小儿肺炎并发心肌损伤心肌钙蛋白I的检测意义(附46例分析)

目的:探讨小儿肺炎并发心肌损伤心肌钙蛋白I的检测意义。方法:采用全自动化学免疫系统检测4 6例肺炎患儿心肌钙蛋白I(CTnI)、肌酸激酶同功酶(CKMB) ,并与2 6例正常小儿进行对照比较。结果:肺炎患儿与正常小儿CTnI、CKMB值比较均有非常显著性差异(P <0 0 1) ,且肺炎越重,越易造成心肌损害,二者值越高。两两比较,除重症肺炎组与普通肺炎组CKMB差异无显著性外(P >0 0 5 ) ,其余均有非常显著性差异(P <0 0 1)。结论:CTnI可作为监测小儿肺炎并发心肌损伤的重要标志物。     

心肌组织力学行为的测试系统

为方便与准确定量地研究心肌组织主动力与被动力的性质,在综合现代实验力学中的光测、电测和步进电机控制等技术的基础上开发了两套实验测试系统。这两个系统也可用于一般生物软组织性质的研究。论述了这两套测试系统各自的工作原理,介绍了硬件和软件的组成部分和功能,以及关键部位力传感器的设计和标定。介绍了心肌力学性质测试的一般方法,初步得到了心肌组织的被动力和主动力的基本性质,和现有的理论模型进行了拟合和比较,表明这两套系统可以完成心肌组织的生物力学性质的测试。     

脉冲电流下对AL6061合金进行熔孔止裂与愈合的仿真研究

Al6061铝合金常应用于航空航天领域蒙皮制造,因其中等硬度与低强度的弱点,在承受复杂载荷时容易出现微裂纹,进而影响服役安全可靠性。脉冲电流是一种极速、非平衡的金属材料微小裂纹修复工艺,可以克服该材料不易焊接修复的短板。本文在既有的实验基础上建立单边预制裂纹缺口模型,采用有限元仿真手段,进行了热-电-力三场耦合数值模拟,计算不同参数下裂纹区域的电场、温度场和应力场分布。使用“生死单元”法模拟止裂熔孔的产生,并获得了不同几何、物理参数下止裂熔孔尺寸变化的规律。结果表明：焦耳热形成的止裂熔孔降低裂尖的集中应力,抑制裂纹扩展,裂纹区域高温区与基体常温区形成温度梯度相互约束产生巨大的热压应力促使裂纹宽度减小,进而直至愈合;初始熔孔尺寸与裂纹长度成正比、与板厚成反比,最佳尺寸直径为0.1mm以内;电流值和电流加载时间均能控制熔孔生长,电流值一定时,当时间达到0.12s形成的熔孔尺寸超出最佳止裂尺寸范围。研究成果为特定金属材料的裂纹止裂与愈合提供了机理参考和仿真方法。     

提取心脏截面图像上内腔的边缘曲线

针对心脏截面图像上内腔边缘形状起伏较大的特点 ,利用一种基本思想称为径向半径搜寻的方法 ,获取内腔边缘的包络曲线 .首先介绍的径向半径搜寻方法较以往的方法提高了对不光滑边缘轮廓提取的精确程度 ,然后对该方法进行改进 ,从而使心脏内腔边缘曲线的提取方法在鲁棒性、准确性方面较以往的方法有较大的提高 ,并具有普遍性     

钢纤维高强砼与普通高强砼力学性能实验研究

本文对钢纤维高强砼和普通精强砼的轴心抗压强度、立方体抗压强度、劈裂抗拉强度、弯曲抗拉强度、弯曲韧性、韧度及弹性模量等力学性能进行试验研究。通过对实验结果的分析，探讨在普通高强砼中择加适量钢纤维对其力学性能的影响，并对钢纤维在砼基材中产生增韧、阻裂效应的原因进行了分析。     

FNN在心率失常判别中的研究

提出了一种基于模糊神经网络(FNN)对心率失常信号进行判别的新方法.首先,根据心电信号特点构建Sugeno型模糊神经网络,然后使用Cam Delta算法对其进行训练,这样可以得到模糊隶属函数,此隶属函数将R-R间期波及QRS波的长度模糊化.随后,用几何法通过计算隶属度实现对心率失常的判别.经MIT-BIH心电数据库和实测数据检验,此方法可有效的对心率失常进行判别.     

