I am writing to you to bring to your attention a new Master Course on Computational Mechanics, which has been awarded the Erasmus Mundus label.

It is an international Master course given jointly in English by the Universidad Politécnica de Cataluña (Barcelona), University of Wales Swansea), Ecole Centrale Nantes and Universität Stuttgart with the collaboration of CIMNE International Centre for Numerical Methods in Engineering, Barcelona). The Erasmus Mundus program:

In his interesting response to our comment posted on 11/28, Ning Wang focused on the transmission of a local force generated at the adhesion site(s). We agree that this is a question important to our understanding of the signaling to the nucleus. The question is not only about the range of the force transmission but also about the magnitude of such force because the nucleus is several times stiffer than the cytoskeleton.

It is commonly assumed that grain boundary sliding can control plastic deformation in fine grained crystalline solids.  Superplasticity is often considered to be controlled by grain boundary sliding, for example.  I have never accepted that view, though my own opinion is very much at odds with the commonly accepted picture.  When I was asked to write a paper in honor of Professor F.R.N. Nabarro's 90th birthday (Prof.

This is a paper by Jizhong Lou and myself, which is in press in Biophysical Journal.

Abstract.  Catch bonds, whose lifetimes are prolonged by force, have been observed in selectin-ligand interactions and other systems. Several biophysical models have been proposed to explain this counter-intuitive phenomenon, but none was based on the structure of the interacting molecules and the noncovalent interactions at the binding interface. Here we used molecular dynamics simulations to study changes in structure and atomic-level interactions during forced unbinding of P-selectin from P-selectin glycoprotein ligand-1. A mechanistic model for catch bonds was developed based on these observations. In the model, "catch" results from forced opening of an interdomain hinge that tilts the binding interface to allow two sides of the contact to slide against each other. Sliding promotes formation of new interactions and even rebinding to the original state, thereby slowing dissociation and prolonging bond lifetimes. Properties of this sliding-rebinding mechanism were explored using a pseudo-atom representation and Monte Carlo simulations. The model has been supported by its ability to fit experimental data and can be related to previously proposed two-pathway models.

We know - or believe - protein function is determined by structure. Crystallographic and NMR studies can provide protein structures with atomic-level details at equilibrium. MD simulations can follow protein conformational changes in time with fs temporal resolution in the absence or presence of a bias mechanism, e.g., applied force, used to induce such changes.

This is a paper that has been accepted for publication in the Journal of the Mechanics and Physics of Solids from our group. The paper describes the combined effect of material inertia and inhomogeneous material property variation on spontaneous cohesive-crack propagation in functionally graded materials. The preprint is attached as a PDF.

Abstract- The effects of combining functionally graded materials of different inhomogeneous property gradients on the mode-3 propagation characteristics of an interfacial crack are numerically investigated. Spontaneous interfacial crack propagation simulations were performed using the newly developed spectral scheme. The numerical scheme derived and implemented in the present work can efficiently simulate planar crack propagation along functionally graded bimaterial interfaces. The material property inhomogeneity was assumed to be in the direction normal to the interface. Various bimaterial combinations were simulated by varying the material property inhomogeneity length scale. Our parametric study showed that the inclusion of a softening type functionally graded material in the bimaterial system leads to a reduction in the fracture resistance indicated by the increase in crack propagation velocity and power absorbed. An opposite trend of increased fracture resistance was predicted when a hardening material was included in the bimaterial system. The cohesive tractions and crack opening displacements were altered due to the material property inhomogeneity, but the stresses ahead of the cohesive zone remained unaffected.

This is a model of a single semiflexible polymer chain under sustained tension. The model captures two key features of the cytoskeletal rheology: a) the power-law behavior; and b) the dependence of the power-law on mechanical prestress. The model also reveals the underlying mechanisms.

The essence of mechanobiology is, probably, the interrelation between mechanical and biochemical factors.  An exciting example of such phenomenon is signaling associated with the interaction between the cell and extracellular matrix (EM).  While some purely biochemical pathways initiated in the area of contact of the cell and EM are known, there are interesting ideas how the mechanical forces, stresses and strains can be involved too. This view goes back to works of Donald Ingber's group in the 90s that showed how perturbations of the adhesion area as a whole and of an individual integrin result in deformation of the cell nucleus. Interestingly, a distinguished oncologist at Johns Hopkins, Donald Coffey, published similar experimental results about the same time, and he also demonstrated that the observed cytoskeleton/nucleus interaction is different in tumor cells. There are several separate pieces of the puzzle that have been resolved: mechanical forces are generated at focal adhesions, the cytoskeleton is involved, nucleus deforms, gene expression changes as a result of perturbation of the adhesions, however, the whole picture of the interrelated mechanical and biochemical factors has yet to be understood. We recently published some results on this topic in the Journal of Biomechanical Engineering (Jean et al., 2004 and 2005). I was glad to find an interest in the same problem from some participants of this website (e.g., N. Wang, Z. Suo,   Long-distance propagation of forces in a cell, 2005 and P.R. LeDuc and R.M. Bellin, Nanoscale Intracellular Organization and Functional Architecture Mediating Cellular Behavior, 2006). This aspect of mechanotransduction is important for many areas beyond mechanics such as cancer, wound healing, cell adhesion and motility, effect of surface micro- and nanopatterning, etc.

Listed below is a recent publication of mine in Science for your possible interest and critics. This is a review article focusing on the multiscale simulation issues in strucutral composites. I will be more than happy to discuss with those of you who are interested. The following is the abstract.

The difficult challenge of simulating diffuse and complex fracture patterns in tough structural composites is at last beginning to yield to conceptual and computational advances in fracture modeling. Contributing successes include the refinement of cohesive models of fracture and the formulation of hybrid stress-strain and traction-displacement models that combine continuum (spatially averaged) and discrete damage representations in a single calculation. Emerging hierarchical formulations add the potential of tracing the damage mechanisms down through all scales to the atomic. As the models near the fidelity required for their use as virtual experiments, opportunities arise for reducing the number of costly tests needed to certify safety and extending the design space to include material configurations that are too complex to certify by purely empirical methods.