Mo-30Cu合金室温变形组织

对Mo-30Cu合金室温拉伸性能进行了研究,并对其断口进行观察分析.通过对Mo-30Cu合金冷轧实验,研究了不同变形量下组织的变化规律.结果表明:Mo-30Cu合金的断裂以Cu相的韧性断裂为主,并伴随着Mo/Cu界面的分离和Mo晶粒的解理断裂.Mo/Cu界面的分离和Mo晶粒的解理断裂是Mo-30Cu合金室温轧制过程中产生裂纹的主要原因.     

Mn含量对铸造高铌TiAl合金组织和性能的影响

选择两种Mn含量不同的高铌TiAl合金Ti46Al8Nb2Mn0.2B和Ti46Al8Nb1.3Mn0.2B,通过热等静压(HIP)及后续热处理,结合组织和力学性能的分析,研究了Mn含量对高铌TiAl合金的组织和性能的影响.XRD和SEM背散射电子实验结果表明:Mn含量较高的Ti46Al8Nb2Mn0.2B合金,经热等静压及循环热处理,得到的双态组织较粗大,并且有少量脆性β相存在;Mn含量较低的Ti46Al8Nb1.3Mn0.2B合金,经热等静压后直接在双相区长时间保温处理,得到了细小的双态组织,并且完全消除了β相.室温拉伸实验表明,Mn含量的降低提高了Ti46Al8Nb1.3Mn0.2B合金的力学性能,其延伸率、屈服强度和断裂强度分别达到2.4%、548MPa和660MPa.断口形貌分析表明,室温下两种合金都属于解理断裂.     

The Reactions of N,N′-Diphenyldithiomalondiamide with Arylmethylidene Meldrum’s Acids

The Michael addition reaction between dithiomalondianilide (N,N′-diphenyldithiomalondiamide) and arylmethylidene Meldrum’s acids, accompanied by subsequent heterocyclization, was investigated along with factors affecting the mixture composition of the obtained products. The plausible mechanism includes the formation of stable Michael adducts which, under the studied conditions, undergo further transformations to yield corresponding N-methylmorpholinium 4-aryl-6-oxo-3-(N-phenylthio-carbamoyl)-1,4,5,6-tetrahydropyridin-2-thiolates and their oxidation derivatives, 4,5-dihydro-3H-[1,2]dithiolo[3,4-b]pyridin-6(7H)-ones. The structure of one such product, N-methylmorpholinium 2,2-dimethyl-5-(1-(2-nitrophenyl)-3-(phenylamino)-2-(N-phenylthiocarbamoyl)-3-thioxopropyl)-4-oxo-4H-1,3-dioxin-6-olate, was confirmed via X-ray crystallography.     

论《追风筝的人》中的背叛与救赎

用文学批评的手法从社会学的角度研究了卡勒德·胡赛尼的作品《追风筝的人》中阿富汗贫富悬殊下的社会伦理和人物冲突,以及身处不同阶级和宗教信仰里友谊与背叛之间的矛盾;并分析了文中风筝的象征意义,探讨了人性的本质与救赎。     

Q235低碳钢高温变形过程的动态组织演化分析

通过Gleeble 2000上的热模拟压缩实验,分析了Q235低碳钢在不同热加工参数下的动态组织演化特征.结果表明:应变速率和温度对Q235钢的奥氏体形变特征影响强烈.在相同变形温度下,应变速率的提高可以明显推迟动态再结晶的发生:应变速率较低时,降低温度同样可以延迟动态再结晶的发生.利用定量金相技术及线性、非线性拟合算法,建立了 Q235钢热变形过程的唯像本构关系及组织演化动力学模型,并将其应用于Autoforge3.1有限元软件平台.压缩过程有限元模拟分析表明,分别采用Arrhenius双曲正弦方程描述Q235钢的唯像本构关系及Yada模型表征Q235钢变形过程的平均晶粒尺寸,可以满足预测精度,与实际变形过程基本吻合.     

