排水粉喷桩(2D工法)加固软土地基对桩周土体强度的影响

排水粉喷桩(简称2D工法)作为一种新的软土地基处理方法,在淮盐公路软基处理中得到试用,效果良好;但是目前对其桩间土强度的变化规律还不是很清楚,本文首次通过大量现场试验,采用静力触探、十字板剪切等试验手段,测得了排水粉喷桩施工后桩间土强度变化的规律。结果显示在排水粉喷桩施工后,桩间土强度先降低,之后随着龄期的增长而提高。     

防护林带：湍流的数学模型与计算机模拟

虽然防护林用于减小风速、控制热量和水汽传递及污染物扩散、 改善气候与环境、增加作物产量等已经有几百年了, 但直到近几十年, 人们才开始系统地研究防护林空气动力学的遮蔽机制.在本综述中,我 们考察了绕防护林带的流动与湍流控制机制,最新的模型与数值模拟 研究情况;通过数值模拟与实验数据的比较,来了解防护林带结构与防 风效果之间的关系;讨论数值分析如何及为什么能够得到所需要的结果. 本文将从多孔隙防护林带流动基本方程组的推导开始,讨论数值模型及 模拟过程,对附体与分离流动进行预测;分析了遮蔽机制与动量交换;对 风向、防护林密度、宽度和三维性对流动与湍流的影响作了系统的论 述.还对热流和土壤水分蒸发的新模型及数值模拟作了简述.最后,我们 对网络工作站、群和高性能分布式并行计算机及其对防护林带模型预 报能力的提高作了讨论.     

下伏软弱层黄土边坡变形机制分析及治理对策研究

本文研究了陕北某电厂夹断层破碎带上覆黄土的泥岩、砂岩互层反倾边坡的变形机制,并研究治理对策及其治理效果。通过边坡工程地质条件及变形破坏特征分析,建立FLAC3D地质模型,采用数值模拟方法研究了边坡变形破坏机制,在此基础上提出削方减载、锚筋桩、锚杆及坡面防护的综合治理措施。研究结果表明,边坡的变形受开挖坡形的影响,坡体浅表层特别是断层带及坡顶黄土部位出现大范围拉应力集中,断层带出现向坡外的挤出变形,带动上部黄土的牵引式变形,引起沿黄土和基岩基覆界面的剪切变形,在黄土中出现大量拉裂缝,在一定条件下潜在滑移面逐渐贯通,坡体将产生整体失稳。边坡的治理应通过削方减载改善坡体应力环境,并重点控制断层带及黄土与基岩基覆界面的变形,数值模拟结果表明,治理后边坡稳定性较好,满足设计要求。     

滑坡防治工程安全性评价研究

滑坡灾害防治是一门综合性工程,防治工程的安全性取决于滑坡勘察、设计以及施工质量,本文就滑坡治理过程中各阶段易出现的问题予以实例说明,探讨滑坡防治工程中应注意的几个问题,对这些经验教训进行总结,同时强调监测在防治工程中的作用,其对于滑坡防治工程具有一定借鉴意义。     

水泥与生石灰处理吹填土对比试验研究

吹填土是由水力吹填形成的,颗粒很细,固结性能差,吹填以后要经过很长时间才能自然沉积固结,待表面形成硬壳后方可进行加固处理,因此,缩短沉积固结时间,使吹填土尽快地从泥浆状态转变为具有一定承载力的地基,是亟待解决的问题。在室内进行模拟加固方法的沉降柱试验,对吹填土加添固化剂以加速其沉积固结。固化剂主要选用水泥和生石灰,对两种添加方式的机理及固结效果进行详尽的分析和研究,初步找出加固效果产生差异的原因,从而揭示其固化机理,为吹填土地基的加固提供一种更加经济可行的方法。     

矿山岩体工程的系统工程

用系统工程学的观点, 重新认识矿山岩体工程的特点。建立矿山岩体工程稳定性的系统的概念。提出地质模型、设计模型、施工模型的构思, 使工程地质、设计、施工三者密切结合, 共同解决矿山岩体工程稳定问题。通过动态监测和信息反馈, 在工程施工的动态过程中不断地获得新的认识, 以便对工程实施做出新的决策。     

Diaminodiacid Bridges to Improve Folding and Tune the Bioactivity of Disulfide‐Rich Peptides

Disulfide‐rich peptides containing three or more disulfide bonds are promising therapeutic and diagnostic agents, but their preparation is often limited by the tedious and low‐yielding folding process. We found that a single cystine‐to‐diaminodiacid replacement could significantly increase the folding efficiency of disulfide‐rich peptides and thus improve their production yields. The practicality of this strategy was demonstrated by the synthesis and folding of derivatives of the μ‐conotoxin SIIIA, the preclinical hormone hepcidin, and the trypsin inhibitor EETI‐II. NMR and X‐ray crystallography studies confirmed that these derivatives of disulfide‐rich peptide retained the correct three‐dimensional conformations. Moreover, the cystine‐to‐diaminodiacid replacement enabled structural tuning, thereby leading to an EETI‐II derivative with higher bioactivity than the native peptide.     

Revealing the Charge‐Transfer Interactions in Self‐Assembled Organic Cocrystals: Two‐Dimensional Photonic Applications

A new crystal of a charge‐transfer (CT) complex was prepared through supramolecular assembly and it has unique two‐dimensional (2D) morphology. The CT nature of the ground and excited states of this new Bpe‐TCNB cocrystal (BTC) were confirmed by electron spin resonance measurements, spectroscopic studies, and theoretical calculations, thus providing a comprehensive understanding of the CT interactions in organic donor–acceptor systems. And the lowest CT₁ excitons are responsible for the efficient photoluminescence (Φ_PL=19 %), which can actively propagate in individual 2D BTCs without anisotropy, thus implying that the optical waveguide property of the crystal is not related to the molecular stacking structure. This unique 2D CT cocrystal exhibits potential for use in functional photonic devices in the next‐generation optoelectronic communications.     

Contact between the β1 and β2 Segments of α‐Synuclein that Inhibits Amyloid Formation

Conversion of the intrinsically disordered protein α‐synuclein (α‐syn) into amyloid aggregates is a key process in Parkinson’s disease. The sequence region 35–59 contains β‐strand segments β1 and β2 of α‐syn amyloid fibril models and most disease‐related mutations. β1 and β2 frequently engage in transient interactions in monomeric α‐syn. The consequences of β1–β2 contacts are evaluated by disulfide engineering, biophysical techniques, and cell viability assays. The double‐cysteine mutant α‐synCC, with a disulfide linking β1 and β2, is aggregation‐incompetent and inhibits aggregation and toxicity of wild‐type α‐syn. We show that α‐syn delays the aggregation of amyloid‐β peptide and islet amyloid polypeptide involved in Alzheimer’s disease and type 2 diabetes, an effect enhanced in the α‐synCC mutant. Tertiary interactions in the β1–β2 region of α‐syn interfere with the nucleation of amyloid formation, suggesting promotion of such interactions as a potential therapeutic approach.