP450) and glutathione (GSH) in liver lobules determine the heterogeneous hepatotoxicity of acetaminophen (APAP). Their interplay in conjunction with blood flow is not well understood. In this paper, we integrate a cellular APAP metabolism model with a sinusoidal blood flow to simulate the temporal-spatial patterns of APAP-induced hepatotoxicity. The heterogeneous distribution of CYP450 and GSH is modeled by linearly varying their reaction rates along the portal triad to the central vein axis of a sinusoid. We found that the spatial distribution of GSH, glutathione S-transferases (GSTs), and CYP450 all contributes to the high acetaminophen protein adduct formation at zone 3 of the lobules. The reversed spatial gradients of CYP450 and GSH cause quick depletion of GSH, which is further accelerated by the distribution of GST. The hepatic flow congestion and hyperperfusion however do not seem to play a significant role in the zonal hepatotoxicity. The simulation results may be useful for understanding the APAP-induced hepatotoxicity and associated pharmaceutical treatment.