顺、反式-3,4′,5-三羟基二苯乙烯的合成

目的通过一种新的简便的方法合成顺、反式3,4′,5三羟基二苯乙烯。方法化合物3和4发生缩合反应形成二苯乙烯骨架,然后经过水解、脱羧、异构化、脱甲基得到反式3,4′,5三羟基二苯乙烯(白藜芦醇),将其进行光异构化得到顺式3,4′,5三羟基二苯乙烯。结果以化合物3和4为起始原料合成顺、反式3,4′,5三羟基二苯乙烯。结论以价廉易得的工业化原料为起始物,建立了一种多羟基顺、反式二苯乙烯类化合物的简易合成方法。     

Fmoc/solid-phase synthesis of Tyr(P)-containing peptides through t-butyl phosphate protection

The synthesis is of Tyr(P)-containing peptides by the use of Fmoc-Tyr(PO₃Me₂)-OH in Fmoc/solid phase synthesis is complicated since, firstly, piperidine causes cleavage of the methyl group from the -Tyr(PO₃ Me₂)-residue during peptide synthesis and, secondly, harsh conditions are needed for its final cleavage. A very simple method for the synthesis of Tyr(P)-containing peptides using t-butyl phosphate protection is described. The protected phosphotyrosine derivative, Fmoc-Tyr(PO₃^tBu₂)-OH was prepared in high yield from Fmoc-Tyr-OH by a one-step procedure which employed di-t-butyl N,N-diethyl-phosphoramidite as the phosphorylation reagent. The use of this derivative in Fmoc/solid phase peptide synthesis is demonstrated by the preparation of the Tyr(P)-containing peptides, Ala-Glu-Tyr(P)-Ser-Ala and Ser-Ser-Ser-Tyr(P)-Tyr(P).     

一些保肝药物对原代培养大鼠肝细胞糖原合成功能的影响

本文参照PO Seglen的方法并加以修改,建立了原代培养大鼠肝细胞糖原合成功能的测定体系。观察到联苯双酯既能使正常肝细胞合成糖原增加88%,又能保护肝细胞完全拮抗四氯化碳对其功能的损伤;银耳多糖能使四氯化碳对肝细胞糖原合成功能的损伤减轻57%;去甲斑蝥素10μg/ml能增加肝细胞糖原合成,浓度增加到100μg/ml时,此作用减弱,1000μg/ml则明显抑制糖原的合成,而且在10～100μg/ml浓度时,即能加强四氯化碳的损伤作用;100μg/ml CL₁₅₀₀和熊果酸二钠单独应用可增加肝细胞糖原合成,但与四氯化碳同时应用,反而加重对糖原合成的抑制作用。     

(E)-3-〔3-4-(氟苯基)-1-(1-甲基乙基)-1H-吲哚-2-基〕-2-丙烯醛的合成

（Ｅ）３〔３（４氟苯基）１（１甲基乙基）１Ｈ吲哚２基〕２丙烯醛（２）是合成氟伐他汀的关键中间体．从苯胺经异丙基化、与２氯１（４氟苯基）乙酮缩合、氯化锌催化的分子内环合、在Ｖｉｌｓｍｅｉｅｒ反应条件下与３（Ｎ甲基Ｎ苯基）丙烯醛反应合成（２），四步反应总收率为５４％．     

2,7,12,18-四甲基-13,17-二(3-羟基丙基)卟啉的合成及其光敏化活性

由氯化高铁次卟啉经脱铁、酯化、还原合成了光敏剂２，７，１２，１８－四甲基－１３，１７－二（３－羟基丙基）卟啉，并测定其光敏活性     

Synthesis and Antitumour Activity of New Derivatives of Flavone-8-acetic Acid (FAA). Part 1: 6-Methyl Derivatives

A range of 17 derivatives of flavone-8-acetic acid (FAA) with a 6-methyl substituent have been prepared and their anti-tumour activity evaluated in vitro against a panel of human and murine tumour cell lines and in vivo against MAC 15A. While many of the compounds show activity comparable to FAA in vitro, this essentially disappears in vivo, possibly due to degradation before the compounds can reach the tumour site.     

“美容牌”染发剂对雄性小鼠生殖细胞非程序DNA合成的诱导

本文应用雄性小鼠生殖细胞非程序DNA合成(UDS)检测方法研究了“美容牌”染发剂对雄性生殖细胞DNA的损伤作用。发现该染发剂诱发的UDS与药物剂量呈线性正相关。提示此类染发剂对雄性生殖细胞DNA有损伤作用。其遗传毒理效应应引起注意。     

Extrapolating global visual field indices from local parameters in the nasal region

The local mean and the average difference of four pairs of test locations within the 26° visual field, situated above and below the horizontal nasal meridian, were used to predict the global field indices MD and CLV of the Gl glaucoma program. Out of 539 examinations (194 eyes suspected of having glaucoma), the local indices NDIFF (describing asymmetrical behavior around the nasal horizontal meridian), ND0 (the mean defect in the nasal region), and the global indices MD and CLV were calculated. Seven hundred fifty-five examinations (446 normal eyes) served as a control group. First and second examinations of 146 glaucoma suspect eyes were used to calculate the retest reliability scores for the indices in question. When analyzing the glaucoma suspects, the local index NDIFF, together with the local mean defect, ND0, yielded highly reliable estimates of the global indices MD and CLV, with a retest correlation r = 0.86 for NDIFF, and r = 0.96 for ND0. The covariance of NDIFF with CLV was r = 0.67, while the co-variance of MD with ND0 was r = 0.95.The ranges of the local indices ND0 and NDIFF were each classified into normal range and range of suspected pathology, in analogy to the normal and pathological ranges of the global field indices. Equivalence of the local indices with the corresponding ranges of MD and CLV was investigated and the results are shown. The establishment of local indices may prove to be a powerful tool in early detection of glaucomatous damage.     

In vivo and in vitro studies of the site of inhibitory action of omeprazole on adrenocortical steroidogenesis

Summary The site of omeprazole inhibition of adrenal steroidogenesis has been sought in vivo by analyzing the patterns of urinary steroid metabolite excretion after 6 days of treatment with placebo/omeprazole.Excretion rates of androsterone, aetiocholanolone, dehydroepiandrosterone, 11 hydroxyandrosterone, tetrahydrocortisone, tetrahydrocortisol and cortolone were reduced, indicating a block at an early step in steroidogenesis, possibly cholesterol side-chain cleavage. In vitro studies have confirmed this finding by measuring conversion of added precursors to cortisol in isolated bovine adrenocortical cells. Cortisol synthesis from added 20 hydroxycholesterol was inhibited by 83% in the presence of 100 µg omeprazole/ml. Conversion from pregnenolone and progesterone and their 17 hydroxylated derivatives was inhibited by 20–40% whereas cortisol production from added 11 deoxycortisol was not affected.These data suggest that omeprazole primarily inhibits cholesterol cleavage and does not inhibit 3 hydroxysteroid dehydrogenase, 17 hydroxylase or 11 hydroxylation; 21 hydroxylase activity may be marginally attenuated.