培养液中钙对碳纳米材料细胞毒性作用机制的同步辐射初步研究

本工作研究了细胞培养液中钙离子和多壁碳纳米管,以及纳米碳黑的相互作用,采用钙荧光标记的显微成像技术和同步辐射X射线荧光技术,研究了HeLa细胞内钙离子浓度的增高及其相关机制。实验结果指出,细胞培养介质中的钙能被碳纳米颗粒(CNPs)大量吸附并载带进入细胞内,因此,CNPs向细胞内输送过量的钙离子可能是造成CNPs细胞毒性的重要原因。本工作为正确检测和评估碳纳米材料细胞毒性提供了新思路。     

合欢、金合欢和银合欢根瘤菌系统发育研究方法比较

利用位于染色体不同位点的多个基因序列进行分析是原核生物分类与系统发育研究的一个热点.本文采用atpD和glnⅡ两个持家基因的部分序列对9株分离自我国合欢、金合欢和银合欢的根瘤菌进行系统发育研究,并与以16S rDNA基因序列构建的系统发育树进行比较.结果表明三者在属水平上基本一致,CCBAU43060、CCBAU61139位于Rhizobium-Agrobacterium系统发育分支内;CCBAU51471、CCBAU35220、CCBAU51276和CCBAU61158属于Mesorhizobium,CCBAU35234、CCBAU61178和CCBAU35085位于Bradyrhizobium系统发育分支;在属内种间个别菌株(CCBAU61158、CCBAU43060、CCBAU61178)的系统发育地位存在差异,表明属内种间存在较广泛的基因交流.因此利用16S rDNA确定属水平的分类地位比较可靠,但利用系统发育的方法研究属内种间亲缘关系应采用多个功能保守的持家基因同时进行分析才能得出比较可靠的结论.     

Tumors exploit FTO-mediated regulation of glycolytic metabolism to evade immune surveillance

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LncRNA CTD-2528L19.6 prevents the progression of IPF by alleviating fibroblast activation

Long non-coding RNAs (lncRNAs) have emerged as critical factors for regulating multiple biological processes during organ fibrosis. However, the mechanism of lncRNAs in idiopathic pulmonary fibrosis (IPF) remains incompletely understood. In the present study, two sets of lncRNAs were defined: IPF pathogenic lncRNAs and IPF progression lncRNAs. IPF pathogenic and progression lncRNAs-mRNAs co-expression networks were constructed to identify essential lncRNAs. Network analysis revealed a key lncRNA CTD-2528L19.6, which was up-regulated in early-stage IPF compared to normal lung tissue, and subsequently down-regulated during advanced-stage IPF. CTD-2528L19.6 was indicated to regulate fibroblast activation in IPF progression by mediating the expression of fibrosis related genes LRRC8C, DDIT4, THBS1, S100A8 and TLR7 et al. Further studies showed that silencing of CTD-2528L19.6 increases the expression of Fn1 and Collagen I both at mRNA and protein levels, promoted the transition of fibroblasts into myofibroblasts and accelerated the migration and proliferation of MRC-5 cells. In contrast, CTD-2528L19.6 overexpression alleviated fibroblast activation in MRC-5 cells induced by TGF-β1. LncRNA CTD-2528L19.6 inhibited fibroblast activation through regulating the expression of LRRC8C in vitro assays. Our results suggest that CTD-2528L19.6 may prevent the progression of IPF from early-stage and alleviate fibroblast activation during the advanced-stage of IPF. Thus, exploring the regulatory effect of lncRNA CTD-2528L19.6 may provide new sights for the prevention and treatment of IPF.Subject terms: Mechanisms of disease, Non-coding RNAs     

免疫检查点抑制剂在慢性乙型肝炎中的研究进展

慢性乙型肝炎病毒(hepatitis B virus,HBV)感染仍是全球主要公共卫生问题之一.尽管目前已有预防性疫苗可有效预防新发HBV感染,但全球仍有约2.5亿慢性HBV感染者,其中每年约有100多万人死于HBV相关的慢性肝病,形势仍不容乐观.抗病毒药物(干扰素和核苷类似物等)可抑制病毒复制,降低乙肝相关并发症,但...