灰树花胞外多糖的结构及免疫调节活性

对灰树花胞外多糖A组分(EXGFP-A)进行结构分析和免疫活性的研究。结构分析结果表明,EXGFP-A是一种主要含有葡萄糖的吡喃型中性多糖。气相结果说明EXGFP-A的单糖组成为鼠李糖、阿拉伯糖、木糖、甘露糖、葡萄糖、半乳糖,摩尔比为0.28∶0.31∶0.30∶0.06∶7.98∶0.61。MTT(3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazo-lium bromide)比色实验表明,当EXGFP-A浓度为80μg/m L,作用48 h时,RAW264.7细胞增殖指数达到最大值,为137.5%。吖啶橙(AO)染色结果表明EXGFP-A能够激活RAW264.7细胞,增强细胞内部核酸代谢水平。EXGFP-A在一定浓度范围内,可以提高RAW264.7细胞中NO的释放量,上调细胞内TNF-α、IL-1β、IL-6、IL-12、IFN-γ细胞因子以及细胞中iNOS的mRNA水平的表达。结果表明,EXGFP-A具有一定的免疫调节活性,为灰树花胞外多糖的结构分析和应用提供了科学依据。     

CX3CR1-Mediated Akt1 Activation Contributes to the Paclitaxel-Induced Painful Peripheral Neuropathy in Rats

Painful peripheral neuropathy is a serious dose-limiting side effect of paclitaxel therapy, which unfortunately often happens during the optimal clinical management of chemotherapy in cancer patients. Currently the underlying mechanisms of the painful peripheral neuropathy remain largely unknown. Here, we found that paclitaxel treatment (3 × 8 mg/kg, cumulative dose 24 mg/kg) upregulated the expression of CX3CR1 and phosphorylated Akt1 in DRG and spinal dorsal horn. Blocking of Akt1 pathway activation with different inhibitor (MK-2206 or LY294002) significantly attenuated mechanical allodynia and thermal hyperalgesia induced by paclitaxel. Furthermore, inhibition of CX3CR1 by using neutralizing antibody not only prevented Akt1 activation in DRG and spinal dorsal horn but also alleviated pain-related behavior induced by paclitaxel treatment. This study suggested that CX3CR1/Akt1 signaling pathway may be a potential target for prevention and reversion of the painful peripheral neuropathy induced by paclitaxel.     

Constructing a linkage–linkage disequilibrium map using dominant-segregating markers

The relationship between linkage disequilibrium (LD) and recombination fraction can be used to infer the pattern of genetic variation and evolutionary process in humans and other systems. We described a computational framework to construct a linkage–LD map from commonly used biallelic, single-nucleotide polymorphism (SNP) markers for outcrossing plants by which the decline of LD is visualized with genetic distance. The framework was derived from an open-pollinated (OP) design composed of plants randomly sampled from a natural population and seeds from each sampled plant, enabling simultaneous estimation of the LD in the natural population and recombination fraction due to allelic co-segregation during meiosis. We modified the framework to infer evolutionary pasts of natural populations using those marker types that are segregating in a dominant manner, given their role in creating and maintaining population genetic diversity. A sophisticated two-level EM algorithm was implemented to estimate and retrieve the missing information of segregation characterized by dominant-segregating markers such as single methylation polymorphisms. The model was applied to study the relationship between linkage and LD for a non-model outcrossing species, a gymnosperm species, Torreya grandis, naturally distributed in mountains of the southeastern China. The linkage–LD map constructed from various types of molecular markers opens a powerful gateway for studying the history of plant evolution.     

