氨基化

Then Doripenem came into the market in the July ,2005. We studied the synthesis of Doripemen.Firstly, we synthesized the chemical 2 from the starting material------o-hydroxylphenylacylamine through Reformastky reaction, alkylation, Diekmann reaction, enolization, esterification and etc. Secondly, we synthesized the chemical 3 from L — hydroxylproline through the protection of carboxyl, amidogen and hydroxyl group, reduction by NaBr, SN_2 substitution and Mitsumobu reaction.

我们以水杨酰胺为起始原料，经Reformatsky反应、烷基化、Diekmann环合、烯醇化、酯化等反应合成双环母核2；再从L-羟基脯氨酸出发，经酯化保护羧基、保护氨基、保护羟基、硼氢化还原酯得醇、Sn2取代和Mitsumobu反应等合成巯基侧链3；最后由化合物3经脱保护、水解得硫醇，和化合物2在二异丙基乙基胺的作用下缩合，最后Pd／C催化脱保护，历经16步反应最终得到产物多尼培南。

A new inequilateral organic polyamine, 2-aminoethyl-bi(3-aminopropyl)amine, was synthesized by the additional and hydrogenation reaction of aminoacetonitrile with acrylonitrile.

利用氨基乙腈及丙烯腈的亲核加成、氢化反应合成了一种新的不等臂有机多胺化合物2-氨基乙基-二（3-氨基丙基）胺。

A series of p-toluene sulfonylamido acetacylhydrazone derivatives were synthesized from p-toluenesulfonyl chloride which reacted with glycine to get the intermediate p-toluene sulfonylamido glycine, then through the esterification, hydrazinolysis to afford another intermediate p-toluene sulfonylamido acethydrazide, which condensed with different aldehydes to obtain the target compounds that were characterized by IR, 1H NMR, 13C NMR spectra and elemental analysis.

魏太保 ；冷艳丽；王永成；张建辉；张有明*摘要：以对甲苯磺酰氯为原料，通过与氨基乙酸反应得到中间体对甲苯磺酰氨基乙酸，再经酯化、肼解得到对甲苯磺酰氨基乙酰肼，然后与相应的醛缩合得一系列对甲苯磺酰胺基乙酰腙类化合物。其结构经元素分析， IR， 1H NMR和13C NMR确证。

The target compound was synthesized from clarithromycin via hydrolyzation,acetylation,cyclic carbonatation,oxidation,decarbonatation,acylation,cyclic carbamatation and cyclization.

方法以克拉霉素为起始原料，经水解、乙酰化、环碳酸酯化、氧化、脱碳酸酯化、酰化、环氨基甲酸酯化和环合等反应合成目标化合物。

Three novel hemicyanine derivatives,-N-(4-sulfopropyl)-4-[2-(4- N, N-diethylaminophenyl)-ethenyl]pyridinium,-N-(4-suMbbutyl)- 4-[2-(4-N, N-diethylaminophenyl)ethenyl]pyridinium (EPS4), and-N-(4- su)fobutyl-4-[2-(4-N, N-diethylaminophenyl)ethenyl]quinolinium (EQS4) with different length of alkyl chains between the adsorbing group (RSO3-) and the chromophore group, were synthesized and their photophysical and photoelectrochemical properties were studied.

设计合成了具有不同空间位阻的吡啶盐类和喹啉盐类半菁染料-N-(4—磺酸根丙基)-4-[2-4（4-N，N-二乙基氨基苯基）乙烯基]吡啶鎓盐，-N-4-磺酸根丁基）-4-[2-(4-N，N-二乙氨基苯基）乙烯基]吡啶鎓盐（EPS4）和-N-（4-磺酸根丁基）-4-2-（4-N，N-二乙基氨基苯基）喹啉鎓盐（EQS4），研究了它们的光物理性质，并将它们用作TiO2纳米晶电极的光敏化剂引入光电化学电池中。

Because of no signal from N-terminal protein sequencing for 43kDa protein directly, a resulting 18kDa peptide from the partial cleavage of 43kDa protein by BrCN had its N-terminal sequences of AFTFKK determined by N-terminal protein sequencing assay. Then, the 43kDa protein was convinced to the enzyme of 3phosphate glycerate kinase (PGK1) by searching YPD.