卷取温度对IF钢组织性能影响规律

 选取IF软钢为研究对象,考虑热轧边部温降的影响,对其热轧卷取温度进行调整试验,并对热轧基料与冷轧成品卷分别进行力学性能、金相组织的分析,研究热轧卷取温度对冷轧成品组织性能的影响。结果表明,卷取温度对IF钢屈服强度、抗拉强度无显著影响,伸长率随温度升高先升高后降低,r值在卷取温度为750 ℃时最高;卷取温度升高时,热轧基料边部出现混晶及组织不均匀现象,冷轧退火会加剧组织不均匀,造成IF钢边部混晶。研究结果对于揭示IF钢板生产工艺与性能之间的内在联系有重要意义,也对指导企业制定低耗高效的轧制工艺参数以获得性能优异的产品具有积极作用。     

Corrosion behaviour of Al1.3CrFeNi chemically complex alloy

In this study, corrosion behaviour of double-phase Al_1.3CrFeNi chemically complex alloy was investigated, including hot corrosion and electrochemical corrosion. Hot corrosion behaviour of Al_1.3CrFeNi alloy was explored in molten 75 wt-% Na₂SO₄?+?25 wt-% NaCl salt. The result revealed that the corrosion kinetic curve of Al_1.3CrFeNi alloy followed the exponential rate rule through mass loss measurement. In addition, it prevented that the formed corrosion layer had obvious stratification including external granular Al₂O₃ and inner porous Cr₂O₃ when corrosion time was up to 100?h. Besides, it should be noted that the Al_1.3CrFeNi alloy was sensitive to the molten salt containing chlorine, which makes the alloy surface leave voids and bring about acceleration of corrosion. Meanwhile, electrochemical corrosion resistance of Al_1.3CrFeNi alloy in NaCl solution with different concentrations (0.6, 1.0 and 2.0?mol?L^?1) was investigated at room temperature. The results revealed that Al_1.3CrFeNi alloy showed superior corrosion resistance in NaCl solution due to the existence of Al and Cr which aid the formation of protective oxide layer.     

The Anxiolytic Drug Buspirone Prevents Rotenone-Induced Toxicity in a Mouse Model of Parkinson’s Disease

A pharmacological and genetic blockade of the dopamine D3 receptor (D3R) has shown to be neuroprotective in models of Parkinson’s disease (PD). The anxiolytic drug buspirone, a serotonin receptor 1A agonist, also functions as a potent D3R antagonist. To test if buspirone elicited neuroprotective activities, C57BL/6 mice were subjected to rotenone treatment (10mg/kg i.p for 21 days) to induce PD-like pathology and were co-treated with increasing dosages of buspirone (1, 3, or 10 mg/kg i.p.) to determine if the drug could prevent rotenone-induced damage to the central nervous system (CNS). We found that high dosages of buspirone prevented the behavioural deficits caused by rotenone in the open field test. Molecular and histological analyses confirmed that 10 mg/kg of buspirone prevented the degeneration of TH-positive neurons. Buspirone attenuated the induction of interleukin-1β and interleukin-6 expression by rotenone, and this was paralleled by the upregulation of arginase-1, brain-derived neurotrophic factor (BDNF), and activity-dependent neuroprotective protein (ADNP) in the midbrain, striatum, prefrontal cortex, amygdala, and hippocampus. Buspirone treatment also improved mitochondrial function and antioxidant activities. Lastly, the drug prevented the disruptions in the expression of two neuroprotective peptides, pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP). These results pinpoint the neuroprotective efficacy of buspirone against rotenone toxicity, suggesting its potential use as a therapeutic agent in neurodegenerative and neuroinflammatory diseases, such as PD.     

Roles of α-Synuclein and Disease-Associated Factors in Drosophila Models of Parkinson’s Disease

α-Synuclein (αSyn) plays a major role in the pathogenesis of Parkinson’s disease (PD), which is the second most common neurodegenerative disease after Alzheimer’s disease. The accumulation of αSyn is a pathological hallmark of PD, and mutations in the SNCA gene encoding αSyn cause familial forms of PD. Moreover, the ectopic expression of αSyn has been demonstrated to mimic several key aspects of PD in experimental model systems. Among the various model systems, Drosophila melanogaster has several advantages for modeling human neurodegenerative diseases. Drosophila has a well-defined nervous system, and numerous tools have been established for its genetic analyses. The rapid generation cycle and short lifespan of Drosophila renders them suitable for high-throughput analyses. PD model flies expressing αSyn have contributed to our understanding of the roles of various disease-associated factors, including genetic and nongenetic factors, in the pathogenesis of PD. In this review, we summarize the molecular pathomechanisms revealed to date using αSyn-expressing Drosophila models of PD, and discuss the possibilities of using these models to demonstrate the biological significance of disease-associated factors.