纳米多孔Co的磷化物制备及其电催化析氢性能

采用脱合金化、水热合成和化学气相沉积制备纳米多孔Co、NiCo(OH)₂/Co和NiCo(OH)₂-P复合电极. 通过X射线衍射仪(XRD)、扫描电子显微镜(SEM)等方法表征电极材料的物相和形貌结构. 在1 mol·L^－1的KOH溶液中,运用线性扫描伏安曲线(LSV)、交流阻抗谱(EIS)、循环伏安曲线(CV)等测试电极的电催化析氢性能. 结果表明:纳米多孔Co、NiCo(OH)₂/Co、NiCo(OH)₂-P电极材料的析氢性能依次增加,化学气相沉积(CVD)磷化后的纳米多孔NiCo(OH)₂-P在10 mA·cm^－2电流密度下,其过电位为139 mV,Tafel斜率为123.57 mV·dec^－1,双电层电容为30.16 mF·cm^－2. 经过1 000圈循环伏安耐久性实验后,纳米多孔NiCo(OH)₂-P电极在10 mA·cm^－2电流密度下,析氢过电位仅相差7 mV,表现出良好的析氢稳定性.     

适用于微传感器的纳米多孔铝膜的制备研究

在单晶硅表面溅射铝,采用两步阳极氧化法制备纳米多孔铝膜.研究了电解液种类、阳极氧化时间、扩孔时间对孔的结构与形貌的影响.结果表明,与硫酸和磷酸相比,草酸是制备纳米孔阵列的相对方便与可靠的电解液;第二步阳极氧化时间对孔的均匀性及孔深度影响较大,对平均孔径的影响较小;扩孔时间的长短对孔径大小及孔的均匀性均影响显著.     

氯碱工业镍-硫电极的研究

应用电化学沉积的方法制备Ni-S和Ni-Co-S合金镀层.通过测量电极的稳态极化曲线,研究电极的电催化活性和析氢反应活化能,考察热处理和电解液中杂质离子等因素对沉积层析氢活性的影响.实验结果显示,Ni-S电极镀层中的硫质量分数为11.59%时,电极的析氢活性最高,镀层呈非晶态或弱晶态结构,电极的析氢反应活化能为22.344 kJ/mol.     

具有纳米多孔结构的WO3薄膜的制备

研究了阶跃加压阳极氧化法在金属钨基底上制备具有多层纳米孔结构形貌的WO3薄膜的工艺,主要研究了阳极氧化条件对生成纳米孔结构的影响及热处理制度对样品形貌和结构的影响.结果表明:在60V电压和20℃反应温度条件下,在含质量分数为005%NH4F的电解液中阳极氧化20min得到的样品表面,具有形貌规则的自组装纳米多层网孔结构,且排列紧密.此外,将阳极氧化制得的样品以5℃/min的速率升温至450℃并保温3h,可使生成的无定形氧化钨薄膜在保持多孔结构形貌基本不变的条件下晶化.     

三维有序介孔镍铁磷化物的制备及电解水析氢性能研究

利用三维SiO₂纳米球阵列作为介孔模板,通过高温磷化合成了不同镍与铁物质的量比的三维有序介孔镍铁磷化物(3DOM Ni_XFe_1-XP);利用透射电子显微镜(TEM)、氮气吸脱附测试(BET)、X射线衍射(XRD)、X射线光电子能谱(XPS)等物理表征方法对所制备材料的形貌和结构进行分析,并通过电化学测试在0.5 mol/L H₂SO₄中系统评价了其电解水析氢(HER)性能。结果表明：3DOM Ni_XFe_1-XP成功地反向复制了SiO₂模板的有序介孔结构,孔道之间排列整齐且相互连通;随着Fe含量的增加,3DOM Ni_XFe_1-XP的HER性能呈现先升高后下降的趋势,在Ni与Fe物质的量比为7∶3时HER性能达到最优;当电流密度达到10 mA/cm²时,3DOM Ni_0.7Fe_0.3P所需过电位为132 mV...     