Predicting the responses of forest distribution and aboveground biomass to climate change under RCP scenarios in southern China

In the past three decades, our global climate has been experiencing unprecedented warming. This warming has and will continue to significantly influence the structure and function of forest ecosystems. While studies have been conducted to explore the possible responses of forest landscapes to future climate change, the representative concentration pathways (RCPs) scenarios under the framework of the Coupled Model Intercomparison Project Phase 5 (CMIP5) have not been widely used in quantitative modeling research of forest landscapes. We used LANDIS‐II, a forest dynamic landscape model, coupled with a forest ecosystem process model (PnET‐II), to simulate spatial interactions and ecological succession processes under RCP scenarios, RCP2.6, RCP4.5 and RCP8.5, respectively. We also modeled a control scenario of extrapolating current climate conditions to examine changes in distribution and aboveground biomass (AGB) among five different forest types for the period of 2010–2100 in Taihe County in southern China, where subtropical coniferous plantations dominate. The results of the simulation show that climate change will significantly influence forest distribution and AGB. (i) Evergreen broad‐leaved forests will expand into Chinese fir and Chinese weeping cypress forests. The area percentages of evergreen broad‐leaved forests under RCP2.6, RCP4.5, RCP8.5 and the control scenarios account for 18.25%, 18.71%, 18.85% and 17.46% of total forest area, respectively. (ii) The total AGB under RCP4.5 will reach its highest level by the year 2100. Compared with the control scenarios, the total AGB under RCP2.6, RCP4.5 and RCP8.5 increases by 24.1%, 64.2% and 29.8%, respectively. (iii) The forest total AGB increases rapidly at first and then decreases slowly on the temporal dimension. (iv) Even though the fluctuation patterns of total AGB will remain consistent under various future climatic scenarios, there will be certain responsive differences among various forest types.     

Capsular polysaccharides facilitate enhanced iron acquisition by the colonial cyanobacterium Microcystis sp. isolated from a freshwater lake

Microcystis sp., especially in its colonial form, is a common dominant species during cyanobacterial blooms in many iron‐deficient water bodies. It is still not entirely clear, however, how the colonial forms of Microcystis acclimate to iron‐deficient habitats, and the responses of unicellular and colonial forms to iron‐replete and iron‐deficient conditions were examined here. Growth rates and levels of photosynthetic pigments declined to a greater extent in cultures of unicellular Microcystis than in cultures of the colonial form in response to decreasing iron concentrations, resulting in the impaired photosynthetic performance of unicellular Microcystis as compared to colonial forms as measured by variable fluorescence and photosynthetic oxygen evolution. These results indicate that the light‐harvesting ability and photosynthetic capacity of colonial Microcystis was less affected by iron deficiency than the unicellular form. The carotenoid contents and nonphotochemical quenching of colonial Microcystis were less reduced than those of the unicellular form under decreasing iron concentrations, indicating that the colonial morphology enhanced photoprotection and acclimation to iron‐deficient conditions. Furthermore, large amounts of iron were detected in the capsular polysaccharides (CPS) of the colonies, and more iron was found to be attached to the colonial Microcystis CPS under decreasing iron conditions as compared to unicellular cultures. These results demonstrated that colonial Microcystis can acclimate to iron deficiencies better than the unicellular form, and that CPS plays an important role in their acclimation advantage in iron‐deficient waters.     

Up-Regulation of microRNA-183 Promotes Cell Proliferation and Invasion in Glioma By Directly Targeting NEFL

Glioblastoma multiforme (GBM) is the most common and lethal type of primary malignant brain tumor. In recent years, increasing reports suggest that discovery of microRNAs (miRNAs) might provide a novel therapeutical target for human cancers, including GBM. The expression and roles of microRNA-183 (miR-183) has been explored in several types of human cancers, including in GBM, and plays important roles in tumor initiation and progression. However, its biological functions in GBM remain largely unknown. In this study, we demonstrated that miR-183 was significantly up-regulated in astrocytoma tissues and glioblastoma cell lines. Introduction of miR-183 mimics into U251 cells could promoted, while its antisense oligos inhibited cell proliferation and invasion. Moreover, we identified neurofilament light polypeptide (NEFL) as a novel target gene of miR-183. The expression levels of NEFL are inversely correlated with that of miR-183 in human astrocytoma clinical specimens. In addition, NEFL-siRNA could significantly attenuate the inhibitory effects of knockdown miR-183 on the proliferation and invasion of U251 cells via mTOR signaling pathway. Overall, This study revealed that miR-183 promotes glioma cell proliferation by targeting NEFL, and also demonstrated that miR-183 could be a potential target for GBM treatment.