No abstract

Particle size distributions of light-duty vehicle brake wear debris are reported with careful attention paid to avoid sampling biases. Electrical low-pressure impactor and micro-orifice uniform deposit impactor measurements yield consistent size distributions, and the net particulate matter mass from each method is in good agreement with gravimetric filter measurements. The mass mean diameter of wear debris from braking events representative of urban driving is 6 microm, and the number-weighted mean is 1-2 microm for three currently used classes of lining materials: low metallic, semimetallic, and non-asbestos organic (NAO). In contrast, the wear rates are very material dependent, both in number and mass of particles, with 3-4 times higher emissions observed from the low metallic linings as compared to the semimetallic and NAO linings. Wind tunnel and test track measurements demonstrate the appearance of micron size particles that correlate with braking events, with approximately 50% of the wear debris being airborne for the test vehicle in this study. Elemental analysis of the wear debris reveals a consistent presence of the elements Fe, Cu, and Ba in both dynamometer and test track samples.

It is remarkable that the thyroid-stimulating autoantibody shows almost identical receptor-binding features to TSH although the structures and origins of these two ligands are very different. Furthermore, our structure of the TSHR and its complex with M22 provide foundations for developing new strategies to understand and control both glycoprotein hormone receptor activation and the autoimmune response to the TSHR.

No abstract

A complex of the TSH receptor extracellular domain (amino acids 22-260; TSHR260) bound to a blocking-type human monoclonal autoantibody (K1-70) was purified, crystallised and the structure solved at 1 . 9 Å resolution. complexes show a root mean square deviation on all C a atoms of only 0 . 51 Å . These high-resolution crystal structures provide a foundation for developing new strategies to understand and control TSHR activation and the autoimmune response to the TSHR.