RNF7 promotes glioma growth via the PI3K/AKT signalling axis

RNF7 has been reported to play critical roles in various cancers. However, the underlying mechanisms of RNF7 in glioma development remain largely unknown. Herein, the expression level of RNF7 was examined in tissues by quantitative real-time PCR, Western blotting and immunohistochemistry. The effect of RNF7 on glioma progression was measured by performing CCK-8 and apoptosis assays, cell cycle-related experiments and animal experiments. The effect of RNF7 on PI3K/AKT signalling pathway was tested by Western blotting. First, we found that RNF7 was upregulated in tumour tissue compared with normal brain tissue, especially in high-grade glioma, and the high expression of RNF7 was significantly related to tumour size, Karnofsky Performance Scale score and a poor prognosis. Second, RNF7 overexpression facilitated tumour cell cycle progression and cell proliferation and suppressed apoptosis. Conversely, RNF7 knockdown suppressed tumour cell cycle progression and cell proliferation and facilitated apoptosis. Furthermore, follow-up mechanistic studies indicated that RNF7 could facilitate glioma cell proliferation and cell cycle progression and inhibit apoptosis by activating the PI3K/AKT signalling pathway. This study shows that RNF7 can clearly promote glioma cell proliferation by facilitating cell cycle progression and inhibiting apoptosis by activating the PI3K/AKT signalling pathway. Targeting the RNF7/PI3K/AKT axis may provide a new perspective on the prevention or treatment of glioma.     

GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin-mediated mitophagy

Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol-3-phosphate dehydrogenase 1-like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy-related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin-mediated mitophagy. However, inhibition of PINK1 reversed GPD1L-mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy.     

胶质母细胞瘤外泌体的作用机制研究进展

胶质母细胞瘤(glioblastoma,GBM)因组织学异质性、侵袭能力强、术后复发快等问题,致使患者经手术治疗、化疗和放疗后的预后差,总体生存期短。GBM细胞来源外泌体(GBM cell-derived exosome,GBM-exo)能够通过其携带的细胞因子、miRNA、DNA和蛋白质等调节GBM细胞的增殖和迁移,通过血管生成蛋白和非编码RNA促进肿瘤血管生成,通过调节因子、蛋白质和药物靶向免疫检查点等介导肿瘤免疫逃逸,以及通过非编码RNA对抗GBM细胞的耐药性,有望成为个性化治疗GBM的重要靶标,且可以作为GBM的诊断和预后标志物。本文阐述了GBM-exo的制备方法和生物学特征,及其在GBM细胞增殖、血管生成、免疫逃逸和耐药性方面的作用和分子机制,为研发诊治GBM的新策略提供参考。     

广西荔浦晚泥盆世法门期竹节石

本文研究了广西荔浦上泥盆统榴江组上部扁豆状灰岩中所含的法门期竹节石2属3种,其产出层位分别为牙形刺化石带的 Palmatolepis crepida带和 Pa.marginifera带。     

Inhibition of the HIV-1 and HIV-2 proteases by curcumin and curcumin boron complexes

Curcumin, a relatively non-toxic natural product isolated from Curcuma longa, is a modest inhibitor of the HIV-1 (1050 = 100 μM) and HIV-2 (IC₅₀ = 250 μM) proteases. Simple modifications of the curcumin structure raise the IC₅₀ value but complexes of the central dihydroxy groups of curcumin with boron lower the IC₅₀ to a value as low as 6 μM. The boron complexes are also time-dependent inactivators of the HIV proteases. The increased affinity of the boron complexes may reflect binding of the orthogonal domains of the inhibitor in intersecting sites within the substrate-binding cavity of the enzyme, while activation of the ,β-unsaturated carbonyl group of curcumin by chelation to boron probably accounts for time-dependent inhibition of the enzyme.     

常绿阔叶林次生演替的一种系统动力学模型

植物群落的演替过程是一个系统,这一系统具有一般系统的基本规律。植物群落演替过程的每个阶段可视为系统的不同状态。就演替系统而言,在一定条件下系统可由一种状态转移到另一种状态。这种系统状态间转移的过程实际上对应着演替过程。植物群落演替系统是动态系统。就是说系统的要素随时间的变化而变化。动态系统都可用微分方程(组)描述其发展变化的规律。这种用微分方程(组)描述的反映系统动态特征的数学表达式称为系统动态数学模型(动力学模型),系统动态数学模型按解决问题目的的不同可分为一     

流式细胞术的发展及在植物研究中的应用

流式细胞术是通过对液流中各种荧光标记的颗粒进行多参数快速高效的定性或定量测定的方法,在科学研究的多个领域发挥重要作用。然而,由于植物组织及细胞壁和次生代谢产物等细胞的特殊成分和结构,限制了其在植物研究领域的应用。本文在介绍流式细胞仪发展和组成分类的基础上,着重讨论了流式细胞术在植物领域的应用、研究进展及应用限制,进而展望该研究领域的发展趋势,为拓宽植物流式细胞术的潜在应用范围提供新的思考方向。     

放养鲢鱼(Hypophthalmichys molitrix C et V)对水库围隔浮游生物群落的影响

本文研究在水库围隔实验生态系统中鲢鱼对浮游生物群落的影响。结果表明,放养鲢鱼后,浮游动物生物量、浮游植物生物量、叶绿素a和浮游植物毛产量分别下降了58.7％、63.6％、52.5％和65.0％;透明度、浮游植物群落多样性指数分别提高了18.2％、32.5％;铜绿微囊藻数量减少了90.6％“水华”得到明显抑制。但小型绿藻(<20μm)数量未出现显著变化,因而其在藻类生物量中所占比例反而提高了82.3％。围隔内可被鲢鱼滤食的大型藻类(硅藻、甲藻、隐藻和绿藻(>20μm))占藻类生物量的85.8％,因此鲢鱼的存在能明显限制浮游植物的生物量。此外,放养鲢鱼还显著降低了水体中的COD,TP,DO和pH值,这表明鲢鱼对水质有净化作用。     

海南岛热带山地雨林林分生物量估测方法比较分析

本文通过对海南岛热带山地雨林林分生物量估测方法的比较分析,表明材积转换法不适宜估算海南岛热带山地雨林林分生物量,其结果与皆伐法相比较一般偏高20％—40％;而用实测资料建立的生物量回归模型,对原始林林分有较好的估测结果,除树枝和树叶生物量外,树干、树皮及地上部分生物量的回归模型值,与皆伐法的结果比较,相对误差一般在±10％以内,为允许误差范围,而对热带山地雨林的更新林生物量的估测则效果较差,应建立相应的估测模型。平均木法有工作量小的优点,且误差也在16％以下,但要注意取样的树种多样性和取样强度,在实际中应当慎用。另外本文对测定热带山地雨林生物量(原始林)的所需面积大小问题作了研究,提出了生物量-面积曲线的概念,确定其最小调查面积为2500m~2以上。