花馔及其氨基酸营养

应用日立835 50型高效氨基酸自动分析仪,对十五种常见食用花卉干样进行了水解蛋白氢基酸成分测定,结果发现:①花馔中酸水解蛋白氨的基酸种类齐全,总氨基酸含量较高,占食用干物质的6.00—29.45％。②花馔中人体必需氨基酸含量丰富,占总氨基酸含量的29.50—42.60％。尤以亮氨酸、苯丙氨酸、赖氨酸和苏氨酸含量为高。③花馔中甜、鲜类氨基酸含量也较高,分别占总氨基酸的25.94—39.89％,23.35—33.38％,花馔是兼有营养、颜色、美味的天然食物,值得人类利用。     

肝胆显像螯合物—氮基三乙酸单酰苯胺及其类似物的合成

本课题合成四个氮基三乙酸单酰苯胺(IDA)类及其类似物肝胆显像螯合物。(1)用家兔做了肝胆显像扫描实验,其显像效果较好。(2)～(3)为未见报道的化合物。     

肺癌患者胸水游离氨基酸分析

本文对11例肺癌患者胸水13种游离氨基酸作了分析,并与28例正常人血浆游离氨基酸水平作了对照,结果表明:肺癌患者胸水的必需及非必需氨基酸普遍高于正常人血浆游离氨基酸,但其胸水谷氨酰胺水平则明显低于正常人血浆水平。     

几种药物对HL-60细胞的诱导分化作用及其过程中蛋白激酶C活力分布的变化

本文就HHT、RA、WB_(852)对HL-60细胞的诱导分化作用及此过程中PKC活力在细胞胞浆部分及膜溶脱部分的变化进行研究。结果表明,在适当的用药浓度下,从细胞生长抑制情况、形态学观察及NBT还原能力测定判断,三种药物对HL-60细胞有明显的诱导分化作用。PKC活力分布变化的研究结果表明,用药组细胞胞浆部分酶活力有不同程度的下降,尤在用药早期(约6h以前)下降显著;而膜部分PKC活力则表现上升、或下降,或活力相差不大的结果。暗示在信息传递过程中起核心作用的PKC对不同的胞外刺激可能采取不同的应答方式。PKC的作用可能主要发生在信息传递的早期。     

视黄酸对人肝癌细胞表面N糖链类型及天线数的影响

本文采用系列凝集素柱层析法,并配合外切糖苷酶处理研究了在视黄酸(RA)作用1—5天过程中人肝癌细胞株SMMC-7721细胞表面N糖链结构的变化。结果表明,RA促进3~H-甘露糖(Man)参入细胞表面N糖链,使高甘露糖型N糖链的百分比下降,复杂型百分比上升,并促进二天线N糖链的生物合成,使多天线特别是四天线和C_2,C_(21)b三天线N糖链的合成减少。结果提示,N糖链结构的这些变化可能是RA诱导SMMC-7721细胞向正常方向分化的结果。     

两株蓖麻蚕核型多角体病毒DNA同源性的研究

两株不同来源的蓖麻蚕核型多角体病毒(ArscsNPV和ArNPV)经提纯后,使用SDS—苯酚抽提病毒核酸,并使用限制性内切酶EcoRI,BamHI酶解后,用分子杂交方法与缺口平移标记的ArscsNPV-DNA探针杂交,分析了两株蓖麻蚕NPV病毒核酸的同源性。EcoRI酶解的ArNPV-DNA产生8个片段,其中5个片段能与ArscsNPV-DNA探针杂交。BamHI酶解ArNPV-DNA产生7个片段,其中6个片段能与ArscsNPV-DNA探针杂交。结果表明:两株蓖麻蚕NPV之间病毒核酸具有很高的同源性。使用斑点杂交方法分析了ArscsNPV与ArNPV,柞蚕NPV及家蚕NPV之间的核酸同源性,结果表明:ArscsNPV与ArNPV,柞蚕NPV具有同源性。而与家蚕NPV无核酸同源性。     

