Progress in combating aeolian desertification (land degradation resulting from wind erosion) has been achieved in an agro-pastoral ecotone of northern China since the mid-1980s. This paper reviews three common measures used to combat and control aeolian desertification in such regions. In addition, it introduces a case study on the recovery of a degraded semi-arid ecosystem to provide regional lessons and support theoretical and practical approaches to desertification prevention and reversal on a global scale. On the basis of the analysis and evaluation of three kinds of typical measures and one regional scale case, this study shows that human-caused aeolian desertified land can be rehabilitated. Although the technologies and management of combating aeolian desertification in an agro-pastoral ecotone of northern China still need further improvement through more experimentation and practical application in the future, the experience gained to date contains important lessons for the recovery of degraded land on a global scale.

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J. Neurochem. (2012) 120, 721–731. Abstract Nogo‐66 is a 66‐amino‐acid‐residue extracellular domain of Nogo‐A, which plays a key role in inhibition neurite outgrowth of central nervous system through binding to the Nogo‐66 receptor (NgR) expressed on the neuron. Recent studies have confirmed that NgR is also expressed on the surface of macrophages/microglia in multiple sclerosis, but its biological effects remain unknown. In the present study, our results demonstrated that Nogo‐66 triggered microglia anti‐adhesion and inhibited their migration in vitro, which was mediated by NgR. We also assessed the roles of small GTP (glycosyl phosphatidylinositol)‐binding proteins of the Rho family as the downstream signal transducers on the microglia adhesion and mobility induced by Nogo‐66. The results showed that Nogo‐66 activated RhoA and reduced the activity of Cdc42 in the meanwhile, which further triggered the anti‐adhesion and migration inhibition effects to microglia. Nogo‐66 inhibited microglia polarization and membrane protrusion formation, thus might eventually contribute to the decreasing capability of cell mobility. Taken together, the Nogo‐66/NgR pathway may modulate neuroinflammation via mediating microglia adhesion and migration in addition to its role in neurons. Better understanding the relationship between Nogo‐66/NgR and neuroinflammation may help targeting NgR for treating central nervous system diseases related with inflammation.