Rate-dependent frictional adhesion in natural and synthetic gecko setae.

Geckos owe their remarkable stickiness to millions of dry, hard setae on their toes. In this study, we discovered that gecko setae stick more strongly the faster they slide, and do not wear out after 30,000 cycles. This is surprising because friction between dry, hard, macroscopic materials typically decreases at the onset of sliding, and as velocity increases, friction continues to decrease because of a reduction in the number of interfacial contacts, due in part to wear. Gecko setae did not exhibit the decrease in adhesion or friction characteristic of a transition from static to kinetic contact mechanics. Instead, friction and adhesion forces increased at the onset of sliding and continued to increase with shear speed from 500 nm s(-1) to 158 mm s(-1). To explain how apparently fluid-like, wear-free dynamic friction and adhesion occur macroscopically in a dry, hard solid, we proposed a model based on a population of nanoscopic stick-slip events. In the model, contact elements are either in static contact or in the process of slipping to a new static contact. If stick-slip events are uncorrelated, the model further predicted that contact forces should increase to a critical velocity (V*) and then decrease at velocities greater than V*. We hypothesized that, like natural gecko setae, but unlike any conventional adhesive, gecko-like synthetic adhesives (GSAs) could adhere while sliding. To test the generality of our results and the validity of our model, we fabricated a GSA using a hard silicone polymer. While sliding, the GSA exhibited steady-state adhesion and velocity dependence similar to that of gecko setae. Observations at the interface indicated that macroscopically smooth sliding of the GSA emerged from randomly occurring stick-slip events in the population of flexible fibrils, confirming our model predictions.

Hypochlorous acid modifies calcium release channel function from skeletal muscle sarcoplasmic reticulum.

We have previously demonstrated that H2O2 at millimolar concentrations induces Ca(2+) release from actively loaded sarcoplasmic reticulum (SR) vesicles and induces biphasic [(3)H]ryanodine binding behavior. Considering that hypochlorous acid (HOCl) is a related free radical and has been demonstrated to be a more effective oxidant of proteins, we evaluated the effects of HOCl on sarcoplasmic reticulum Ca(2+)-channel release mechanism. In a concentration-dependent manner, HOCl activates the SR Ca(2+) release channel and induces rapid release of Ca from actively loaded vesicles. HOCl-induced Ca(2+) release is inhibited in the presence of millimolar concentrations of DMSO. High-affinity [(3)H]ryanodine binding is also enhanced at concentrations from 10 to 100 microM. At HOCl concentrations of >100 microM, equilibrium binding is inhibited. HOCl stimulation of binding is inhibited by the addition of dithiothreitol. The direct interaction between HOCl and the Ca(2+) release mechanism was further demonstrated in single-channel reconstitution experiments. HOCl, at 20 microM, activated the Ca(2+) release channel after fusion of a SR vesicle to a bilayer lipid membrane. At 40 microM, Ca(2+)-channel activity was inhibited. Pretreatment of SR vesicles with HOCl inhibited the fluorescence development of a fluorogenic probe specific to thiol groups critical to channel function. These results suggest that HOCl at micromolar concentrations can modify SR Ca(2+) handling.