Impact of Soil Water on the Spectral Characteristics and Accuracy of Energy-Dispersive X-ray Fluorescence Measurement.

Soil water is a major interference in the on-site analysis of soil by energy-dispersive X-ray fluorescence. Apparent consequences of this interference include lowered readings for elemental concentrations and significant changes in spectral characteristics in wet soils compared with dry soils. A rigorous interpretation on this issue remains unresolved. Thus, this study evaluated the impact of soil water on the detection of Ca, Ti, Mn, Fe, Cu, Zn, As, Rb, Sr, and Pb. Specimens were prepared from 11 certified reference soils and 3 field soils with water contents from 0 to ∼40 wt %. Results from three commercial models revealed that the readings were subjected to respective internal quantification algorithms; therefore, they could not provide a fundamental perspective of this issue. We analyzed the spectra to examine the mechanism underlying this phenomenon. The spectra of wet soils feature elevated baseline, increased Compton and Rayleigh scatter peaks, and lowered characteristic peaks of elements. Previous studies attributed the lowered characteristic peaks to the absorption of fluorescent X-rays by water and considered soil water and dry soil as separate layers in the calculation. This work argues that wet soils should be treated as mixtures. Water becomes part of the soil matrix and leads to lower attenuation capability, which could be explained by the matrix effect. Meanwhile, the mass fraction of analytes is lowered because of dilution. Results confirmed that dilution lowers the characteristic peaks, whereas the matrix effect heightens them. When estimating the elemental concentrations on a wet weight basis, the matrix effect becomes the major interference. The Compton compensation method provided satisfying results on correcting the matrix effect caused by soil water on Zn, As, Rb, Sr, and Pb.

MicroRNA-21 regulates non-small cell lung cancer cell proliferation by affecting cell apoptosis via COX-19.

AIMS: This study is to investigate the regulatory effect of microRNA-21 (miR-21) on bone metastasis of non-small cell lung cancer (NSCLC). METHODS: In this study, 18 patients were diagnosed with vertebral column metastasis of NSCLC. MiR-21 or small interfering RNAs were transfected into H2170 cells using Lipofectamine 2000. Real-time PCR was performed to detect miR-21 expression. Western blotting was used to measure the expression of COX-19 protein. Enzymatic activity tests were performed to measure the activity of cytochrome C oxidase. Flow cytometry was used to monitor changes in cell apoptotic rate. MTT assay was used to determine the capability of cell proliferation. RESULTS: Bone metastasis of NSCLC enhanced the levels of miR-21 in NSCLC patients. Proliferation capability of cells with high expression of miR-21 was greater than that of cells with the inhibition of miR-21 expression. High expression of miR-21 promoted cell proliferation by inhibiting cell apoptosis. COX-19 was a key factor in the inhibition of apoptosis by miR-21. Inhibition of COX-19 expression reduced cell proliferation by enhancing cell apoptosis. CONCLUSIONS: This study demonstrates that inhibition of miRNA-21 suppresses NSCLC cell proliferation by promoting cell apoptosis via the decrease of COX-19 expression.

A conditionally immortal clonal stem cell line from human cortical neuroepithelium for the treatment of ischemic stroke.

Transplantation of neural stem cells into the brain is a novel approach to the treatment of chronic stroke disability. For clinical application, safety and efficacy of defined, stable cell lines produced under GMP conditions are required. To this end, a human neural stem cell line, CTX0E03, was derived from human somatic stem cells following genetic modification with a conditional immortalizing gene, c-mycER(TAM). This transgene generates a fusion protein that stimulates cell proliferation in the presence of a synthetic drug 4-hydroxy-tamoxifen (4-OHT). The cell line is clonal, expands rapidly in culture (doubling time 50-60 h) and has a normal human karyotype (46 XY). In the absence of growth factors and 4-OHT, the cells undergo growth arrest and differentiate into neurons and astrocytes. Transplantation of CTX0E03 in a rat model of stroke (MCAo) caused statistically significant improvements in both sensorimotor function and gross motor asymmetry at 6-12 weeks post-grafting. In addition, cell migration and long-term survival in vivo were not associated with significant cell proliferation. These data indicate that CTX0E03 has the appropriate biological and manufacturing characteristics necessary for development as a therapeutic cell line.

Schwann cells as regulators of nerve development.

Myelinating and non-myelinating Schwann cells of peripheral nerves are derived from the neural crest via an intermediate cell type, the Schwann cell precursor [K.R. Jessen, A. Brennan, L. Morgan, R. Mirsky, A. Kent, Y. Hashimoto, J. Gavrilovic. The Schwann cell precursor and its fate: a study of cell death and differentiation during gliogenesis in rat embryonic nerves, Neuron 12 (1994) 509-527]. The survival and maturation of Schwann cell precursors is controlled by a neuronally derived signal, beta neuregulin. Other factors, in particular endothelins, regulate the timing of precursor maturation and Schwann cell generation. In turn, signals derived from Schwann cell precursors or Schwann cells regulate neuronal numbers during development, and axonal calibre, distribution of ion channels and neurofilament phosphorylation in myelinated axons. Unlike Schwann cell precursors, Schwann cells in older nerves survive in the absence of axons, indicating that a significant change in survival regulation occurs. This is due primarily to the presence of autocrine growth factor loops in Schwann cells, present from embryo day 18 onwards, that are not functional in Schwann cell precursors. The most important components of the autocrine loop are insulin-like growth factors, platelet derived growth factor-BB and neurotrophin 3, which together with laminin support long-term Schwann cell survival. The paracrine dependence of precursors on axons for survival provides a mechanism for matching precursor cell number to axons in embryonic nerves, while the ability of Schwann cells to survive in the absence of axons is an absolute prerequisite for nerve repair following injury. In addition to providing survival factors to neurones and themselves, and signals that determine axonal architecture, Schwann cells also control the formation of peripheral nerve sheaths. This involves Schwann cell-derived Desert Hedgehog, which directs the transition of mesenchymal cells to form the epithelium-like structure of the perineurium. Schwann cells thus signal not only to themselves but also to the other cellular components within the nerve to act as major regulators of nerve development.