碳布基底上Sn-Co双金属协同电催化CO2为甲酸

通过采用电镀的方法在不同的摩尔比镀液中制备了以碳布(carbon clothes,CC)为基底的锡－钴双金属电极材料(SnxCoy/CC).采用XRD、SEM、XPS、EDS和BET等测试方法对该催化材料的组成、微观形貌和结构进行了表征,结果表明Sn-Co双金属在碳布基底上电沉积成功.并利用线性循环伏安法、计时电流法以及EIS阻抗分析评价了该电极材料对CO2还原的电催化性能.结果表明,当双金属渡液中Co掺杂的含量为40%时,在碳钎维上生长出稻穗形貌的立方状双金属微粒,且该电催化材料具有最低的电荷转移电阻和最高的电导率,XPS分析表明双金属电极的表面金属元素都以催化效果较好的氧化态SnOx、Co3O4的形式存在.在电解电压为－1.16 V(vs.RHE)时,Sn60Co40/CC电催化产甲酸的法拉第效率可达57.4%,高于单金属Sn的产甲酸的法拉第效率42.3%,表明通过掺杂Co元素和调控形貌可以有效提高单金属Sn的电催化性能.     

Effect of TiO<Subscript>2</Subscript> nanoparticles on hydrogen evolution reaction activity of Ni coatings

The electrocatalytic activity of electrodeposited Ni and Ni-TiO₂ coatings with regard to the alkaline hydrogen evolution reaction (HER) was investigated. The Ni coatings were electrodeposited from an acid chloride bath at different current densities, and their HER activities were examined in a 1.0-mol·L-1 KOH medium. The variations in the HER activity of the Ni coatings with changes in surface morphology and composition were examined via the electrochemical dissolution and incorporation of nanoparticles. Electrochemical analysis methods were used to monitor the HER activity of the test electrodes; this activity was confirmed via the quantification of gases that evolved during the analysis. The obtained results demonstrated that the Ni-TiO₂ nanocomposite test electrode exhibited maximum activity toward the alkaline HER. The surface appearance, composition, and the phase structure of all developed coatings were analyzed using scanning electron microscopy (SEM), energy dispersive spectroscopy (EDS), and X-ray diffraction (XRD), respectively. The improvement in the electrocatalytic activity of Ni-TiO₂ nanocomposite coating toward HER was attributed to the variation in surface morphology and increased number of active sites.     

双金属层表面等离子体共振传感器品质因子的研究

基于光学薄膜理论,研究了银-金双金属层表面等离子体共振(SPR)传感器品质因子的特征。 首先,通过共振角处最低反射率的计算得到了双金属层的最佳厚度配比;其次,研究了最佳厚度配比下双金属层 SPR 传感器的线宽、灵敏度以及品质因子的特征。 研究结果表明,随着双金属层中银膜厚度的增加(或金膜厚度的减小),传感 器的灵敏度和线宽均减小,而传感器的品质因子增大。 当双金属层 SPR 传感器中金膜厚度减小至 0 nm 时(单层银膜 SPR 传感器),传感器的品质因子达到最大值 96.35 RIU-1 。     

Structure of the extracellular region of HER2 alone and in complex with the Herceptin Fab

HER2 (also known as Neu, ErbB2) is a member of the epidermal growth factor receptor (EGFR; also known as ErbB) family of receptor tyrosine kinases, which in humans includes HER1 (EGFR, ERBB1), HER2, HER3 (ERBB3) and HER4 (ERBB4). ErbB receptors are essential mediators of cell proliferation and differentiation in the developing embryo and in adult tissues, and their inappropriate activation is associated with the development and severity of many cancers. Overexpression of HER2 is found in 20-30% of human breast cancers, and correlates with more aggressive tumours and a poorer prognosis. Anticancer therapies targeting ErbB receptors have shown promise, and a monoclonal antibody against HER2, Herceptin (also known as trastuzumab), is currently in use as a treatment for breast cancer. Here we report crystal structures of the entire extracellular regions of rat HER2 at 2.4 A and human HER2 complexed with the Herceptin antigen-binding fragment (Fab) at 2.5 A. These structures reveal a fixed conformation for HER2 that resembles a ligand-activated state, and show HER2 poised to interact with other ErbB receptors in the absence of direct ligand binding. Herceptin binds to the juxtamembrane region of HER2, identifying this site as a target for anticancer therapies.     

脉冲电镀制备Ni-Mo合金镀层及其析氢性能

研究了脉冲电镀法制备Ni-Mo合金镀层过程中电镀条件对Ni-Mo合金镀层组成、表观形貌以及析氢性能的影响.当n(Ni)∶n(Mo)<1时,随着钼盐的加入,镀层中的Mo含量逐渐下降,镀层的析氢过电位升高;利用脉冲电镀制备的Ni-Mo合金镀层均匀、平整、致密,其中w(Mo)在30%左右的Ni-Mo合金镀层呈非晶态结构,具有更高的催化活性(80℃,η200=62 mV)以及较高的耐蚀性.经100 h电解后(33%NaOH溶液中),镀层非晶态结构被破坏.随着Mo的溶出,镀层孔隙率增大并出现鼓泡现象.     

