基于地学信息图谱的重庆岩溶石漠化植被恢复演替研究

重庆岩溶石漠化区的植被恢复演替动态变化研究对于该地区的石漠化治理和生态恢复具有十分重要的指导意义。而多时相的遥感数据和地学图谱分析法为植被恢复的研究提供了一种动态性和综合性的研究方法。以重庆市中梁山的典型植被恢复区为例,在基于1996、2001、2007和2013年4期遥感影像解译分类的基础上,采用"空间代替时间"的生态学植被演替研究方法,建立重庆市中梁山区退耕还林前后的植被恢复演替图谱,并结合地学图谱的相关分析方法,得到该区的植被恢复演替动态格局演变规律,体现了空间信息科学技术、生态学方法和地学信息图谱分析法在植被恢复演替研究中的有效结合。结果表明:(1)运用BP神经网络和BP算法进行分类,分类精度达到87.42%,比传统监督分类提高了5.57%。(2)自2002年全国范围内的"退耕还林(草)"工程全面启动后,该区域植被恢复演变特征明显,耕地面积明显减少而植被面积明显增加。(3)从2001—2013年,植被演替在该时期内依然存在着进展演替和逆向演替两个方向。虽然逆向演替比例仅占到18.63%,但它却使该区的演替研究变得复杂。(4)质心反映了各植被类型在恢复演替过程中的聚散与迁移,1996—2013年,马尾松群落和落叶阔叶林群落的质心变化较小,其他植被群落的质心都有很明显的变化。     

PTTG3P promotes gastric tumour cell proliferation and invasion and is an indicator of poor prognosis

Pseudogenes play a crucial role in cancer progression. However, the role of pituitary tumour‐transforming 3, pseudogene (PTTG3P) in gastric cancer (GC) remains unknown. Here, we showed that PTTG3P expression was abnormally up‐regulated in GC tissues compared with that in normal tissues both in our 198 cases of clinical samples and the cohort from The Cancer Genome Atlas (TCGA) database. High PTTG3P expression was correlated with increased tumour size and enhanced tumour invasiveness and served as an independent negative prognostic predictor. Moreover, up‐regulation of PTTG3P in GC cells stimulated cell proliferation, migration and invasion both in vitro in cell experiments and in vivo in nude mouse models, and the pseudogene functioned independently of its parent genes. Overall, these results reveal that PTTG3P is a novel prognostic biomarker with independent oncogenic functions in GC.     

Hypoxia promotes HO-8910PM ovarian cancer cell invasion via Snail-mediated MT1-MMP upregulation

The molecular mechanisms of ovarian cancer cell invasion under hypoxia remain unclear. Here we employed a 3D collagen model and chick chorioallantoic membrane (CAM) invasion assay to explore the influence of hypoxia on ovarian cancer cell invasion. Hypoxia (both 1% O₂ and CoCl₂ 150 and 250 µM) induced HO-8910PM ovarian cancer cell invasion in 3D collagen and collagenolysis determined by hydroxyproline. Pretreatment with a hypoxia inducible factor-1α inhibitor, YC-1, or MMP inhibitor, GM6001, significantly inhibited 3D collagen invasion and degradation and cell proliferation. Hypoxia stimulated both mRNA and protein expressions of membrane-type 1 matrix metalloproteinase (MT1-MMP) and promoted MT1-MMP translocation to the cell surface in an YC-1 sensitive manner. MT1-siRNA transfection inhibited hypoxia-induced invasion, proliferation, and collagen degradation of cells in 3D collagen. Hypoxia stimulated Snail mRNA and protein expression as well as translocation to nucleus in an YC-1 sensitive manner. Overexpression of Snail with a recombinant plasmid in HO-8910PM cells resulted in an enhanced invasion in 3D collagen. Transfection with Snail-specific siRNA significantly decreased MT1-MMP expression and 3D collagen invasion. Hypoxia-treated cells significantly broke the upper CAM surface of 11-day-old chick embryos and infiltrated interstitial tissue, completely blocked in the presence of YC-1 or GM6001, or after MT1-MMP siRNA or Snail siRNA transfection. Together, these data suggest that hypoxia promotes HO-8910PM ovarian cancer cell traffic through 3D matrix via Snail-mediated MT1-MMP upregulation, a possible molecular mechanism of ovarian cancer cell invasion under hypoxia.     

Growth asymmetry precedes differential auxin response during apical hook initiation in Arabidopsis

The development of a hook-like structure at the apical part of the soil-emerging organs has fascinated botanists for centuries, but how it is initiated remains unclear. Here, we demonstrate with highthroughput infrared imaging and 2-D clinostat treatment that, when gravity-induced root bending is absent, apical hook formation still takes place.In such scenarios, hook formation begins with a de novo growth asymmetry at the apical part of a straightly elongating hypocotyl. Remarkably, suchde novo ...     

Protective effect of pinitol against D-galactosamine-induced hepatotoxicity in rats fed on a high-fat diet

The protective effect of pinitol against D-galactosamine (GalN)-induced liver damage was examined. Forty male Sprague-Dawley rats were divided into normal control, GalN control, and pinitol groups (0.5%, 1%, and 2%). After 8 weeks of feeding, a single dose of GalN (650 mg/kg) was administered 24 h before their sacrifice. The serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor-alpha (TNF-alpha) levels were significantly increased after an injection with GalN (P<0.05), but pinitol supplementation at the level of 0.5% reversed these changes to normal levels. Significant decreases in serum triglyceride and cholesterol and increases in hepatic cholesterol were observed in GalN-intoxicated rats. However, supplementation with pinitol significantly attenuated these trends. In addition, pinitol elevated the Mn-superoxide dismutase, glutathione reductase, and catalase activities, prevented hepatic lipid peroxidation, and restored the hepatic GSH levels and cytochrome P450 2E1 function. Thus, 0.5% pinitol supplementation protected the rats from the hepatotoxicity induced by GalN, at least part of its effect being attributable to attenuation of the oxidative stress and inflammatory process promoted by GalN.     

Impact of Nox5 Polymorphisms on Basal and Stimulus-Dependent ROS Generation

Nox5 is an EF-hand containing, calcium-dependent isoform of the NADPH oxidase family of reactive oxygen species (ROS) generating enzymes. Altered expression and activity of Nox5 has been reported in cardiovascular diseases and cancers but the absence of Nox5 in rodents has precluded a greater understanding of its physiological and pathophysiological roles. Multiple polymorphisms have been identified within the coding sequence of human Nox5, but whether this translates into altered enzyme function is unknown. Herein, we have generated 15 novel mutants of Nox5β to evaluate the effect of exonic SNPs on basal and stimulated enzyme activity. Compared to the WT enzyme, ROS production was unchanged or slightly modified in the majority of mutants, but significantly decreased in 7. Focusing on M77K, Nox5 activity was dramatically reduced in unstimulated cells and following challenge with both calcium- and phosphorylation-dependent stimuli despite equivalent levels of expression. The M77K mutation did not influence the Nox5 phosphorylation or the ability to bind Hsp90, but in cell-free assays with excess co-factors and calcium, ROS production was dramatically reduced. A more conservative substitution M77V arising from another SNP yielded a different profile of enzyme activity and suggests a critical role of M77 in calcium-dependent ROS production. Two C-terminal mutants, R530H and G542R, were observed that had little to no activity and relatively high minor allele frequency (MAF). In conclusion, we have identified 7 missense SNPs in Nox5 that result in little or no enzyme activity. Whether humans with dysfunctional Nox5 variants have altered physiology or disease remains to be determined.