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.

The five unsymmetrical ligands 2- [1-(2,6-dibenzhydryl-4-tert-butylphenylimino)and the symmetrical ligand 2,6-bis(1-(2,6-dibenzhydryl-4-tertbutylphenylimino)ethyl)pyridine (L6) have been prepared and characterized by FT IR and 1 H/ 13 C NMR spectroscopy and elemental analysis. The treatment of L1−L6 with FeCl 2 •4H 2 O afforded the corresponding ferrous chloride complexes (Fe1− Fe6) in excellent yields. A distorted-square-pyramidal geometry with a τ 5 value of 0.13 is a feature of the X-ray structure of Fe3; broad paramagnetically shifted peaks are revealed in the 1 H NMR spectra for all the iron complexes in solution. On activation with either MAO or MMAO cocatalyst, all iron complexes displayed high activities with modest variations in activities at elevated temperature (up to 12.0 × 10 6 , 12.4 × 10 6 , 12.8 × 10 6 , and 13.1 × 10 6 g of PE (mol of Fe) −1 h −1 at 50, 60, 70, and 80 °C, respectively). The activity at 80 °C is approximately 5 times higher than that of Brookhart/Gibosn's classical iron precatalyst (Fe0) under identical conditions. Moreover, the nature of the methylaluminoxane cocatalyst employed had a marked effect in defining the end groups of the polymer chain. For example, using MAO cocatalyst, vinyl and n-propyl end groups are formed with a relative ratio of 0.66/0.44, whereas for the MMAO cocatalyst, polymer chains undergo termination with isobutyl, n-propyl, and vinyl end groups having a relative ratio of 0.49/0.33/0.18, indicating that both chain transfer to Al(R) 3 and β-hydride elimination mechanisms are functional.

Long noncoding RNAs have been implicated in neuropathy. Here, we identify and validate a long noncoding RNA, MRAK009713, as the primary regulator of neuropathic pain in chronic constriction injury (CCI) rats. MRAK009713 expression was markedly increased in CCI rats associated with enhanced pain behaviors, and small interfering RNA against MRAK009713 significantly reduced both mechanical and thermal hyperalgesia in the CCI rats. MRAK009713 is predicted to interact with the nociceptive P2X3 receptor by CatRAPID, a bioinformatics technology. Overexpression of MRAK009713 markedly increased expression of P2X3 in the dorsal root ganglia of the control rats, and MRAK009713 small interfering RNA significantly inhibited the P2X3 expression in the dorsal root ganglia of the CCI rats. MRAK009713 directly interacted with the P2X3 protein heterologously expressed in the human embryonic kidney (HEK) 293 cells and potentiated P2X3 receptor function. Thus, MRAK009713 is a novel positive regulator of neuropathic pain in rats through regulating the expression and function of the P2X3 receptor.

Mixed carbocyclic-fused bis(arylimino)pyridine-cobalt(ii) chlorides, on activation with either MAO or MMAO, displayed high activities for ethylene polymerization affording linear polyethylene waxes; high selectivity for vinyl end-groups is a feature of MAO-promoted systems.

Background: The protective effect of metformin (MET) on abdominal aortic aneurysm (AAA) has been reported. However, the related mechanism is still poor understood. In this study, we deeply investigated the role of metformin in AAA pathophysiology. Methods: Angiotensin II (Ang-II) was used to construct the AAA model in ApoE −/− mice. The related mechanism was explored using Western blot and quantitative real time PCR (qRT-PCR). We also observed the morphological changes in the abdominal aorta and the influence of metformin on biological behaviors of rat abdominal aortic VSMCs. Results: The PI3K/AKT/mTOR pathway was activated in aneurysmal wall tissues of AAA patients and rat model. Treatment with metformin inhibited the breakage and preserved the elastin structure of the aorta, the loss of collagen, and the apoptosis of aortic cells. In addition, metformin significantly suppressed the activation of the PI3K/AKT/mToR pathway and decreased the mRNA and protein levels of LC3B and Beclin1, which were induced by Ang-II. Moreover, PI3K inhibitors enhanced the effect of metformin while PI3K agonists largely reversed this effect. Interestingly, the cell proliferation, apoptosis, migration and autophagy of vascular smooth muscle cells (VSMCs) induced by Ang-II were also decreased following metformin treatment. PI3K inhibitors and agonists strengthened and weakened the effects of metformin in VSMCs, respectively. Conclusions: Metformin represses the pathophysiology of AAA by inhibiting the activation of PI3K/AKT/mTOR/ autophagy pathway. This repression may be useful as a new therapeutic strategy for AAA.

Kisspeptins are natural ligands of G protein-coupled receptor-54. Activation of KiSS1/G protein-coupled receptor-54 signaling pathways results in potent activation of the hypothalamus-pituitary-gonadal axis and initiates puberty. Recent data have shown that in female mice, KiSS1 is positively regulated by estradiol (E(2)) in the anteroventral periventricular nucleus, an important reproductive neuroendocrine brain region, but negatively regulated in the arcuate nucleus. However, little is known about the molecular mechanisms governing E(2)-modulated KiSS1 expression. Here, we demonstrate that the expression level of the KiSS1 gene was up-regulated with the administration of E(2) in estrogen receptor alpha (ERalpha)-positive hypothalamic GT1-7 cells. Using transient transfection of human KiSS1 gene promoter coupled to a luciferase reporter, E(2) increases promoter activity in the presence of ERalpha. Deletion analysis of KiSS1 promoter indicates that the E(2)-regulated increase in promoter activity depends on the Sp1 sites of the proximal promoter region. Using both EMSAs and chromatin immunoprecipitation analysis, we determined that both Sp1 and Sp3 proteins constitutively associate with the four putative Sp1 sites in vitro, whereas the association of ERalpha with the KiSS1 promoter is dependent on E(2) exposure. Sp1 and ERalpha form a complex in vivo to mediate the E(2)-induced activation of KiSS1 promoter. Interestingly, Sp1 transactivates KiSS1 promoter activity, whereas Sp3 functions as a transcriptional repressor. Together, these results demonstrate that E(2)-dependent transcriptional activation of KiSS1 gene is mediated by ERalpha through the interaction of Sp1/Sp3 proteins with the GC-rich motifs of KiSS1 promoter, providing a molecular mechanism of how steroid hormone feedback regulates KiSS1 expression.