Pt／Au纳米双金属簇的制备及表征

采用硼氢化钠还原法制得聚乙烯吡咯烷酮(PVP)保护的Pt/Au纳米双金属簇,用TEM、UV-VIS吸收光谱进行了表征,从制备方法、还原顺序、金属不同摩尔比等方面对双金属簇的影响进行了研究。分别制得了Pt/Au合金及Pt/Au核壳结构的直径在2~5nm的纳米双金属簇。     

通过合金和去合金过程制备一种海绵状的纳米多孔铂以及对氧的电催化还原

采用一种简易的方法制备了海绵状的球形纳米多孔铂,首先是用循环伏安法在玻碳电极上电沉积得到铂铜合金,然后在浓硝酸中刻蚀合金去掉铜．用到场发射扫描电镜、X射线光电子能谱、X射线衍射和循环伏安法对其进行了表征．也对制备此种铂催化剂的条件进行了优化．此种铂修饰电极对氧的还原表现出很高的电催化活性,其氧的还原峰电流是相应纳米铂修饰电极的四倍．这种制备海绵状纳米多孔结构的方法以及所得到得到铂修饰电极可能在燃料电池和生物传感器等领域有着很大的应用前景．     

层状分子基磁体:{[ML][Fe~ⅡFe~Ⅲ(ox)_3·1.5H_2O]}_∞的合成和波谱表征(M=Co~(2+),Mn~(2+))

合成和表征了两种新的Schiff碱配合物[CoL(ClO4)·3H2O(1)和MnL(ClO4)·3H2O(2),其中L是由摩尔比为1∶1的水杨醛和二乙撑三胺缩合而成的Schiff碱。1(或2)、FeSO4·7H2O和K3[Fe(ox)3]·3H2O进一步反应,生成了层状分子基磁体{[ML][FeⅡFeⅢ(ox)3]·1.5H2O}∞,其中M=Co2+(3)orMn2+(4)。红外光谱和Mo¨ssbauer谱测定结果表明,3和4具有二维层状结构,其阴离子层由[FeⅡFeⅢ(ox)3]-单元构成。     

Co-Mn 金属有机骨架衍生的双金属硫化物及其在锂离子电池负极材料中的应用

介绍了一种通过简单的室温搅拌合成具有多孔结构的 Co-Mn 金属有机框架(metal-organic-framework, MOF)材料的方法, 并对制备的双金属 MOF 进行气相硫化, 得到多孔 CoS介绍了一种通过简单的室温搅拌合成具有多孔结构的Co-Mn金属有机框架(metalorganic-framework,MOF)材料的方法,并对制备的双金属MOF进行气相硫化,得到多孔CoS_2/MnS双金属复合材料.与相同方法制备的单金属MnS与CoS2材料对比发现,CoS_2/MnS双金属复合材料表现出了类似花瓣状的多孔片状结构以及更小的粒径,在作为锂离子电池电极材料使用时表现出了最好的储锂性能.这主要归因于类花瓣状的多孔结构:一方面为锂离子提供了更短的传输路径以及更多的接触位点;另一方面也缓解了材料锂化/去锂化过程的体积变化.此外,两种金属硫化物的有机结合也抑制了材料在循环过程中由于体积变化而导致的容量快速衰减.最后,MOF有机配体衍生的碳骨架也为增强材料的导电性起到了积极的作用.     

双金属改性碳纳米管选择性氧化苯酚研究

以苯酚选择性氧化合成苯醌为模型反应,考察不同双金属、金属质量分数、金属原子比和溶液不同氧含量等因素对改性单壁碳纳米管阴极电极性能的影响。结果显示经金属质量分数为20%,Ag/Co(金属原子比)=2∶1改性的单壁碳纳米管阴极电极能有效催化激活分子氧,提高苯醌收率及其选择性。     

Characterization and Preparation of Bimetallic Nanoparticles

1 Results Bimetallic particles in the nanometer size range are of substantial interest due to their vast applications in catalysis[1].The synthesis of bimetallic nanoparticles with definite size with a well-control over their nanostructure remains a challenging problem.Thus there exists a great demand for both synthesis and atomic level characterization of nanostructure of bimetallic nanoparticles (NPs).With the recent advent of high-intensity tunable sources of X-rays,now available at synchrotron radia...     

