Promotion of Myelopoiesis in Myelosuppressed Mice by Ganoderma lucidum Polysaccharides

Our previous studies demonstrated that Ganoderma lucidum polysaccharides (Gl-PS) exhibit potent immunomodulating effects. Immunomodulation plays an important role in hematopoiesis. To investigate the possible mechanism by which Gl-PS promote myelopoiesis during myelosuppression induced by cyclophosphamide, mice were injected intraperitoneally (i.p.) once daily with 2.5 mg/kg of Gl-PS for 10 days and were treated i.p. once daily with cyclophosphamide (100 mg/kg) on days 2 through 4. In the present study in vivo and in vitro, we find that Gl-PS selectively bind to bone marrow stromal cells, stimulate the secretion of hematopoietic growth factors, and enhance the clonogenic activities of hematopoietic and stromal cells to promote hematopoiesis in myelosuppressed mice

Method of determining cosmological parameter ranges with samples of candles with an intrinsic distribution

In this paper, the effect of the intrinsic distribution of cosmological candles is investigated. We find that, in the case of a narrow distribution, the deviation of the observed modulus of sources from the expected central value could be estimated within a ceratin range. We thus introduce a lower and upper limits of $\chi ^{2}$, $\chi_{\min}^{2}$ and $\chi_{\max}^{2}$, to estimate cosmological parameters by applying the conventional minimizing $\chi ^{2}$ method. We apply this method to a gamma-ray burst (GRB) sample as well as to a combined sample including this GRB sample and an SN Ia sample. Our analysis shows that: a) in the case of assuming an intrinsic distribution of candles of the GRB sample, the effect of the distribution is obvious and should not be neglected; b) taking into account this effect would lead to a poorer constraint of the cosmological parameter ranges. The analysis suggests that in the attempt of constraining the cosmological model with current GRB samples, the results tend to be worse than what previously thought if the mentioned intrinsic distribution does exist.Comment: 6 pages,4 figures,1 tables.Data updated. Main conclusion unchange

Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma

<p>Abstract</p> <p>Background</p> <p>Downregulation of the putative tumor suppressor gene <it>SLC22A18 </it>has been reported in a number of human cancers. The aim of this study was to investigate the relationship between <it>SLC22A18 </it>downregulation, promoter methylation and the development and progression of human glioma.</p> <p>Method</p> <p><it>SLC22A18 </it>expression and promoter methylation was examined in human gliomas and the adjacent normal tissues. U251 glioma cells stably overexpressing <it>SLC22A18 </it>were generated to investigate the effect of <it>SLC22A18 </it>on cell growth and adherence <it>in vitro </it>using the methyl thiazole tetrazolium assay. Apoptosis was quantified using flow cytometry and the growth of <it>SLC22A18 </it>overexpressing U251 cells was measured in an <it>in viv</it>o xenograft model.</p> <p>Results</p> <p><it>SLC22A18 </it>protein expression is significantly decreased in human gliomas compared to the adjacent normal brain tissues. <it>SLC22A18 </it>protein expression is significantly lower in gliomas which recurred within six months after surgery than gliomas which did not recur within six months. <it>SLC22A18 </it>promoter methylation was detected in 50% of the gliomas, but not in the adjacent normal tissues of any patient. SLC22A18 expression was significantly decreased in gliomas with <it>SLC22A18 </it>promoter methylation, compared to gliomas without methylation. The <it>SLC22A18 </it>promoter is methylated in U251 cells and treatment with the demethylating agent 5-aza-2-deoxycytidine increased <it>SLC22A18 </it>expression and reduced cell proliferation. Stable overexpression of <it>SLC22A18 </it>inhibited growth and adherence, induced apoptosis <it>in vitro </it>and reduced <it>in vivo </it>tumor growth of U251 cells.</p> <p>Conclusion</p> <p><it>SLC22A18 </it>downregulation via promoter methylation is associated with the development and progression of glioma, suggesting that <it>SLC22A18 </it>is an important tumor suppressor in glioma.</p