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The sorption and rheological properties of an acidic polyaromatic compound (C5PeC11), which can be used to further our understanding in the behavior of asphaltenes, are determined experimentally. The results show that C5PeC11 exhibits the type of pH-dependent surface activity and interfacial shear rheology observed in C6-asphaltenes with a decrease in the interfacial tension concomitant to the elastic modulus when the pH increases. Surface pressure-area (Π-A) isotherms show evidence of aggregation behavior and π-π stacking at both the air/water and oil/water interfaces. Similarly, interactions between adsorbed C5PeC11 compounds are evidenced through desorption experiments at the oil/water interface. Contrary to indigenous asphaltenes, adsorption is reversible, but desorption is slower than for noninteracting species. The reversibility enables us to create layers reproducibly, whereas the presence of interactions between the compounds enables us to mimic the key aspects of interfacial activity in asphaltenes. Shear and dilatational rheology show that C5PeC11 forms a predominantly elastic film both at the liquid/air and the liquid/liquid interface. Furthermore, a soft glassy rheology model (SGR) fits the data obtained at the liquid/liquid interface. Yet, it is shown that the effective noise temperature determined from the SGR model for C5PeC11 is higher than for indigenous asphaltenes measured under similar conditions. Finally, from a colloidal and rheological standpoint, the results highlight the importance of adequately addressing the distinction between the material functions and true elasticity extracted from a shear measurement and the apparent elasticity measured in dilatational-pendant drop set-ups.

Interfacial transport phenomena play an important role in the dynamics of liquid interfaces found in emulsions, foams, and membranes. Both macroscopic and microscopic measurements of interfacial transport and rheology can be made, the former typically relying on the use of at least millimeter-scale probes, and the latter exploiting the motion of micrometer-scale probes. Recent publications have shown multiple orders of magnitude differences between experimentally observed diffusivities in passive microrheology, and the diffusivities expected based on macroscopic measurements of the surface rheology. In the present work, interfacial rheological measurements were made with both microrheological and macrorheological methods and the results are compared for different monolayers at an air-water interface. We have identified multiple aspects of particle-tracking microrheology that can contribute to orders-of-magnitude disagreement with macrorheological methods. In particular, unintentional tracking of particles not residing at the interface, the presence of large-scale interfacial heterogeneities, and underestimating static noise can all decrease estimates of surface viscosity from particle-tracking microrheology by orders of magnitude. After taking care to address these artifacts, we show that viscosities obtained from both methods agree well for poly(tert-butyl methacrylate) (PtBMA), and for dipalmitoylphosphatidylcholine (DPPC), but disagree by orders of magnitude for hexadecanol. In poly(tert-butyl acrylate) (PtBA), large-scale heterogeneities prevented us from obtaining representative surface viscosities. By making surface viscosity measurements in an interfacial stress rheometer (ISR) with needles of different aspect ratio, we show that compressibility or Marangoni stress related effects may be contributing to the orders of magnitude disagreement in micro and macrorheological measurements observed in the hexadecanol system.

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A 3-step process regulated by hemodynamics was necessary for robust thrombus propagation: First, immobilized tissue factor initiates coagulation and fibrin deposition within a low flow niche defined by a secondary vortex in the pocket of a model venous valve. Second, a primary vortex delivers platelets to the fibrin interface in a red blood cell-dependent manner. Third, platelets adhere to fibrin, activate through glycoprotein VI, express phosphatidylserine, and subsequently promote thrombus growth beyond the valve sinus and into the bulk flow.