靶向沉默人HER2/neu基因的RNA干扰

针对人HER2/neu基因的mRNA序列, 设计并构建shRNA干扰载体, 经聚合酶链式反应(PCR)及测序鉴定后转染SK-BR-3细胞, 并检测HER2/neu mRNA和蛋白抑制情况及SK-BR-3细胞迁移能力的变化. 实验结果表明： 构建了3个HER2/neu shRNA真核表达质粒; 3个重组质粒均可不同程度下调HER2/neu mRNA和蛋白表达水平, 并抑制SK BR 3细胞的迁移; 其中1号重组质粒效应最强, 对mRNA和蛋白的抑制率分别为84.65%和7498%.     

TiO2/PbS/Ru(bpy)2(NCS)2纳米多孔膜电极的光电化学研究

用染料Ru(bpy)2(NCS)2对ITO/TiO2/PbS复合半导体纳米多孔膜电极进行敏化,用光电化学方法研究ITO/TiO2/PbS/Ru(bpy)2(NCS)2电极的光电化学行为及组成光电池的能量转换效率.结果表明,该电极作为太阳能电池光阳极的能量转换效率与TiO2/PbS 复合半导体中PbS的含量有关.     

Correlation of matrix metalloproteinase－2, －9, tissue inhibitor－1 of matrix metalloproteinase and CD44 variant 6 in head and neck cancer metastasis

This study aimed to explore the molecular mechanism in tumor invasion and metastasis. The expression of matrix metalloproteinase-2, -9 (MMP-2, MMP-9), tissue inhibitor-1 of matrix metalloproteinase (TIMP-1), cell adhesion molecule 44 variant 6 (CD44v6), HER2/neu and p53 was investigated in 154 patients with head and neck squamous cell carcinoma (SCC) by ABC and ImmunoMax immunohistochemical method. Their clinical relevance and correlation were analysed. The expression of MMP-2, MMP-9, TIMP-1, CD44v6, HER2/neu and p53 was found in cancer cells in 87.01%, 85.71%, 68.18%, 98.05%, 55.19% and 50.65% cases respectively. Linear regression and correlation analysis revealed that there was close positive relationship (P<0.05) between the expression of MMP-2 and MMP-9, TIMP-1 and CD44v6, HER2/neu and MMP-9, MMP-2 and p53. Up-regulation of MMP-2 was accompanied by advanced T stage (P<0.01). There was also a trend of MMP-2 expression being related with tumor metastasis. Increased expression of HER2/neu was found in patients with tumor recurrence(P<0.05). The expression of TIMP-1 was higher in laryngeal cancer than that in pharyngeal cancer, and higher in keratinizing and non-keratinizing SCC than that in basaloid SCC(P<0.05). These findings suggested that MMP-2 and MMP-9, HER2/neu and MMP-9, MMP-2 and p53 had a coordinate function in aggression of tumor; that MMP-2 had a more important function than MMP-9 in tumor invasion and metastasis; and that HER2/neu might serve as a biomarker for poor prognosis in HNSCC.     

Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3

Oncogenic tyrosine kinases have proved to be promising targets for the development of highly effective anticancer drugs. However, tyrosine kinase inhibitors (TKIs) against the human epidermal growth factor receptor (HER) family show only limited activity against HER2-driven breast cancers, despite effective inhibition of epidermal growth factor receptor (EGFR) and HER2 in vivo. The reasons for this are unclear. Signalling in trans is a key feature of this multimember family and the critically important phosphatidylinositol-3-OH kinase (PI(3)K)/Akt pathway is driven predominantly through transphosphorylation of the kinase-inactive HER3 (refs 9, 10). Here we show that HER3 and consequently PI(3)K/Akt signalling evade inhibition by current HER-family TKIs in vitro and in tumours in vivo. This is due to a compensatory shift in the HER3 phosphorylation-dephosphorylation equilibrium, driven by increased membrane HER3 expression driving the phosphorylation reaction and by reduced HER3 phosphatase activity impeding the dephosphorylation reaction. These compensatory changes are driven by Akt-mediated negative-feedback signalling. Although HER3 is not a direct target of TKIs, HER3 substrate resistance undermines their efficacy and has thus far gone undetected. The experimental abrogation of HER3 resistance by small interfering RNA knockdown restores potent pro-apoptotic activity to otherwise cytostatic HER TKIs, re-affirming the oncogene-addicted nature of HER2-driven tumours and the therapeutic promise of this oncoprotein target. However, because HER3 signalling is buffered against an incomplete inhibition of HER2 kinase, much more potent TKIs or combination strategies are required to silence oncogenic HER2 signalling effectively. The biologic marker with which to assess the efficacy of HER TKIs should be the transphosphorylation of HER3 rather than autophosphorylation.