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As an initial step towards understanding the molecular mechanisms by which plants become invasive, we present here the first transcriptome analysis for an invasive weed Mikania micrantha. The analysis was based on the 75-nucleotide short reads data generated by the Illumina Genome Analyzer II system. A total of 31 131 unique sequences were assembled de novo based on 8.7 million filtered paired-end sequence reads for the transcriptome of an individual M. micrantha growing in the field. 73 % of the unique sequences showed significant similarity to existing proteins in the NCBI database, and 21 448 could be grouped based on gene ontology assignments. Of particular interest are the sequences that share homology with genes involved in genome evolution, plasticity, secondary metabolism and defense responses.

Background. Crescentic glomerulonephritis (CGN) presents a rapidly progressive glomerulonephritis clinically, in which macrophages play a crucial role in the pathogenesis. However, the precise molecular mechanism of macrophage recruitment and activation has not been fully elucidated. C-C chemokines, monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α and β (MIP-1α and MIP-1β), are major chemoattractants for macrophages. We attempted to study the expression of C-C chemokines and their correlation with CD68-positive macrophages in crescentic glomeruli to investigate further their possible roles in crescent formation and progression to fibrosis in different types of human CGN. Methods. The expression of MCP-1, MIP-1α, MIP-1β and CD68 was detected in glomeruli with different forms of crescents (cellular, fibrocellular and fibrous crescents) by immunohistochemistry in serial sections of renal biopsies taken from 32 patients with biopsy-proven CGN including eight patients with anti-glomerular basement membrane (GBM) disease (type I CGN), 12 patients with immune complex-mediated CGN (type II CGN) and another 12 patients with pauci-immune CGN (type III CGN) enrolled in this study. Eight normal human kidneys were obtained from cadaveric renal transplant donors whose kidneys were technically unsuitable for transplantation, serving as controls. Results. MCP-1, MIP-1α, MIP-1β and CD68 were undetectable in glomeruli of normal kidney. In crescentic biopsies, MCP-1, MIP-1α, MIP-1β and CD68 were detected in fibrocellular crescents and were even more prominent in cellular crescents, but were undetectable in fibrous crescents. Using consecutive sections for staining, it was demonstrated that a high proportion of infiltrating CD68-positive macrophages, mainly localized to the area of the expression of chemokines, were MCP-1, MIP-1α and MIP-1β positive in crescents. Chemokines were expressed mainly by CD68-positive macrophages and parietal epithelial cells in crescents. The number of MCP-1- and MIP-1α-positive cells in glomeruli with cellular crescents was positively correlated with the number of CD68-positive cells (r = 0.568 and 0.749, respectively, both P < 0.01). The number of MCP-1- and MIP-1α-positive cells and the incidence of Bowman''s capsule rupture in glomeruli of patients with type I CGN were higher than those of type II and type III CGN. Conclusions. These observations suggest that the expressed C-C chemokines, MCP-1, MIP-1α and MIP-1β, may mediate the inflammatory process of crescent formation and progression to fibrosis. The strong correlation of MCP-1 and MIP-1α with infiltrating macrophages within glomeruli with cellular crescents suggested that these chemokines might be of particular importance for macrophage recruitment to this site. MCP-1 and MIP-1α were correlated to type I CGN with its more severe inflammatory course and worse prognosis. The variance of glomerular expression of C-C chemokines may contribute to the difference in histopathological features and prognosis in these three types of CGN. [ABSTRACT FROM AUTHOR]

This work demonstrates, by frequency-dependent electrical measurements, significant variation associated with interfacial defects in Co/ZnO nanocomposites (NCs) for electrical and magnetic transport. Radio-frequency impedance measurements showed that heat treatment in an ultrahigh vacuum (UHV) increased interfacial defect density. Interfacial defects-assisted transport reduced the magnetoresistance (MR) ratio from 5.04% for the as-grown sample to 0.17% following heat treatment in UHV. The evolution of the onset frequency of power-law dispersion conductivity revealed that the increase in the interfacial defect density in Co/ZnO NCs upon heat treatment was consistent with the change in MR. [ABSTRACT FROM AUTHOR]

Summary The three dimensional elasto-viscoplastic composite element method is formulated in this paper for rock masses reinforced by a fully-grouted bolt. If a bolt segment penetrates a finite element representing the rock mass, then a composite element is formed including five sub-elements corresponding to the rock material, the grout material, the bolt material, the rock-grout interface and the bolt-grout interface. The displacements in each sub-element are interpolated from the corresponding nodal displacements of the composite element. By the virtual work principle the governing equation for the solution of the nodal displacements can be formulated. The elasto-viscoplastic characteristics of the materials are considered in the formulation. The new model can be incorporated into the conventional finite element analysis grid, in which several composite elements have fully grouted bolts embedded. In this way the mesh generation of large scale bolted rock structures becomes convenient and feasible. The model has been implemented in a FEM program, and a comparative study between the numerical analysis and a pull out field test has been carried out, from which the validity and the robustness of the new model are justified. [ABSTRACT FROM AUTHOR]

The intrinsic flux noise observed in superconducting quantum interference devices (SQUIDs) is thought to be due to the fluctuation of electron-spin impurities, but the frequency and temperature dependence observed in experiments do not agree with the usual 1/f models. We present theoretical calculations and experimental measurements of flux noise in rf SQUID flux qubits that show how these observations, and previous reported measurements, can be interpreted in terms of a spin-diffusion constant that increases with temperature. We fit measurements of flux noise in 16 devices, taken in the 20-80 mK temperature range, to the spin-diffusion model. This allows us to extract the spin-diffusion constant and its temperature dependence, suggesting that the spin system is close to a spin-glass phase transition. [ABSTRACT FROM AUTHOR]

Activated microglia may be detrimental to neuronal survival in a number of neurodegenerative diseases. Thus, strategies that reduce microglial neurotoxicity may have therapeutic benefit. Stimulation of group II metabotropic glutamate (mGlu) receptors on rat primary microglia with the specific group II agonist 2S,2'R,3'R-2-(2',3'-dicarboxy-cyclopropyl)glycine for 24 h induced microglial activation and resulted in a neurotoxic microglial phenotype. These effects were attributable to preferential mGlu2 stimulation, because N-acetyl-L-aspartyl-L-glutamate, a specific mGlu3 agonist, did not induce microglial activation or neurotoxicity. Stimulation of microglial mGlu2 but not mGlu3 induced caspase-3 activation in cerebellar granule neurons in culture, using microglial-conditioned media as well as cocultures. Stimulation of microglial mGlu2 induced tumor necrosis factor-alpha (TNFalpha) release, which contributed to microglial neurotoxicity mediated via neuronal TNF receptor 1 and caspase-3 activation. Stimulation of microglial group I or III mGlu receptors did not induce TNFalpha release. TNFalpha was only neurotoxic in the presence of microglia or microglial-conditioned medium. The toxicity of TNFalpha could be prevented by coexposure of neurons to conditioned medium from microglia stimulated by the specific group III agonist L-2-amino-4-phosphono-butyric acid. The neurotoxicity of TNFalpha derived from mGlu2-stimulated microglia was potentiated by microglial-derived Fas ligand (FasL), the death receptor ligand. FasL was constitutively expressed in microglia and shed after mGlu2 stimulation. Our data suggest that selective and inverse modulation of microglial mGlu2 and mGlu3 may prove a therapeutic target in neuroinflammatory diseases such as Alzheimer's disease and multiple sclerosis.