电动自行车用蓄电池正极板活性物质与板栅结合力的探讨

增强活性物质和板栅之间的结合力,可解决电动自行车用蓄电池”早期容量衰减”的问题。经过生产实践,总结出采用合适的固化方法可增强活性物质和板栅之间的结合力,并详细介绍了固化方法的要领。本文还认为,在电动自行车电池正极活性物质配方中添加铋的化合物、聚四氟乙烯（PTFE）乳液及短纤维时,这3种物质可组成强固的网络,在电池整个循环寿命周期内,保持正极活性物质不脱落,正极板孔率不降低,从而延长电动自行车电池的循环寿命。     

基于变异粒子群算法的过程挖掘

为实现过程挖掘,克服标准粒子群算法易陷入局部极值的缺点,提出基于变异操作的粒子群过程挖掘方法。在标准粒子群算法进化中,所有粒子追随最优粒子在解空间搜索,导致种群多样性迅速下降,出现早熟收敛。受遗传算法启发,通过对进化中的粒子增加变异操作,使算法摆脱易于陷入局部极值点的束缚,增强算法跳出局部最优的能力。仿真结果表明,基于变异粒子群算法的过程挖掘在求解的精度和速度方面都得到了好的效果。     

正交Alopex算法在机械优化设计中的应用

针对Alopex算法对初值敏感的特性及正交设计可以使初始种群在空间分布更加均匀的特点,提出了正交Alopex算法。该算法为了克服后期"早熟"收敛的缺陷,引入了变异操作。数值仿真结果及两个工程优化问题的求解结果表明,所提出的算法能有效避免"早熟"收敛,且求解结果优于传统优化及比较算法。     

轮胎胶应力诱导脱硫化及PE-HD动态交联热塑性弹性体制备

采用在废旧轮胎胶粉(GTR)与高密度聚乙烯(PE-HD)的熔融挤出过程中提高双螺杆挤出机螺杆转速的高剪切应力诱导方法,研究了双螺杆挤出机的螺杆转速、挤出反应温度及脱硫促进剂仲丁醇、烷基酚多硫化物(420或450)和正丁胺对轮胎胶脱硫共混物的凝胶含量、熔体流动速率、溶胶红外吸收光谱及轮胎胶脱硫共混物/三元乙丙橡胶(EPDM)动态交联热塑性弹性体力学性能的影响。结果表明:高转速同向双螺杆挤出机的高剪切作用可诱发废旧轮胎胶共混物中交联网络的断链和解交联反应,引起脱硫共混物凝胶含量的下降、未熔融凝胶颗粒尺寸的减小及熔体流动速率的增加;4种促进剂均具有明显促进脱硫反应的作用,其中450或正丁胺的促进脱硫效果较好,并引起脱硫共混物凝胶含量下降、熔体流动速率上升及动态交联热塑性弹性体力学性能的明显改善;当以正丁胺为脱硫促进剂时,最佳脱硫反应条件(240℃和1000r/min)下,脱硫共混物/EPDM动态交联热塑性弹性体的拉伸强度和断裂伸长率分别达到12.5MPa和440.6%。     

应变速率对Fe-Mn-Si-Cr-Ni合金组织和力学性能的影响

目前的TRIP钢由于Mn、Si含量较低,室温条件下仅保留约10%的残余奥氏体,结果使变形过程中材料产生的相变诱发塑性量有限,不能满足一些要求产生更大相变诱发塑性场合的需要。研究表明：提高钢中Mn、Si含量并辅以适量其它合金元素（如铬和镍）是提高材料相变诱发塑性的有效途径。研究了Fe-17Mn-5Si-10Cr-4Ni合...     

石竹菜不同贮藏条件下衰老指标的研究

分别对石竹莱在不同贮藏条件下的几项衰老指标进行了测定,结果表明:对照组(25℃)和保鲜组(25℃)采后出现明显的衰老代谢特征,表现为呼吸速率上升,MDA含量增加,POD、CAT活性升高;其中,对照组贮藏第4d各项指标达最大值,之后下降;保鲜组第6d达最大值,之后下降;冷藏组(4℃)在贮藏期间维持了较低的呼吸速率、MDA含量和较低的POD、CAT活性。     

