Road surface mirage： A bunch of hot air？

The inferior mirage from road surfaces is a common phenomenon, which can be easily seen in everyday life. It has been recognized in the literature as a light refraction phenomenon due to the refractive index gradient caused by the temperature gradient in the air strata above the road surfaces. However, it was also suggested that the mirage is just a phenomenon of specular reflection at grazing incidence. Because of the lack of reasonable and quantitative evidence, the generally accepted light refraction theory has not yet been refuted. Here we show some mirror-like reflection images captured from a road surface stretch in Yujiashan North Road, Wuhan, China, when there was no obvious temperature gradient on or above the road, measured on a winter day in December 2009. This provided direct evidence to doubt the temperature induced light refraction mechanism of the inferior mirage. Furthermore, the critical grazing angle of about 0.2° to the road plane where the mirror-like reflection appears could not make the rough surface scatter incident light as a smooth surface according to the Rayleigh criterion. Therefore the phenomenon is a mirrorlike observation effect of scattering from the surface, which cannot be entirely explained by light refraction via air strata. The results demonstrate that the image-formation mechanism and the observer-based-analysis method shown here potentially offer a means of understanding a wide range of scattering phenomena from rough surfaces at grazing angle; for example, the superior mirages of unusual brightness occasionally observed over frozen lakes and the off-specular reflection phenomenon.     

Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6

Toll-like receptors (TLRs) are activated by pathogen-associated molecular patterns to induce innate immune responses and production of pro-inflammatory cytokines, interferons and anti-inflammatory cytokines. TLRs activate downstream effectors through adaptors that contain Toll/interleukin-1 receptor (TIR) domains, but the mechanisms accounting for diversification of TLR effector functions are unclear. To dissect biochemically TLR signalling, we established a system for isolating signalling complexes assembled by dimerized adaptors. Using MyD88 as a prototypical adaptor, we identified TNF receptor-associated factor 3 (TRAF3) as a new component of TIR signalling complexes that is recruited along with TRAF6. Using myeloid cells from TRAF3- and TRAF6-deficient mice, we show that TRAF3 is essential for the induction of type I interferons (IFN) and the anti-inflammatory cytokine interleukin-10 (IL-10), but is dispensable for expression of pro-inflammatory cytokines. In fact, TRAF3-deficient cells overproduce pro-inflammatory cytokines owing to defective IL-10 production. Despite their structural similarity, the functions of TRAF3 and TRAF6 are largely distinct. TRAF3 is also recruited to the adaptor TRIF (Toll/IL-1 receptor domain-containing adaptor-inducing IFN-beta) and is required for marshalling the protein kinase TBK1 (also called NAK) into TIR signalling complexes, thereby explaining its unique role in activation of the IFN response.