A heavy dust fell in Beijing on April [16][17] 2006. The dust storm formed in middle and western Inner Mongolia, China, under a strong Mongolian Cyclone. During the dust fall, the near-surface wind speed was insignificant in Beijing. The minimal wind speed at ground level indicates that the dust must have been transported by upper northwestern winds, and the local dust of Beijing contributed little to dust fall. The lack of a contribution from local dust differed from previous dust fall events in Beijing. Therefore, this dust fall provides good information on the dust source. Dust samples colleted during this event and Pleistocene loess samples from the Beijing area were analyzed for magnetic susceptibility, bulk particle and quartz grain size distributions, bulk particle and quartz micro-textures, mineralogy, carbonate content, major element concentrations, trace element and rare earth element (REE) concentrations, and the oxygen isotope composition of quartz. The results indicate the following. (1)

Macrophages infiltration and activation in myocardium is a pivotal immunopathological lead to hypertensive cardiac micro-injury, but underlying mechanisms remain elusive. We have found that CD8 KO or CD8+ T cells depletion by antibody significantly reduce cardiac pro-fibrotic inflammatory responses induced by angiotensin II (Ang II) infusion, whereas CD8 KO mice reconstituted with CD8+ T cells became sensitive. More importantly, CD8+ T cells are required for macrophage infiltration in myocardium and subsequent activation to express pro-inflammatory cytokines and chemokines, including MCP-1. Furthermore, transwell experiments showed that macrophage activation requires direct contact with activated CD8+ T cells, but with TCR dispensable. TCR-independent activation of macrophage is further confirmed in vivo, where OT-I transgenic mice show a similar cardiac pro-inflammatory response to Ang II as wt mice. Finally, IFNγ seems required for influx and activation of CD8+ T cells in myocardium in response to Ang II, that subsequently activate macrophages in the onset of cardiac inflammation. Thus, TCR-independent innate nature of CD8+ T cells is both necessary and sufficient for macrophage-induced hypertensive cardiac fibrosis. In conclusion, TCR-independent activation of macrophages by CD8+ T cells casts yet a novel innate function of T cells that is required to activate inflammatory response of macrophages to danger signals.