膨胀土改良技术研究综述

由于膨胀土危害性大,造成的工程问题突出,对膨胀土的研究已成为当前岩土工程的重要研究方向之一,并成为世界性的共同课题。为了确保膨胀土地区工程建设的安全,需对膨胀土进行处治。在诸多加固处理方法中,膨胀土改良方法越来越得到重视和应用。就近年来我国在膨胀土改良技术研究方面所取得的主要研究成果进行较为系统分析介绍,以期反映了目前膨胀土改良技术研究的现状,为今后改良膨胀土的理论分析和试验研究提供参考。     

基于频响函数曲率的结构损伤检测

结构的损伤能够引起结构动力参数的变化。为了更明确地显示损伤,文中用频响函数曲率、频响函数曲率差、频响函数曲率比三种指标来进行损伤诊断。考虑到单处损伤及多处损伤情况,对简支梁进行数值模拟,并用上述三种指标进行了诊断。对比结果表明,在单损情况时,频响函数曲率差及曲率比都对损伤位置敏感;但在多损情况时,频响函数曲率比对损伤位置更加敏感。     

Sensitive voltammetric detection of DNA damage at carbon electrodes using DNA repair enzymes and an electroactive osmium marker

This paper presents a new approach to electrochemical sensing of DNA damage, using osmium DNA markers and voltammetric detection at the pyrolytic graphite electrode. The technique is based on enzymatic digestion of DNA with a DNA repair enzyme exonuclease III (exoIII), followed by single-strand (ss) selective DNA modification by a complex of osmium tetroxide with 2,2'-bipyridine. In double-stranded DNA possessing free 3'-ends, the exoIII creates ss regions that can accommodate the electroactive osmium marker. Intensity of the marker signal measured at the pyrolytic graphite electrode responded well to the extent of DNA damage. The technique was successfully applied for the detection of (1) single-strand breaks (ssb) introduced in plasmid DNA by deoxyribonuclease I, and (2) apurinic sites generated in chromosomal calf thymus DNA upon treatment with the alkylating agent dimethyl sulfate. The apurinic sites were converted into the ssb by DNA repair endonuclease activity of the exoIII enzyme. We show that the presented technique is capable of detection of one lesion per approximately 10(5) nucleotides in supercoiled plasmid DNA.     

氯化1-辛基-3-甲基咪唑对EMT6细胞的毒性及其DNA损伤作用

研究了氯化1-辛基-3-甲基咪唑([C8mim][Cl])对EMT6细胞的毒性大小及其可能的遗传机制.不同浓度(0.06、0.25、1.00mmol·L-1)的[C8mim][Cl]对EMT6细胞染毒12h,WST-1比色法检测了细胞活力,ELISA方法检测了Bcl-2蛋白的表达,Hoechst 33342染色检测了细胞核形态的变化,单细胞凝胶电泳(SCGE)检测了细胞DNA的损伤,流式细胞仪检测了细胞周期和细胞DNA的含量.结果显示,经[C8mim][Cl]染毒后,EMT6细胞活力下降,并且呈剂量依赖关系.当[C8mim][Cl]浓度高于0.25mmol·L-1时,与对照相比,差异显著.[C8mim][Cl]染毒使Bcl-2蛋白表达下调,引起了细胞核形态改变,造成了DNA的断裂损伤和含量下降,诱导了细胞凋亡.从而可以得出结论,DNA损伤参与了[C8mim][Cl]诱导的细胞凋亡.     

Theoretical studies of damage to 3'-uridine monophosphate induced by electron attachment

Low-energy electrons (LEE) are well known to induce nucleic acid damage. However, the damage mechanisms related to charge state and structural features remain to be explored in detail. In the present work, we have investigated the N1-glycosidic and C3'-O(P) bond ruptures of 3'-UMP (UMP=uridine monophosphate) and the protonated form 3'-UMPH with -1 and zero charge, respectively, based on hybrid density functional theory (DFT) B3 LYP together with the 6-31+G(d,p) basis set. The glycosidic bond breakage reactions of the 3'UMP and 3'UMPH electron adducts are exothermic in both cases, with barrier heights of 19-20 kcal mol(-1) upon inclusion of bulk solvation. The effects of the charge state on the phosphate group are marginal, but the C2'-OH group destabilizes the transition structure of glycosidic bond rupture of 3'-UMPH in the gas phase by approximately 5.0 kcal mol(-1). This is in contrast with the C3'-O(P) bond ruptures induced by LEE in which the charge state on the phosphate influences the barrier heights and reaction energies considerably. The barrier towards C3'-O(P) bond dissociation in the 3'UMP electron adduct is higher in the gas phase than the one corresponding to glycosidic bond rupture and is dramatically influenced by the C2'-OH group and bulk salvation, which decreases the barrier to 14.7 kcal mol(-1). For the C3'-O(P) bond rupture of the 3'UMPH electron adduct, the reaction is exothermic and the barrier is even lower, 8.2 kcal mol(-1), which is in agreement with recent results for 3'-dTMPH and 5'-dTMPH (dTMPH=deoxythymidine monophosphate). Both the Mulliken atomic charges and unpaired-spin distribution play significant roles in the reactions.     

