Collagen and myosin fibrils are endogenous harmonophores that both give rise to Second Harmonic Generation (SHG). By combining four polarization SHG images provided by a scanning microscope, we show that the orientation of the principal axis of the nonlinear susceptibility tensor chi(2) can be determined for each pixel of the image. The ratio rho = chi33/chi15 of the principal components of chi(2) of collagen and myosin was obtained with the same method, and found within the range 1.6-1.8 and 0.5-0.6 respectively. The orientation of the principal axis of chi(2) is shown to be correlated to the orientation of the fibrils themselves. This provides a straightforward method, which we call Orientation Field-Second Harmonic Microscopy (OF-SHM), to reconstruct orientation fields of fibrils at various scales and resolutions in different biological systems (from muscle sarcomere to the whole embryo).

Background: E-selectin interactions with glycoprotein ligands mediate the initial capturing of cells out of flow. Results: Adopting a Biacore-based immunoprecipitation binding assay unraveled differential binding kinetics of monomeric (m) versus dimeric (d) E-selectin to endogenous ligands. Conclusion: Although mE-selectin binds transiently, dE-selectin binds with remarkably slow on-and off-rates. Significance: Transitioning from monomeric to dimeric E-selectin could enable fast but firm capturing of cells out of flow.

The adult vasculature is comprised of three distinct compartments: the arteries, which carry blood away from the heart and display a divergent flow pattern; the capillaries, where oxygen and nutrient delivery from blood to tissues, as well as metabolic waste removal, occurs; and the veins, which carry blood back to the heart and are characterized by a convergent flow pattern. These compartments are organized in series as regard to flow, which proceeds from the upstream arteries to the downstream veins through the capillaries. However, the spatial organization is more complex, as veins may often be found paralleling the arteries. The factors that control the morphogenesis of this hierarchically branched vascular network are not well characterized. Here, we explain how arteries exert a morphological control on the venous pattern. Indeed, during vertebrate development, the following transition may be observed in the spatial organization of the vascular system: veins first develop in series with the arteries, the arterial and venous territories being clearly distinct in space ͑cis-cis configuration͒. But after some time, new veins grow parallel to the existing arteries, and the arterial and venous territories become overlapped, with extensive and complex intercalation and interdigitation. Using physical arguments, backed up by experimental evidence ͑biological data from the literature and in situ optical and mechanical measurements of the chick embryo yolk-sac and midbrain developing vasculatures͒, we explain how such a transition is possible and why it may be expected with generality, as organisms grow. The origin of this transition lies in the remodeling of the capillary tissue in the vicinity of the growing arteries. This remodeling lays down a prepattern for further venous growth, parallel to the existing arterial pattern. Accounting for the influence of tissue growth, we show that this prepatterned path becomes favored as the body extends. As a consequence, a second flow route with veins paralleling the arteries ͑cis-trans configuration͒ emerges when the tissue extends. Between the cis-cis and cis-trans configurations, all configurations are in principle possible, and self-organization of the vessels contributes to determining their exact pattern. However, the global aspect depends on the size at which the growth stops and on the growth rate.

The coupling between cell-cell and cell-matrix adhesion systems is known to affect the stability of the adhesive status of cells, as well as tissue cohesion. In this work, we perform quantitative assays of integrin-cadherin cross talk in controlled and reproducible conditions. This is achieved by plating cells on microprinted fibronectin patterns of different sizes, and simulating the formation of an intercellular contact with a microbead coated with E-cadherin extracellular domains and brought to the cell membrane. Using an optical trap, we measure the average rigidity modulus of the E-cadherin bead-cell contact as a function of the contact incubation time and of the cell spreading area. For a given incubation time, this rigidity modulus decreases by three orders of magnitude as the cell-matrix contact area, A, increases from 100 to 700 μm(2). In a similar way, the dynamics of formation of the bead-cell contact gets slower as this area increases. This is clear evidence for a strong negative feedback from cell-fibronectin onto cell-cell adhesive contacts, for which we discuss some possible mechanisms.