TiNi合金的耐磨机制及其摩擦学应用研究

TiNi合金是一种新型的性能优异的摩擦学材料,其摩擦学特性主要与相变超弹性有关,快速应变硬化、耐腐蚀及抗疲劳等特性也对合金的耐磨性能有很大帮助.本研究从相变超弹性产生机制、产生条件及影响因素等方面揭示了其优异摩擦学特性的原因,介绍了提高和充分发挥相变超弹性的措施,回顾了超弹TiNi合金在摩擦学方面的应用研究进展,提出了若干发展方向及亟待解决的问题.     

荔枝果壳原花青素对中波紫外线诱导HaCaT细胞氧化损伤的保护作用

为评价荔枝果壳原花青素对中波紫外线（ultraviolet B,UVB）（波长280～320 nm）诱导人永生化角质形成细胞（HaCaT）氧化损伤的保护作用。构建UVB辐射HaCaT细胞氧化损伤模型,研究荔枝果壳低聚原花青素（litchi pericarp oligomolymeric procyanidins,LPOPC）及从中分离鉴定的6 种单体化合物对HaCaT细胞氧化损伤的保护作用。实验分为对照组、UVB照射组、实验组（阳性对照对氨基苯甲酸（para-aminobenzoic acid,PABA）、LPOPC及6 种单体化合物）,以CCK-8法测定各组细胞活力,采用试剂盒检测各组细胞内活性氧自由基（reactive oxygen species,ROS）相对含量,超氧化物歧化酶（superoxide dismutase,SOD）、过氧化氢酶（catalase,CAT）、谷胱甘肽过氧化物酶（glutathione peroxidase,GSH-Px）活力,还原型谷胱甘肽（glutathione,GSH）及丙二醛（malondialdehyde,MDA）含量。结果表明：LPOPC及6 种单体化合物的干预处理均可明显提高UVB诱导氧化损伤的HaCaT细胞活力,减少细胞内ROS和MDA的生成,增加SOD、CAT、GSH-Px的活力和GSH水平。6 种单体化合物中,原花青素A2的保护作用最明显,与阳性药物PABA的效果相当。结论：LPOPC及6 种单体化合物均可通过增强细胞内抗氧化能力、抑制脂质过氧化来明显改善受损细胞氧化应激损伤,对UVB诱导氧化损伤的HaCaT细胞具有良好的保护作用,提示原花青素A2是荔枝果壳原花青素中对氧化应激损伤防护作用最强的活性组分。     

自增强高性能聚合物的成型工艺同力学性能间相关性研究——2.超拉伸高聚物的弹性模量同其起始结构和成型工艺间的关系

本文提出一种表征超拉伸高聚物的拉伸模量新方法,从应力诱导结晶理论出发,推出了超拉伸高聚物的弹性模量同其起始结构和成型工艺条件间的定量关系式。当引入等速拉伸和起始分子量分布按Schultz-Flory 分布后,便得到其拉伸模量同起始数均分子量、超拉伸比、拉伸速率和试样长径比等间的定量关系式。采用该关系式处理了大量的实验数据,均得到了预期的直线。当引入超拉伸比和起始分子量趋近于无穷大后,就得到了预期的理论模量。     

Phase transformation behaviors and shape memory effects of TiNiFeAl shape memory alloys

Measurements of electrical resistivity, X-ray diffraction, and tensile test at room temperature and ?196°C were performed to investigate the effects of Al addition substituting Ni on the phase transformation behaviors, the mechanical properties, and the shape memory effects of Ti50Ni47Fe2Al1 and Ti50Ni46.5Fe2.5Al1 alloys. It is found that 1at% Al addition dramatically decreases the martensitic start transformation temperature and expands the transformation temperature range of R-phase for TiNiFeAl alloys. The results of tensile test indicate that 1at% Al improves the yield strength of Ti50Ni47Fe2Al1 and Ti50Ni46.5Fe2.5Al1 alloys by 40% and 64%, but de- creases the plasticity to 11% and 12% from 26% and 27% respectively. Moreover, excellent shape memory effect of 6.6% and 7.5% were found in Ti50Ni47Fe2Al1 and Ti50Ni46.5Fe2.5Al1 alloys, which results from the stress-induced martensite transformation from the R-phase.     

