丙烯在镍离子高分散催化剂上反应过程的TPSR EPR XPS UV-DRS研究

用ＴＰＳＲ法对丙烯在硫酸镍高分散型催化剂上反应过程进行考察；用ＮＨ３－ＴＰＤ法对ＮＨ３吸附中心进行跟踪，发现除强弱两类酸中心外，确有第三类活性中心，此第三类活性中心可能就是配位催化活性中心。     

内扩散控制下异丁烯齐聚反应宏观动力学研究

利用工业硅铝小球固体酸催化剂，排除了外扩散的影响后，在高压微反实验装置上进行了异丁烯齐聚反应的宏观动力学研究。结果表明，在相同的实验条件下，反应的宏观动力学行为与本征动力学行为有较大的不同，异丁烯的反应级数受内扩散影响由2级变为1．5级，异辛烯的反应级数则为0级。在本征动力学方程的基础上，利用集总的方法建立了内扩散控制下的异丁烯齐聚复杂反应动力学模型，并采用数值计算方法对该模型进行了求解，获得了异丁烯齐聚的集总宏观动力学方程。模拟结果与实验结果吻合良好。     

新型高效钯催化下不同取代炔烃的低聚反应

报道了不同取代炔在钯络合物催化下发生低聚反应生成芳环衍生物或偶联产物,探讨了反应立体选择性及收率,反应催化、溶剂体系,炔化合物取代因素,反应时间、温度及可能机理.     

以Nafion为催化剂的异丁烯齐聚反应的研究

考察了反应温度、 空速对Nafion催化异丁烯齐聚反应的影响. 探讨了催化剂在反应中的稳定性和变化特点. 在30～60 ℃范围内, 异丁烯的转化率随反应温度升高迅速增加, 低温时液体产物以二聚体为主. 当反应温度高于60 ℃时异丁烯转化率大于86%, 液体产物以三聚体为主. Nafion的催化活性随可接近磺酸基团的增加而提高. 高温有利于提高Nafion的溶胀度, 使体相内的磺酸基团更易接近. 由温度变化引起磺酸基团浓度稳定增加但可逆, 经低温处理后可以复原. 将Nafion担载在大比表面的载体上, 在低温下可获得更多的异丁烯二聚体.     

异丁烯齐聚反应催化剂的制备与评价

研究了Fe2(SO4)3(NiSO4)/γ-Al2O3催化剂对异丁烯齐聚反应的催化性能,考察了催化剂焙烧温度、活性组分担载量、Fe与Fe+Ni的摩尔比n(Fe):n(Fe+Ni)及催化剂成型对催化性能的影响.结果表明:n(Fe):n(Fe+Ni)为0.67时催化剂活性最佳;活性组分担载量为7%,500℃下焙烧的催化剂具有较好的异丁烯齐聚反应活性;催化剂成型(三叶型)后,其活性降低约6%,但目的产物(二聚物)的选择性提高约8%,二、三聚物的总选择性变化不大.     

Signaling versus punching hole: How do Bacillus thuringiensis toxins kill insect midgut cells?

Cry proteins, produced by Bacillus thuringiensis (Bt), are widely used for the control of insect pests in agriculture as spray products or expressed in transgenic crops, such as maize and cotton. Little was known regarding the mechanism of action of these toxins when the first commercial Bt product was introduced fifty years ago. However, research on the mechanism of action over the last two decades has enhanced our knowledge of toxin interaction with membrane receptors and their effects in insect midgut cells. All this information allowed for the rational design of improved toxins with higher toxicity or toxins that overcome insect resistance, which could compromise Bt use and effectiveness in the field. In this review we discuss and evaluate the different models of the mode of action of Cry toxins, including a discussion about the role of various receptors in toxin action. Received 13 June 2008; received after revision 05 November 2008; accepted 11 November 2008     

