Collective behavior of asperities as a model for friction and adhesion

Understanding friction and adhesion in static and sliding contact of surfaces is important in numerous physical phenomena and technological applications. Most surfaces are rough at the microscale, and thus the real area of contact is only a fraction of the nominal area. The macroscopic frictional and adhesive response is determined by the collective behavior of the population of evolving and interacting microscopic contacts. This collective behavior can be very different from the behavior of individual contacts. It is thus important to understand how the macroscopic response emerges from the microscopic one. In this thesis, we develop a theoretical and computational framework to study the collective behavior. Our philosophy is to assume a simple behavior of a single asperity and study the collective response of an ensemble. Our work bridges the existing well-developed studies of single asperities with phenomenological laws that describe macroscopic rate-and-state behavior of frictional interfaces. We find that many aspects of the macroscopic behavior are robust with respect to the microscopic response. This explains why qualitatively similar frictional features are seen for a diverse range of materials. We first show that the collective response of an ensemble of one-dimensional independent viscoelastic elements interacting through a mean field reproduces many qualitative features of static and sliding friction evolution. The resulting macroscopic behavior is different from the microscopic one: for example, even if each contact is velocity-strengthening, the macroscopic behavior can be velocity-weakening. The framework is then extended to incorporate three-dimensional rough surfaces, long- range elastic interactions between contacts, and time-dependent material behaviors such as viscoelasticity and viscoplasticity. Interestingly, the mean field behavior dominates and the elastic interactions, though important from a quantitative perspective, do not change the qualitative macroscopic response. Finally, we examine the effect of adhesion on the frictional response as well as develop a force threshold model for adhesion and mode I interfacial cracks.

Establishing the C. elegans uterine seam cell (utse) as a novel model for studying cell behavior

The molecular inputs necessary for cell behavior are vital to our understanding of development and disease. Proper cell behavior is necessary for processes ranging from creating one’s face (neural crest migration) to spreading cancer from one tissue to another (invasive metastatic cancers). Identifying the genes and tissues involved in cell behavior not only increases our understanding of biology but also has the potential to create targeted therapies in diseases hallmarked by aberrant cell behavior.

A well-characterized model system is key to determining the molecular and spatial inputs necessary for cell behavior. In this work I present the C. elegans uterine seam cell (utse) as an ideal model for studying cell outgrowth and shape change. The utse is an H-shaped cell within the hermaphrodite uterus that functions in attaching the uterus to the body wall. Over L4 larval stage, the utse grows bidirectionally along the anterior-posterior axis, changing from an ellipsoidal shape to an elongated H-shape. Spatially, the utse requires the presence of the uterine toroid cells, sex muscles, and the anchor cell nucleus in order to properly grow outward. Several gene families are involved in utse development, including Trio, Nav, Rab GTPases, Arp2/3, as well as 54 other genes found from a candidate RNAi screen. The utse can be used as a model system for studying metastatic cancer. Meprin proteases are involved in promoting invasiveness of metastatic cancers and the meprin-likw genes nas-21, nas-22, and toh-1 act similarly within the utse. Studying nas-21 activity has also led to the discovery of novel upstream inhibitors and activators as well as targets of nas-21, some of which have been characterized to affect meprin activity. This illustrates that the utse can be used as an in vivo model for learning more about meprins, as well as various other proteins involved in metastasis.