Dynamic analysis of DNA damage induced miRNAs in colon cancer cells

It is known that microRNAs （miRNAs） expression profile shows substantial changes in cells under DNA damage. Here, we did miRNA microarray and quantitative real-time PCR to comprehensively identify the differentially expressed miRNAs in colon cancer cell lines HCT116 p53＋/＋ and HCT116 p53-/-. Cluster analysis revealed a panel of differentially expressed miRNAs which are regulated by p53 and/or UV-C induced DNA damage. These altered miRNAs tend to be located in chromosomes 13, X and 17. Moreover, pathways enrichment analysis estimated that MAPK pathway, focal adheren pathway, p53 pathway and Wnt pathway were mediated by these miRNAs to exert their functions in DNA damage response. Additionally, we found that miR- 320a, one of the UV-C induced miRNAs, play a role in protecting cells from DNA damage. Taken together, our results show that miRNAs are dynamic regulated in p53- dependent or -independent manners in different cell contexts and different situations following DNA damage.     

大强度运动对青年男子淋巴细胞凋亡的影响

设计训练组(T组,14名男性田径运动员)和对照组(C组,14名男性普通大学生)均完成一次大强度运动,并于运动前、运动后即刻以及运动后12h取血液淋巴细胞测定淋巴细胞计数、凋亡率、羟自由基(·OH)和8-氧鸟嘌呤(8-oxodG)含量,对比运动员和普通大学生在一次大强度运动前后淋巴细胞DNA损伤的变化,探讨长期运动训练对淋巴细胞凋亡的影响及其可能机制.结果显示,运动后即刻:组内前后比较,两组所有指标均显著性升高(P<0.05或P<0.01);组间比较,T组指标变化的幅度均低于C组(P<0.01).运动后12h:组内前后比较,C组淋巴细胞凋亡率和8-oxodG含量升高(P<0.01),淋巴细胞计数降低(P<0.01),·OH含量恢复(P>0.05),T组8-oxodG含量升高(P<0.05),其他指标均恢复至运动前水平;组间比较,T组8-oxodG含量升高幅度明显低于C组(P<0.01).以上结果表明:一次大强度运动诱导淋巴细胞自由基产生增多并造成DNA氧化损伤,细胞凋亡增加;长期运动训练则可降低淋巴细胞DNA氧化损伤和细胞凋亡并加速凋亡恢复,防止运动应激后淋巴细胞数量的减少.     

水电站坝下游面钢衬钢筋混凝土管道损伤和承载特性

基于混凝土塑性损伤模型,对某水电站坝下游面钢衬钢筋混凝土管道的损伤和承载特性进行了非线性有限元分析.结果表明:在正常运行工况下,裂缝主要出现在位于坝体之外的背管部分,数条贯穿性裂缝将由主变平台延伸至上弯段;主变平台附近管道受力状态复杂,管道断面出现贯通性损伤,可能出现短小而密集的裂缝;温度变化对结构受力影响明显,特别是温降荷载将引起管道外侧损伤区进一步发展,靠近管壁外侧的钢筋拉应力明显上升,因此应注意管道表面的保温和防护.     

夹层玻璃结构的抗鸟撞分析

抗鸟撞设计是飞机设计过程中一个复杂、关键的步骤.通过建立SPH-FEM耦合的鸟撞夹层结构数值计算模型,分析由常用的航空透明材料,如无机玻璃、聚氨酯（PU）、聚碳酸酯（PC）和聚甲基丙烯酸甲酯（PMMA）组合构成的夹层玻璃（板）风挡的鸟撞响应.PU、PC和PMMA的材料参数通过材料各自的准静态、动态试验结果得到.在有限元软件LS-DYNA中计算夹层结构的鸟撞过程,得到夹层结构的破坏失效过程,并分析不同材料组成的夹层结构的抗鸟撞性能.发现由无机玻璃和高分子聚合物组成的夹层结构的抗鸟撞性能最佳.