功能绝缘材料加工工艺对电润湿显示器性能的影响

电润湿显示器是基于氟树脂层（如AF1600）作为疏水绝缘层,通过外加电压来改变液体在其表面润湿性来达到显示效果的装置,为了使光刻胶层和氟树脂层有很好的粘结性能,对氟树脂表面进行离子刻蚀来增大其润湿性. 光刻后需恢复氟树脂疏水性以恢复其电润湿特性. 常用方法是通过高温回流(High Temperature Reflow Method)的方法使刻蚀后的氟树脂表面熔融流平,但高温会造成光刻胶材料黄变,像素格变形等缺陷. 本文通过蒸汽溶解法(Vapor Redissolve Method)代替高温回流法来恢复氟树脂层的疏水性能,使用氟碳溶剂（HFE7100）蒸汽溶解氟树脂层粗糙表面形成溶胶状态,加热蒸发溶剂后使表面恢复疏水性质. 本文针对蒸汽溶解法溶解时间、干燥温度和干燥时间等条件进行探究,并对高温回流法和蒸汽溶解法对电润湿显示器产生的物理和光电影响进行了对比研究.     

基于相变操控的电润湿显示油墨填充与封装工艺研究

彩色油墨的填充与封装工艺是电润湿显示制造技术的核心,如何提高填充均匀性和制程效率仍然是电润湿显示技术量产的关键挑战之一。本文提出一种基于相变操控的电润湿显示油墨创新填充和封装方法,即在空气环境中完成油墨液相填充,经低温凝固后投入液体环境完成封装。该方法有效规避了在传统液下环境中填充涉及的油/水/固三相界面操控的复杂性,提高了填充工艺的兼容性和稳定性。对油墨厚度的分析结果表明,基于相变操控填充油墨厚度与像素墙高度的相关性更好,较传统自组装填充具有更好的膜厚控制性。相变操控填充电润湿显示器件的光电响应处于合理水平。本研究有效解决了电润湿显示油墨填充的技术瓶颈,对推进电润湿显示技术的应用具有重要意义。     

Application of Method-of-Lines to Charging-Up Process in Pipelines with Entrapped Air

Introduction The initial charging-up process is an important opera-tion in an intermittent,undulating pipeline system.Re-cently,the charging-up process has received attention with the aim of predicting the effective duration of supply in different regions…     

变数据窗阻抗算法的频域分析方法研究

分析典型变数据窗阻抗算法的估计原理和特点 ,提出了一种适用于不同阻抗估计算法的新型频率响应计算方法 ,为不同算法的频域特性分析和比较提供了共同的基础 .该方法也可用于对算法抑制非周期分量的性能进行分析研究     

Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy

Auditory neuropathy is a particular type of hearing impairment in which neural transmission of the auditory signal is impaired, while cochlear outer hair cells remain functional. Here we report on DFNB59, a newly identified gene on chromosome 2q31.1-q31.3 mutated in four families segregating autosomal recessive auditory neuropathy. DFNB59 encodes pejvakin, a 352-residue protein. Pejvakin is a paralog of DFNA5, a protein of unknown function also involved in deafness. By immunohistofluorescence, pejvakin is detected in the cell bodies of neurons of the afferent auditory pathway. Furthermore, Dfnb59 knock-in mice, homozygous for the R183W variant identified in one DFNB59 family, show abnormal auditory brainstem responses indicative of neuronal dysfunction along the auditory pathway. Unlike previously described sensorineural deafness genes, all of which underlie cochlear cell pathologies, DFNB59 is the first human gene implicated in nonsyndromic deafness due to a neuronal defect.     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.     

Preparation and characterization of doubly substituted microwave absorbing material by sol-gel technique for super high frequency applications

Rare earth Dy~(3+)and divalent Mn~(2+)elements substituting W-type hexagonal ferrites Ba_(1-x)Dy_xZn_2Fe_(16-y)Mn_yO_(27)(x=0,0.02,0.06,0.1 and y=0,0.1,0.3,0.5)were prepared by sol-gel method.The thermo-gravimetric analysis(TGA)and differential scanning calorimetry(DSC)was carried out to find the temperature at which single phase can be obtained.XRD patterns indicate the presence of the single phase for all the synthesized samples with the absence of any extra peak due to unreacted material and secondary phases.The occurrence of absorption bands at low wave numbers(563 and 446 cm~(-1)),can be assigned to the stretching vibration of metal and oxygen ions in FTIR spectra,which also confirms the single hexagonal phase for prepared material.The grains are of platelet like structure,which enhances the microwave absorption properties of hexagonal ferrites.The synthesized material exhibits the minimum reflection loss of-20.9 dB at 11.8 GHz frequency,which reflects the applications of this material in super high frequency devices.The microwave conductivity of the material increases with frequency.     

形变双奇核1944Au中的强耦合带

利用重离子融合蒸发反应159Tb（29Si,4nγ）194Au布居了形变双奇核184Au的高自旋态,用GASP探测器阵列进行了在束γ实验测量．通过对实验数据的深入分析,新发现了一条可归属于184Au核的强耦合转动带．基于对转动带有效K值的分析以及从实验数据中提取出的带内B（M1）／B（E2）值与理论计算值的比较,建议了转动带的准粒子组态和能级的自旋宇称值．     

Purification and cloning of amyloid precursor protein beta-secretase from human brain

Proteolytic processing of the amyloid precursor protein (APP) generates amyloid beta (Abeta) peptide, which is thought to be causal for the pathology and subsequent cognitive decline in Alzheimer's disease. Cleavage by beta-secretase at the amino terminus of the Abeta peptide sequence, between residues 671 and 672 of APP, leads to the generation and extracellular release of beta-cleaved soluble APP, and a corresponding cell-associated carboxy-terminal fragment. Cleavage of the C-terminal fragment by gamma-secretase(s) leads to the formation of Abeta. The pathogenic mutation K670M671-->N670L671 at the beta-secretase cleavage site in APP, which was discovered in a Swedish family with familial Alzheimer's disease, leads to increased beta-secretase cleavage of the mutant substrate. Here we describe a membrane-bound enzyme activity that cleaves full-length APP at the beta-secretase cleavage site, and find it to be the predominant beta-cleavage activity in human brain. We have purified this enzyme activity to homogeneity from human brain using a new substrate analogue inhibitor of the enzyme activity, and show that the purified enzyme has all the properties predicted for beta-secretase. Cloning and expression of the enzyme reveals that human brain beta-secretase is a new membrane-bound aspartic proteinase.