戊型肝炎病毒中国XT—179株全基因组Cdna克隆及其核苷酸和氨基酸序列分析

本文报道对中国新疆东部一起戊型肝炎流行高峰期间,由ＨＥ患者烘便中分离到的型肝炎病毒中国ＸＴ－１７９株进行全基因ｃＤＮＡ克隆、核苷酸和氨基酸序列测定及分析结果。所阐明的ＨＥＶ－ＸＴ－１７９株基因组全序列由７１９４个核苷酸和３＇端的多聚腺嘌呤核苷酸尾组成。四种核苷酸的含量腺嘌呤（Ａ）为１７．０％,胞嘧啶（Ｃ）为３１．９％,鸟嘌呤（Ｇ）为２６．０,尿嘧啶（Ｕ）为２５．１％。Ｇ＋Ｃ含量为５７．９％。全基因     

骨缘当归的化学成分

骨缘当归Angellica cartilaginomarginata var.foliata Yuan et Shen,别名:山藁本、野芹菜（江苏）,仅分布于江苏和浙江。在江苏镇江等地用干燥全草作山藁本入药,其化学成分未见报道。 样品采自江苏省句容县。将干根磨粉,提取物经中性氧化铝层析,根据色谱及光谱鉴定为两种脂肪酸、四种已知香豆素和一种植物甾醇即:正葵酸（n-capric acid）、月桂酸（lauric acid）、骨缘当归素（cartilaginomarginadin）、蝉翼素（pteryxin）、白花前胡素F（praeruptorin F）、佛手柑内酯（bergapten）及β-谷甾醇（β-sitosterol）。     

Proteomics analysis of meclofenamic acid-treated small cell lung carcinoma cells revealed changes in cellular energy metabolism for cancer cell survival

Small cell lung carcinoma (SCLC) is a highly aggressive cancer with low survival rate. Although initial response to chemotherapy in SCLC patients is well-rated, the treatments applied after the disease relapses are not successful. Drug resistance is accepted to be one of the main reasons for this failure. Therefore, there is an urgent need for new treatment strategies for SCLC. Meclofenamic acid, a nonsteroidal anti-inflammatory drug, has been shown to have anticancer effects on various types of cancers via different mechanisms. The aim of this study was to investigate the alterations that meclofenamic acid caused on a SCLC cell line, DMS114 using the tools of proteomics namely two-dimensional gel electrophoresis coupled to MALDI-TOF/TOF and nHPLC coupled to LC-MS/MS. Among the proteins identified by both methods, those showing significantly altered expression levels were evaluated using bioinformatics databases, PANTHER and STRING. The key altered metabolism upon meclofenamic acid treatment appeared to the cellular energy metabolism. Glycolysis was suppressed, whereas mitochondrial activity and oxidative phosphorylation were boosted. The cells underwent metabolic reprogramming to adapt into their new environment for survival. Metabolic reprogramming is known to cause drug resistance in several cancer types including SCLC. The identified differentially regulated proteins in here associated with energy metabolism hold value as the potential targets to overcome drug resistance in SCLC treatment.     

Identification of Products from Oxidation of Uric Acid Induced by Hydroxyl Radicals

The aim of the present study was to separate and characterise products formed by oxidation of uric acid by hydroxyl radicals with a view to probing for these products in vivo in clinical contexts. Aerated solutions of 200 μM uric acid, or its oxidation products, allantoin or parabanic acid, were exposed to gamma radiolysis, (52.0 Gy/min), as a source of HO- radicals, at pH 3.4 and 7.4. Aliquots were taken every 5 minutes for 20 minutes and oxidation products were separated by HPLC and analysed with a diode array detector. Identities of oxidation products were confirmed on the basis of similarity of retention times and absorbance spectra and peak purity parameters of known standards. Hydroperoxides were measured by tri-iodide formation in the 20 minute sample. Exposure of uric acid to such HO fluxes produced a net loss of the parent compound with formation of a complex mixture of products with allantoin and parabanic acid being the predominant products at pH 3.4. The rate of uric acid degradation at physiological pH was slower and the distribution of oxidation products was different. A small but significant amount of uric acid hydroperoxide was detected at both pHs. A mechanism for uric acid oxidation under these conditions is presented.