由于43kDa蛋白直接进行蛋白质氨基端序列测定时没有信号，因而用溴化氰部分化学裂解43kDa蛋白，得到的18 kDa多肽经蛋白质氨基端序列测定，得到其氨基端前6个氨基酸残基序列为AFTFKK，通过计算机检索YPD，确定43 kDa蛋白是3—磷酸甘油酸激酶（PGK1）。

Tetrachloroterephthalic acid was prepared by chlorinating terephthalic acid, oleumsolvent and iodine catalyst. Tetrachloroterephthalic acid was acylated by sulphurous oxychloride in the presence of DMF to form tetrachloroterephthaloyl chloride. The acyl chloride product was fluorinated by potassium fluoride and esterified by methanol to synthesize dimethyl tetrafluoroterephthalate. The ester was reduced with potassium borohydride and lithium chloride to give tetrafluoroterephthalyl alcohol. The above product was bromated in the hydrobromic acid to obtain 4-bromomethyl-2,3,5,6-tetrafluoro-benzene methanol. 4-Methyl-2,3,5,-6-tetrafluorobenzene ethanol was obtained by reducing the bromide with magnesium. In the exist of DCC and DMAP, tefluthrin was got by the condensation reaction between 4-methyl-2,3,5,6-tetrafluoro-benzene methanol and-(1RS,3RS)- 3-(2- chloro-3,3,3-trifluoro-1-propenyl)-2,2-dimethyl cycolpropanecar-boxylate acid.

对苯二甲酸与氯气在碘存在下以发烟硫酸为溶剂进行氯化制备四氯对苯二甲酸；再以DMF为催化剂与二氯亚砜反应生成四氯对苯二甲酰氯；以氟化钾为氟化剂，环丁砜为溶剂置换氟化，再与甲醇酯化得到四氟对苯二甲酸甲酯；以KBH4-LiCl为还原剂二甲醚为溶剂反应制得四氟对苯二甲基苄醇；以氯苯为溶剂在溴化氢溶液中溴化得到溴化产物；在乙醇溶液中经镁粉还原得到4-甲基-2，3，5，6-四氟苄醇；甲基苄醇与功夫酸在催化剂二环己基碳二亚胺和4-二甲氨基吡啶作用下缩合得到七氟菊酯，总收率达43.6%。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

The intermediate which obtained from oximation of 7a-e reacted withmethyl N-(2-bromomethylphenyl)-N-methoxycarbamate to synthesize oxime ether methyl carbamate 3a-e.

以邻位卤代苯甲醛和3-丁烯-2-醇为原料通过钯催化&一锅法&反应合成了2-乙酰基茚7a-e，7a-e 肟化之后和N-(2-溴甲基苯基)-N-甲氧基氨基甲酸甲酯反应合成了肟醚类氨基甲酸甲酯3a-e，进一步胺解之后得到了肟醚类氨基甲酰甲胺3f-j。

The recent research progress of oxidation carbonylation of amines/β-amino alcohols, alkoxycarbonylation of epoxides, carbonylative Suzuki coupling, carbonylative Sonogashira, and double carbonylation of aryl iodides has been presented, focusing on the carbonylation reactions studied by us in the past few years, with 81 references.

综述了胺／氨基醇类化合物氧化羰化、环氧化合物氢酯基化、碘代芳烃的羰化Suzuki偶联、羰化Sonogashira以及双羰基化等重要羰基化反应的研究状况，特别是结合本课题组近年来在该领域中的工作，并对羰基化反应的发展及应用前景进行了展望。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。