除尘脱硝一体化玻纤/P84复合毡覆膜滤料制备及性能研究

介绍了除尘脱硝一体化玻纤/P84复合毡覆膜滤料的制备和性能研究。通过基材的结构设计等关键技术研发,制备了除尘脱硝一体化玻纤/P84复合毡覆膜滤料,性能测试结果为颗粒物排放4.36 mg/m³,氮氧化物排放38 mg/m³,结果优于环保要求。     

聚酰亚胺P84纤维与玄武岩纤维复合耐高温过滤毡

本实用新型一种聚酰亚胺P84纤维与玄武岩纤维复合耐高温过滤毡,在玻璃纤维基布的上、下各粘有一层聚酰亚胺P84纤维与玄武岩纤维混合纤维层,在迎尘面的聚酰亚胺P84纤维与玄武岩纤维混合纤维层上覆盖有聚四氟乙烯PTFE涂层。本实用新型的优点是耐高温,     

针刺炭布／网胎复合织物中的纤维转移和损伤研究

将T-300炭纤维平纹布和聚丙烯腈(PAN)预氧化纤维网胎预复合后,使用15×16×36×3C222G73012型刺针,接力层叠针刺制备炭布/网胎复合织物。通过SEM研究了刺针对纤维的转移作用及损伤情况。结果表明,网胎纤维在刺针倒钩带动下,沿垂直方向转移后,以"销钉"作用形成"板钉"状网络结构,和平面织物一起构成复合织物的准三维网络结构;在针刺过程中,刺针对网胎和炭布纤维造成不同程度的损伤,特别是炭布纤维的损伤造成平面内强度的大幅度降低,在针刺密度为8针/cm2,针刺深度为12mm的情况下,炭布拉伸强力经向从2140N下降为1440N,纬向从1970N下降为1280N。损伤的炭布纤维在z向基本无转移增强作用。     

DBDPE-Sb2O3复合阻燃长玻纤增强聚丙烯性能的研究

采用十溴二苯乙烷(DBDPE)协同三氧化二锑(Sb2O3)组成复合阻燃剂DBDPE-Sb2O3阻燃长玻纤增强聚丙烯(LGFPP),通过氧指数测定仪、水平-垂直燃烧试验仪、锥形量热仪、万能试验机和冲击试验机研究了DBDPE-Sb2O3的用量对DBDPE-Sb2O3/LGFPP复合材料的阻燃性能、热稳定性能、燃烧性能和力学性能的影响。结果表明,当DBDPE-Sb2O3复合阻燃剂质量分数为16%时,DBDPE-Sb2O3/LGFPP复合材料的氧指数和垂直燃烧等级分别达到了26.54%和FV-0级,且力学性能最优;DBDPE-Sb2O3提高了复合材料的热稳定性,降低了复合材料的热释放速率平均值及峰值,延缓了复合材料的引燃时间。     

岔30断块S/P二元复合驱实验研究

针对华北岔30断块90℃高温、地层水矿化度18765.1 mg/L的特点,筛选得到了石油磺酸盐CDS-1与疏水缔合聚合物HNT201-3二元复合体系。0.05%CDS-1/HNT201-3二元复合体系与原油的界面张力可降到10^-2mN/m数量级;当HNT201-3浓度为1250mg/L时,复合体系的表观粘度为23.7 mPa.s。非均质岩心（模拟油层非均质变异系数和平均空气渗透率）驱油试验结果表明,注入驱油体系0.3PV、后续保护段塞0.1PV（聚合物HNT201-3浓度1250mg/L）时,可比水驱提高采收率19.73%OOIP。     

过滤用玻纤复合针刺毡的研发

介绍了玻纤针刺毡的概念、特点及加工工艺。着重介绍了新型过滤材料一玻纤复合针刺毡的原料选择和加工工艺的确定。     

燃烧合成Cf/TiC-TiB2复合材料过程中碳纤维的损断机理

采用燃烧合成结合准热等静压的方法制备了Cf/TiC-TiB2复合材料,详细分析了材料制备过程中碳纤维的损断机理。研究结果表明,在剪短、湿混以及加压过程中会造成纤维的物理损伤和断裂;Ti和O原子与碳纤维表面C原子反应会造成纤维的化学损伤;残余应力导致纤维的高温损伤和断裂。     

Examination of Longitudinal Alterations in Alzheimer’s Disease-Related Neurogenesis in an APP/PS1 Transgenic Mouse Model,and the Effects of P33, a Putative Neuroprotective Agent Thereon

Neurogenesis plays a crucial role in cognitive processes. During aging and in Alzheimer’s disease (AD), altered neurogenesis and neuroinflammation are evident both in C57BL/6J, APP_Swe/PS1_dE9 (Tg) mice and humans. AD pathology may slow down upon drug treatment, for example, in a previous study of our group P33, a putative neuroprotective agent was found to exert advantageous effects on the elevated levels of APP, Aβ, and neuroinflammation. In the present study, we aimed to examine longitudinal alterations in neurogenesis, neuroinflammation and AD pathology in a transgenic (Tg) mouse model, and assessed the putative beneficial effects of long-term P33 treatment on AD-specific neurological alterations. Hippocampal cell proliferation and differentiation were significantly reduced between 8 and 12 months of age. Regarding neuroinflammation, significantly elevated astrogliosis and microglial activation were observed in 6- to 7-month-old Tg animals. The amounts of the molecules involved in the amyloidogenic pathway were altered from 4 months of age in Tg animals. P33-treatment led to significantly increased neurogenesis in 9-month-old animals. Our data support the hypothesis that altered neurogenesis may be a consequence of AD pathology. Based on our findings in the transgenic animal model, early pharmacological treatment before the manifestation of AD symptoms might ameliorate neurological decline.