PROGRESSIVE DAMAGE ARREST MECHANISM IN TAILORED LAMINATED PLATES WITH A CUTOUT

This study addresses the effectiveness of a simple stiffness tailoring concept to delay damage initiation, control damage progression, and improve residual strength in tensile-loaded composite plates with a central circular cutout. The tailoring concept is to simply reposit all axially oriented （0°） material into regions near the edge of the plate away from the cutout. This tailoring is done in a way so as not to affect the weight of the plate. This accomplishes several beneficial changes in the way that the plate resists loading with no increases in material cost or weight. Lowering the axial stiffness of the laminate surrounding the cutout lowers the stress concentration. Increasing the axial stiffness near edges of the plate attracts loading away from the vicinity of the cutout to further lower stresses in the critical cutout region. This study focuses on in-plane response including damage progression and residual strength as a function of the degree of tailoring and cutout size. Strength and stiffness properties typical of IM7/8551-7 preperg material were assumed and a modified version of the Hashin failure criteria was used to identify the local damage. Results show that tailoring can significantly increase the damage initiation load and the residual strength. In some cases, observed evidence shows that tailoring performs as a damage arrest mechanism.     

Rational molecular targeting of the inter-subunit interaction between human cardiac troponin hcTnC and hcTnI using switch peptide-competitive biogenic medicines

The human cardiac troponin (hcTn) has been implicated in diverse cardiovascular diseases (CDs). The protein function is regulated by the inter-subunit interaction between the N-terminal domain of hcTnC and the C-terminal switch peptide of hcTnI; disruption of the interaction has been recognized as a potential therapeutic strategy for CDs. Here, we report use of biogenic medicines as small-molecule competitors to directly disrupt the protein–protein interaction by competitively targeting the core binding site (CBS) of hcTnC NTD domain. A multistep virtual screening protocol is performed against a biogenic compound library to identify competitor candidates and competition assay is employed to verify the screening results. Consequently, two compounds Collismycin and Compound e are identified as strong competitors (CC₅₀ < 10 μM) with hcTnI for hcTnC CBS site, while other tested compounds are found to have moderate (CC₅₀ = 10–100 μM), low (CC₅₀ > 100 μM) or no (CC₅₀ = N.D.) potency. The competitor ligands are anchored at the core groove of hcTnC CBS site through aromatic and hydrophobic interactions, while few peripheral hydrogen bonds are formed to further confer specificity for domain–compound recognition. These molecular-level findings would benefit from further in vitro and in vivo studies at cellular and animal levels, which can help to practice the ultimate therapeutic purpose.     

Substituent-regulated highly X-ray sensitive Os(Ⅵ)nitrido complex for low-toxicity radiotherapy

A high efficiency and low toxicity radiosensitizer,OsN(PhenOH)Cl_3,was designed and synthesized through substituent regulation.To the best of our knowledge,this is the first osmium-based coordination complex radiosensitizer.The experimental results shown that this radiosensitizer induced G2/M cell cycle arrest mainly through induction of intracellular ROS overproduction.     

Synthesis,structure, characterization and biological evaluation of 3‐substituted 1‐pyridin‐2‐ylimidazo[1,5‐a]pyridine‐based copper(I)–phosphine complexes for anticancer drug screening

Copper(I) complexes of the types [Cu(N–N)(PPh₃)₂]NO₃ (LC41–LC44) and [Cu(N–N)(PPh₃)(NO₃)] (LC45) carrying 3‐substituted 1‐pyridine‐2‐ylimidazo[1,5‐a]pyridine (N–N) derivatives and triphenylphosphine (PPh₃) ligands have been prepared. The synthesized copper(I)–phosphine complexes were fully characterized by NMR, IR, ESI‐MS and UV–visible spectroscopy as well as by cyclic voltammetry. Selected structures such as LC42, LC43 and LC45 were additionally analysed by single‐crystal X‐ray method, which show that copper(I) centre adopts a highly distorted tetrahedral geometry. The ¹H and ¹³C NMR spectral data of the complexes throw light on the nature of metal–ligand bonding. They display dπ–π* metal‐to‐ligand charge transfer (MLCT) transition and show quasireversible Cu^I/Cu^II metal oxidation. Among the copper(I)–phosphine complexes, LC41–LC44 exhibit moderate cytotoxicity (IC₅₀: 24 h, 67–74 μM; 48 h, 58–70 μM) against human lung epithelial adenocarcinoma A549 cells, whereas LC45 displays the best activity (IC₅₀: 24 h, 42 μM; 48 h, 34 μM) for A549 cancer cell line, which is better than that of the commercial antitumor drug cisplatin. All the complexes also displayed excellent selectivity by being relatively inactive against the human lung epithelial L132 normal cell line with selectivity index (SI) values ranging from 3.4 to 7.4. The complexes block cell cycle progression of A549 cells in G₀/G₁ phase. FACSVerse analyses are suggestive of reactive oxygen species (ROS) generation and apoptotic cell death induced by the LC41, LC43 and LC45. The induction of apoptosis in A549 cells was shown by Annexin V with propidium iodide (PI) and 4′,6‐diamidino‐2‐phenylindole (DAPI) staining methods and established the ability of LC41, LC43 and LC45 to accumulate in the cell nuclei.