合成光学活性紫苏醇的简易方法

本文介绍了经二步法合成光学活性的紫苏醇 ,首先用过乙酸氧化 β-蒎烯 ,生成的环氧化产物在硝基甲烷中用硝酸铵异构化即得紫苏醇。经分析测试证明产物与文献报道值相符。     

Polarization Pyrometry of Layered Semiconductor Structures under Conditions of Low-Temperature Technological Processes

Principal issues of using pyrometry for temperature monitoring in low-temperature processes in the technology of production of semiconductor structures are considered by an example of growing mercury–cadmium–telluride (MCT) layers on the GaAs substrate by the method of molecular beam epitaxy. Optical and thermophysical models are proposed to describe the processes of radiant heat transfer in a vacuum chamber. Based on these models, it is demonstrated that radiation from the heater and the signal reflected from the chamber walls, which are comparable in magnitude with the measured radiation emitted by the sample, should be taken into account in interpreting data measured by a pyrometer. Methods of useful signal identification are found. Experiments on temperature measurement by a pyrometer mounted on the MCT growth chamber are performed. Results of these experiments are in good agreement with theoretical predictions.     

微波促进硫酸铁铵催化合成环己酮乙二醇缩酮

用十二水硫酸铁铵作催化剂,微波辐射催化合成环己酮乙二醇缩酮。讨论了酮醇物质的量比、催化剂用量、微波功率和辐射时间对反应收率的影响。得出最佳反应条件为: n (环己酮) ∶n (乙二醇)=1∶1.4,催化剂用量为反应物总质量的3.5%,辐射功率450 W,辐射时间7 min,产物收率达88.1%。     

含羰基β-环糊精的合成及对苯乙烯的不对称环氧化

由β-环糊精合成单-2-羟丙基-β-环糊精,再利用二氧杂环丙烷氧化成单-2-丙酮基-β-环糊精。以过氧硫酸氢钾复合盐与单-2-丙酮基-β-环糊精产生的二氧杂环丙烷作氧化剂,考察了单-2-丙酮基-β-环糊精与苯乙烯不同物质的量比、NaHCO₃用量、过氧硫酸氢钾复合盐用量、以及反应时间和温度等对苯乙烯不对称环氧化的影响。结果表明,单-2-丙酮基-β-环糊精能诱导苯乙烯的不对称环氧化;当反应时间5 h和单-2-丙酮基-β-环糊精、过氧硫酸氢钾复合盐、NaHCO₃和苯乙烯的物质的量比为2∶6∶12∶1时,ee值可达到13%。     

Dawson型磷钨杂多盐催化氧化苯乙烯制苯甲醛

考察了在丙酮中以过氧化氢为氧化剂,二缺位Dawson型杂多化合物K10Na2H2P2W16O60为催化剂氧化苯乙烯合成苯甲醛的反应。发现该工艺中主要生成苯甲醛,少量副产物是环氧苯乙烷和苯乙醛等。在催化剂、苯乙烯、过氧化氢摩尔比为1∶100∶300的条件下,65℃反应10 h,苯乙烯转化率达95.4%,苯甲醛选择性为95.6%。该工艺产物分离简便,不使用含氯原料和有害的重金属,苯甲醛可达食品级标准。     

SOLUBILITY AND DIFFUSIVITY OF GASES IN AN ORGANIC SOLUTION OF AMINE

Solubilities and diffusivities of carbon dioxide and nitrous oxide in a mixture of toluene and isopropanol organic solution of cyclohexylamine were measured at 20°C in the range of pressures of solute from 1 to 3 bars. This was performed with an original chromatographic technique taking into account the presence of the product of the reaction.     

生物质化学品5-乙氧基甲基糠醛的催化合成进展

5-乙氧基甲基糠醛（5-EMF）被认为是新一代具有重要潜力的生物质液体燃料和精细化学品。概括和总结了近年来以生物质及其衍生物为原料制备5-EMF的研究进展,阐述了由生物质原料如纤维素合成5-EMF的反应路径和机理,综述了多相酸催化体系的特点、制备方法及催化行为,强调了合成5-EMF的最新催化工艺。在此基础上,提出了今后的发展方向是由生物质一步转化为5-EMF。     

有机碱催化下乳酸乙酯乙酸酯的合成

在1-甲基咪唑等有机碱催化下,乳酸乙酯与乙酸酐经乙酰化反应高效合成乳酸乙酯乙酸酯。单因素优化法得到适宜的反应条件为：1-甲基咪唑为催化剂,催化剂用量为乳酸乙酯物质的量的5.00%,n(乳酸乙酯)∶n(乙酸酐)=1∶1.2,回流反应2 h,目标产物乳酸乙酯乙酸酯收率为98.5%。该方法反应时间短,产物收率高,操作简便,具有工业化应用前景。     

Crk protein binds to PDGF receptor and insulin receptor substrate-1 with different modulating effects on PDGF- and insulin-dependent signaling pathways

We have studied the involvement of murine c-Crk, an SH2/SH3 containing adaptor protein, in signaling pathways stimulated by different receptor tyrosine kinases. We show here that c-Crk is associated with components of insulin- and PDGF-dependent signaling pathways. Insulin treatment of murine myoblast cells induces the formation of stable complex of endogenous c-Crk with insulin receptor substrate-1 (IRS-1) mediated via the SH2 domain of Crk. The ligand dependent physical association of c-Crk with IRS-1 is direct. However IRS-1 is also co-precipitated with c-Crk from quiescent L6 cells. The association of IRS-1 with c-Crk in quiescent cells is probably not direct since Far Western blot analysis did not reveal the binding of neither SH2 domain nor amino-terminal SH3 domain of c-Crk to IRS-1 from unstimulated cells. We also show that PDGF treatment of murine myoblast cells induces association of c-Crk with the PDGF receptor and tyrosine phosphorylation of c-Crk. Overexpression of c-Crk enhanced insulin- but not PDGF-induced activation of MAP kinases when compared to parental cell lines. Thus, the formation of the direct IRS-1/Crk complex appears to be crucial for Crk-mediated insulin-induced activation of MAP kinase, whereas Crk is probably involved in other PDGF-induced responses. These data provide support to the hypothesis that insulin and PDGF employ different mechanisms for activation of MAP kinase cascade.