Hepatic Senescence Accompanies the Development of NAFLD in Non-Aged Mice Independently of Obesity

Senescence is considered to be a cardinal player in several chronic inflammatory and metabolic pathologies. The two dominant mechanisms of senescence include replicative senescence, predominantly depending on age-induced telomere shortening, and stress-induced senescence, triggered by external or intracellular harmful stimuli. Recent data indicate that hepatocyte senescence is involved in the development of nonalcoholic fatty liver disease (NAFLD). However, previous studies have mainly focused on age-related senescence during NAFLD, in the presence or absence of obesity, while information about whether the phenomenon is characterized by replicative or stress-induced senescence, especially in non-aged organisms, is scarce. Herein, we subjected young mice to two different diet-induced NAFLD models which differed in the presence of obesity. In both models, liver fat accumulation and increased hepatic mRNA expression of steatosis-related genes were accompanied by hepatic senescence, indicated by the increased expression of senescence-associated genes and the presence of a robust hybrid histo-/immunochemical senescence-specific staining in the liver. Surprisingly, telomere length and global DNA methylation did not differ between the steatotic and the control livers, while malondialdehyde, a marker of oxidative stress, was upregulated in the mouse NAFLD livers. These findings suggest that senescence accompanies NAFLD emergence, even in non-aged organisms, and highlight the role of stress-induced senescence during steatosis development independently of obesity.     

Modeling of the Senescence-Associated Phenotype in Human Skin Fibroblasts

Modern understanding of aging is based on the accumulation of cellular damage during one’s life span due to the gradual deterioration of regenerative mechanisms in response to the continuous effect of stress, lifestyle, and environmental factors, followed by increased morbidity and mortality. Simultaneously, the number of senescent cells accumulate exponentially as organisms age. Cell culture models are valuable tools to investigate the mechanisms of aging by inducing cellular senescence in stress-induced premature senescence (SIPS) models. Here, we explain the three-step and one-step H₂O₂-induced senescence models of SIPS designed and reproduced on different human dermal fibroblast cell lines (CCD-1064Sk, CCD-1135Sk, and BJ-5ta). In both SIPS models, it was evident that the fibroblasts developed similar aging characteristics as cells with replicative senescence. Among the most noticeable senescent biomarkers were increased β-Gal expression, high levels of the p21 protein, altered levels of cell-cycle regulators (i.e., CDK2 and c-Jun), compromised extracellular matrix (ECM) composition, reduced cellular viability, and delayed wound healing properties. Based on the significant increase in senescence biomarkers in fibroblast cultures, reduced functional activity, and metabolic dysfunction, the one-step senescence model was chosen as a feasible and reliable method for future testing of anti-aging compounds.     

热诱发ε马氏体量对Co-30Ni合金形状记忆效应的影响

为了明确具有ε马氏体转变的Co-Ni基合金形状记忆效应的来源,通过控制不同变形温度,在Co-30Ni合金中获得不同数量的热诱发ε马氏体,在此基础上利用OM和XRD研究了变形时预先存在的热诱发ε马氏体的演化及其对应力诱发ε马氏体转变的影响,并采用弯曲法表征了合金的形状记忆效应。结果表明:合金的形状记忆效应都随热诱发和应力诱发ε马氏体数量的增加而升高,但原位金相未观察到热诱发ε马氏体在应力下的长大合并。Co-Ni基合金的形状记忆效应来源于应力诱发ε马氏体转变,而不是热诱发ε马氏体在应力下的长大合并。低的母相屈服强度是Co-Ni合金形状记忆效应差的原因。预先形成的热诱发ε马氏体能提高母相的屈服强度,因而有利于形状记忆效应的提高。     

NiTi-Nb原位复合材料的准线性超弹性变形EI北大核心CSCD

据文献报道,Nb纳米线增强NiTi记忆合金复合材料可展现超常的准线性超弹特性。为揭示该准线性超弹特性的产生和变形机制,通过真空感应熔炼、锻造、拔丝方法原位合成了NiTi-Nb复合材料丝材。TEM显微分析表明,Nb纳米线沿丝材轴向平行分布在纳米晶NiTi基体中。该材料在经历一次9%的预变形后会展现准线性超弹特性,其屈服强度达1.7 GPa,表观Young's模量约34 GPa,准线性超弹性应变接近5.5%。同步辐射高能X射线原位拉伸实验结果表明,准线性超弹性的产生与以下2点原因有关:(1)复合材料经历预变形后,Nb纳米线和NiTi基体间会产生耦合力,再次加载时,NiTi所受的耦合拉应力可以将局部区域应力诱发马氏体相变所需的外应力降低到零附近,并且耦合力越大,加载初期的相变速率越高,经过适当的预变形后,加载初始就能够持续发生高速率相变;(2) NiTi中耦合拉应力呈梯度分布,使相变应力-应变曲线不再是常见的“平台型”,转变为“硬化型”斜线。