水分胁迫对冷藏韭菜叶片衰老和活性氧代谢的影响

与保水处理韭菜相比,对照(CK)韭菜冷藏期间,失水很快,遭受严重水分胁迫,其叶片叶绿素含量和色调角(hueangle)值显著降低。水分胁迫降低了韭菜抗氧化剂、类胡萝卜素和抗坏血酸含量,抑制了抗氧化酶特别是SOD(超氧化物歧化酶)和CAT(过氧化氢酶)活性,促进了H2O2和膜脂过氧化产物MDA(丙二醛)的积累。采后水分胁迫促进了冷藏韭菜衰老,其机制与水分胁迫促进活性氧代谢失调和膜脂过氧化有关。     

Potential of Telomerase in Age-Related Macular Degeneration—Involvement of Senescence,DNA Damage Response and Autophagy and a Key Role of PGC-1α

Age-related macular degeneration (AMD), the main cause of vision loss in the elderly, is associated with oxidation in the retina cells promoting telomere attrition. Activation of telomerase was reported to improve macular functions in AMD patients. The catalytic subunit of human telomerase (hTERT) may directly interact with proteins important for senescence, DNA damage response, and autophagy, which are impaired in AMD. hTERT interaction with mTORC1 (mTOR (mechanistic target of rapamycin) complex 1) and PINK1 (PTEN-induced kinase 1) activates macroautophagy and mitophagy, respectively, and removes cellular debris accumulated over AMD progression. Ectopic expression of telomerase in retinal pigment epithelium (RPE) cells lengthened telomeres, reduced senescence, and extended their lifespan. These effects provide evidence for the potential of telomerase in AMD therapy. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) may be involved in AMD pathogenesis through decreasing oxidative stress and senescence, regulation of vascular endothelial growth factor (VEGF), and improving autophagy. PGC-1α and TERT form an inhibitory positive feedback loop. In conclusion, telomerase activation and its ectopic expression in RPE cells, as well as controlled clinical trials on the effects of telomerase activation in AMD patients, are justified and should be assisted by PGC-1α modulators to increase the therapeutic potential of telomerase in AMD.     

花后干旱条件下冬小麦顺序和非顺序衰老同化物积累及转运特性--测试文章

以小麦顺序衰老（正置茎）和非顺序衰老（倒置茎）茎为材料,比较研究了自然天气和干旱条件下小麦正置茎和倒置茎叶片绿叶面积、光合速率、蔗糖磷酸转运酶活性以及地上器官同化物积累和转运特性,旨为进一步研究小麦叶片非顺序衰老的生理生化机制提供思路和理论指导。试验表明：无论是自然天气条件还是干旱条件,温麦19、豫麦19和兰考矮早8倒置茎倒二叶的绿叶面积、光合速率和叶片干重均明显高于旗叶,表现出旗叶早于倒二叶衰老的特征;倒置茎花后同化物转运量、转运率和对籽粒的贡献率、穗重以及叶片蔗糖磷酸合成酶活性均明显高于正置茎。表明小麦叶片的非顺序衰老与花后同化物的快速转运有关,这种衰老方式对小麦籽粒的后期充实是有利的,并且对干旱条件有较强的适应能力。     

The Role of AKT/mTOR Pathway in Stress Response to UV-Irradiation: Implication in Skin Carcinogenesis by Regulation of Apoptosis,Autophagy and Senescence

Induction of DNA damage by UVB and UVA radiation may generate mutations and genomic instability leading to carcinogenesis. Therefore, skin cells being repeatedly exposed to ultraviolet (UV) light have acquired multilayered protective mechanisms to avoid malignant transformation. Besides extensive DNA repair mechanisms, the damaged skin cells can be eliminated by induction of apoptosis, which is mediated through the action of tumor suppressor p53. In order to prevent the excessive loss of skin cells and to maintain the skin barrier function, apoptotic pathways are counteracted by anti-apoptotic signaling including the AKT/mTOR pathway. However, AKT/mTOR not only prevents cell death, but is also active in cell cycle transition and hyper-proliferation, thereby also counteracting p53. In turn, AKT/mTOR is tuned down by the negative regulators being controlled by the p53. This inhibition of AKT/mTOR, in combination with transactivation of damage-regulated autophagy modulators, guides the p53-mediated elimination of damaged cellular components by autophagic clearance. Alternatively, p53 irreversibly blocks cell cycle progression to prevent AKT/mTOR-driven proliferation, thereby inducing premature senescence. Conclusively, AKT/mTOR via an extensive cross talk with p53 influences the UV response in the skin with no black and white scenario deciding over death or survival.