Nonlinear description of transversal motion in a laminar boundary layer with streaks

The nonlinear streamwise growth of a spanwise periodic array of steady streaks in a flat plate boundary layer is numerically computed using the well known Reduced Navier-Stokes formulation. It is found that the flow configuration changes substantially when the amplitude of the streaks grows and the nonlinear effects come into play. The transversal motion (in the wall normal-spanwise plane), which is normally not considered, becomes non-negligible in the nonlinear regime, and it strongly distorts the streamwise velocity profiles, which end up being quite different from those predicted by the linear theory. We analyze in detail the resulting flow patterns for the nonlinearly saturated streaks, and compare them with available experimental results.

Nonlinear description of transversal motion in a laminar boundary layer with streaks

The nonlinear streamwise growth of a spanwise periodic array of steady streaks in a flat plate boundary layer is numerically computed using the well known Reduced Navier- Stokes formulation. It is found that the flow configuration changes substantially when the amplitude of the streaks grows and the nonlinear effects come into play. The transversal motion (in the wall normal-spanwise plane), which is normally not considered, becomes non-negligible in the nonlinear regime, and it strongly distorts the streamwise velocity profiles, which end up being quite different from those predicted by the linear theory. We analyze in detail the resulting flow patterns for the nonlinearly saturated streaks, and compare them with available experimental results.

Controlled unzipping of a bacterial surface layer with atomic force microscopy

We have combined high-resolution atomic force microscopy (AFM) imaging and force spectroscopy to gain insight into the interaction forces between the individual protomers of the hexagonally packed intermediate (HPI) layer of Deinococcus radiodurans. After imaging the HPI layer, the AFM stylus was attached to individual protomers by enforced stylus-sample contact to allow force spectroscopy experiments. Imaging of the HPI layer after recording force-extension curves allowed adhesion forces to be correlated with structural alterations. By using this approach, individual protomers of the HPI layer were found to be removed at pulling forces of ≈300 pN. Furthermore, it was possible to sequentially unzip entire bacterial pores formed by six HPI protomers. The combination of high-resolution AFM imaging of individual proteins with the determination of their intramolecular forces is a method of studying the mechanical stability of supramolecular structures at the level of single molecules.

Induction of resistance to diabetes in non-obese diabetic mice by targeting CD44 with a specific monoclonal antibody

Inflammatory destruction of insulin-producing β cells in the pancreatic islets is the hallmark of insulin-dependent diabetes mellitus, a spontaneous autoimmune disease of non-obese diabetic mice resembling human juvenile (type I) diabetes. Histochemical analysis of diabetic pancreata revealed that mononuclear cells infiltrating the islets and causing autoimmune insulitis, as well as local islet cells, express the CD44 receptor; hyaluronic acid, the principal ligand of CD44, is detected in the islet periphery and islet endothelium. Injection of anti-CD44 mAb 1 hr before cell transfer of diabetogenic splenocytes and subsequently on alternate days for 4 weeks induced considerable resistance to diabetes in recipient mice, reflected by reduced insulitis. Contact sensitivity to oxazolone was not influenced by this treatment. A similar antidiabetic effect was observed even when the anti-CD44 mAb administration was initiated at the time of disease onset: i.e., 4–7 weeks after cell transfer. Administration of the enzyme hyaluronidase also induced appreciable resistance to insulin-dependent diabetes mellitus, suggesting that the CD44–hyaluronic acid interaction is involved in the development of the disease. These findings demonstrate that CD44-positive inflammatory cells may be a potential therapeutic target in insulin-dependent diabetes.