微尾鼩的食性与防治初探

通过对微尾鼩胃容物的检验及个体饲养研究,以确定其食物组成和取食特性,并结合其生态地位来对其种群进行防治。结果表明微尾鼩主食蚯蚓及各类昆虫、肉类等,对各类作物的种子也有明显的喜好性,偶尔会取食某些绿色植物的茎杆、叶片。分析结果表明,可使用能降低其繁殖力的非毒杀饵料来控制其种群数量。     

优势黄杆菌对蒽、菲、芘混合物的降解特征研究

为探索混合多环芳烃的生物降解特征，利用两株优势黄杆菌，对混合蒽、菲、芘进行了降解研究．高效液相色谱分析表明，混合多环芳烃的降解56．3％～69．6％在前10h内完成，其生物降解进程和单基质相似，但降解效率低于单基质．混合体系中蒽、菲、芘在不同菌株作用下有按特定优先顺序降解的特征，但两株黄杆菌(FCN1和FCN2)的混合菌并不促进混合多环芳烃的降解．降解130h后，体系中蒽、菲、芘消除，但总有机碳去除率仅达到60．1％～72．7％，说明部分多环芳烃转化为中间代谢产物．菌数测定表明，FCN1和FCN2利用多环芳烃及其降解中间产物繁殖生长，菌数最高时分别增长200倍和100倍，但菌数增长滞后于多环芳烃的浓度变化．研究表明，混合多环芳烃之间具有降解竞争抑制特征，且其生物降解具有规律性．     

热网络法预测车内温度的理论和实验研究

为对车内温度水平进行预测,采用热网络法对车辆停车和行驶状态下的车内温度进行计算。太阳辐射是影响车内温度水平的主要因素,而热网络法通过建立和求解节点热平衡方程,获得各节点的温度,尤其适用于以辐射为主的换热问题。车内外的对流换热采用实验关联式进行计算。由热网络法建立的节点热平衡方程组为非线性方程组,采用牛顿迭代法进行了求解。计算结果与实测温度值的比较显示,两者吻合较好,表明热网络法用于车内温度预测的有效性。另外,计算结果也显示车窗玻璃的透射率对车内温度有明显影响,在考虑安全的前提下,选取合适透射率的车窗玻璃材料可起到减少车辆能耗的作用。     

Nb微合金化对低合金高强钢耐海水腐蚀性能的影响

利用室内模拟海水加速腐蚀试验及电化学分析,研究了Nb微合金化对Cu-Cr-Ni-P系低合金高强钢耐海水腐蚀性能的影响。结果表明,含Nb钢与不含Nb钢组织均由铁素体和珠光体构成,但Nb微合金化后钢中珠光体组织减少且晶粒细化明显,其在模拟海水介质中的平均腐蚀速率与不含Nb钢相比,降低了约12%,阳极腐蚀电流密度也有所降低。由此可见,在Cu-Cr-Ni-P系低合金高强钢中加入Nb元素有助于提高其耐海水腐蚀性能。     

1000 mm2 cross-section wire a led four tension exhibition put to traction practice

文章介绍了宁东一山东±660 kV直流输电示范工程(晋4标段)1 000 mm2大截面导线一牵四张力展放施工中,使用4个转向滑车转向布置牵引场的实践过程及施工中的注意事项.     

粒度组成对KR搅拌头用浇注料性能的影响

以Andreassen颗粒紧密堆积理论为基础,研究KR搅拌头外衬莫来石浇注料临界粒度和粒度组成对其密度、强度和热震稳定性的影响.结果表明,随着临界粒度的增大,浇注料干燥和烧结后冷态密度与强度均明显提高;临界粒度一定时,粒度组成对浇注料冷态密度、强度以及热震稳定性的影响基本一致,但临界粒度不同的浇注料试样达到最佳性能所对应的粒度组成并不完全相同;与冷态性能相比,浇注料热震稳定性受临界粒度的影响较小.     

铁掺杂TiO_2-SBA-15催化剂制备及光催化降解甲基橙研究

采用溶胶-凝胶法,将TiO_2负载到介孔分子筛SBA-15上,再通过FeCl3浸渍的方法,将不同量的铁掺杂到TiO_2-SBA-15上.通过FT-IR、XRD、N2吸附-脱附和TEM等手段对铁掺杂TiO_2-SBA-15催化剂进行表征.结果表明:负载TiO_2后的SBA-15依然为高度有序的二维六方结构,比表面积略有减小,说明SBA-15的孔道结构有利于TiO_2的分散.掺铁后的TiO_2-SBA-15的结构改变不大,且TiO_2晶形仍为锐钛矿型.最后以光催化降解甲基橙探究不同铁掺杂量的TiO_2-SBA-15催化活性.结果表明:铁离子掺杂量为0.035%(质量分数),紫外光照射200min时,甲基橙降解率达最高值98.2%.     

热处理对以Al2O3为绝缘层的并五苯薄膜晶体管性能的影响

采用阳极氧化法制备了Al_2O_3绝缘材料,并制备了以Al_2O_3为绝缘层的并五苯薄膜晶体管器件(OTFT)。Al_2O_3绝缘层经过10 min 350℃氢热处理后,OTFT迁移率比未经氢热处理的增大近20倍,且阈值电压降到了-7 V。Al_2O_3膜MIS结构电容—电压(C–V)特性的平带电压平移量数据表明,Al_2O_3膜经过热处理后,并五苯半导体与Al_2O_3绝缘体界面处以及绝缘体内缺陷态密度显著地降低,Al_2O_3绝缘层和并五苯半导体层之间的接触得到改善,这使得经热处理Al_2O_3膜的OTFT器件性能得到显著的改善。     

HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS

A prominent feature of late-onset neurodegenerative diseases is accumulation of misfolded protein in vulnerable neurons. When levels of misfolded protein overwhelm degradative pathways, the result is cellular toxicity and neurodegeneration. Cellular mechanisms for degrading misfolded protein include the ubiquitin-proteasome system (UPS), the main non-lysosomal degradative pathway for ubiquitinated proteins, and autophagy, a lysosome-mediated degradative pathway. The UPS and autophagy have long been viewed as complementary degradation systems with no point of intersection. This view has been challenged by two observations suggesting an apparent interaction: impairment of the UPS induces autophagy in vitro, and conditional knockout of autophagy in the mouse brain leads to neurodegeneration with ubiquitin-positive pathology. It is not known whether autophagy is strictly a parallel degradation system, or whether it is a compensatory degradation system when the UPS is impaired; furthermore, if there is a compensatory interaction between these systems, the molecular link is not known. Here we show that autophagy acts as a compensatory degradation system when the UPS is impaired in Drosophila melanogaster, and that histone deacetylase 6 (HDAC6), a microtubule-associated deacetylase that interacts with polyubiquitinated proteins, is an essential mechanistic link in this compensatory interaction. We found that compensatory autophagy was induced in response to mutations affecting the proteasome and in response to UPS impairment in a fly model of the neurodegenerative disease spinobulbar muscular atrophy. Autophagy compensated for impaired UPS function in an HDAC6-dependent manner. Furthermore, expression of HDAC6 was sufficient to rescue degeneration associated with UPS dysfunction in vivo in an autophagy-dependent manner. This study suggests that impairment of autophagy (for example, associated with ageing or genetic variation) might predispose to neurodegeneration. Morover, these findings suggest that it may be possible to intervene in neurodegeneration by augmenting HDAC6 to enhance autophagy.