以丝光沸石为载体的异丁烯齐聚反应催化剂的研究

研究了以丝光沸石为载体的催化剂对异丁烯齐聚反应的催化作用。以NH4NO3作为离子交换溶液,在微型反应器上考察了改性丝光沸石催化剂的酸中心量、浸渍液浓度、焙烧温度等制备条件对异丁烯齐聚反应转化率及选择性的影响,得到了适宜的制备条件。在此基础上,研究了温度、压力、进料速率等反应条件的影响。结果表明,最佳制备条件为换铵两次、铵浓度0.5 mol/L、焙烧温度400℃;最佳操作条件为反应温度100℃、反应压力3.0 MPa、进料速率1~2 mL/min。     

Membrane translocation and oligomerization of hBok are triggered in response to apoptotic stimuli and Bnip3

hBok is a human pro-apoptotic member of the Bcl-2 family. By fluorescence in situ hybridization and in silico analysis, hBok was found to be located on chromosome 2q37.3. Its expression was detected in various organs and several hormonally regulated cancer cells. Expression of hBok was shown to be upregulated in estrogen-dependent breast cancer by estrogen deprivation and in myocardial cells during hypoxia. Confocal laser scanning microscopy examinations and subcellular fractionation studies showed that hBok was distributed in both the cytosol and intracellular membranes of healthy cells. Upon overexpression of hBok or stimulation of apoptosis, hBok became integrated into the membrane. Furthermore, apoptosis and oligomerization were promoted by BH3-only proteins, such as Bid, Bnip3 and p53, but prevented by BFL-1. hBok was found to interact with Bnip3. Our findings suggest that functional BH3-only proteins facilite the oligomerization and insertion of hBok into the membrane to activate it.Received 7 December 2004; received after revision 23 February 2005; accepted 4 March 2005     

Collapsin response mediator protein-2 is a calmodulin-binding protein

Collapsin response mediator protein-2 (CRMP-2) plays a crucial role in axonal guidance and neurite outgrowth during neural development and regeneration. We have studied the interaction between calmodulin (CaM) and CRMP-2 and how Ca²⁺/CaM binding modulates the biological functions of CRMP-2. We have shown that CRMP-2 binds to CaM directly in a Ca²⁺-dependent manner. The CaM binding site of CRMP-2 is proposed to reside in the last helix of the folded domain, and in line with this, a synthesized peptide representing this helix bound to CaM. In addition, CaM binding inhibits a homotetrameric assembly of CRMP-2 and attenuates calpainmediated CRMP-2 proteolysis. Furthermore, a CaM antagonist reduces the number and length of process induced by CRMP-2 overexpression in HEK293 cells. Take together, our data suggest that CRMP-2 is a novel CaM-binding protein and that CaM binding may play an important role in regulating CRMP-2 functions. Received 26 June 2008; received after revision 18 November 2008; accepted 24 November 2008     

Functionally independent subunits in the oligomeric structure of the GABA cotransporter rGAT1

We have combined structural and functional approaches to investigate the role of oligomerization in the operation of the GABA transporter rGAT1. Xenopus laevis oocytes were induced to express, either separately or simultaneously, the wild-type form of rGAT1 and a mutated (Y140W) form, unable to translocate GABA and to generate transport currents, although its intramembrane charge movement properties are only slightly affected. These characteristics, together with the insensitivity of Y140W to the blocking action of SKF89976A, were used to study the possible functional interaction of the two forms in an heteromeric structure. The electrophysiological data from oocytes coexpressing wild-type and Y140W rGAT1 were consistent with a completely independent activity of the two forms. Oligomerization was also studied by fluorescence resonance energy transfer (FRET) in tsA201 cells expressing the transporters fused with cyan and yellow fluorescent proteins (ECFP and EYFP). All combinations tested (WT-ECFP/WTEYFP, Y140W-ECFP/Y140W-EYFP and WT-ECFP/ Y140W-EYFP) were able to give rise to FRET, confirming the formation of homo- as well as heterooligomers. We conclude that, although rGAT1 undergoes structural oligomerization, each monomer operates independently. Received 18 July 2005; received after revision 21 September 2005; accepted 6 October 2005