稀土农用毒性评价及抑癌作用机理的研究

稀土农用毒性评价及抑癌作用机理的研究纪云晶崔明珍一、问题的由来早在７０年代初，我国就开始了稀土农用的研究。但一方面由于试验不细致，重复少，施用技术缺乏针对性；另一方面对于施用稀土后是否可能有放射性污染、残留毒性问题得不到回答，因此在１９７８年前中断了...     

抑癌基因的研究进展

抑癌基因的研究进展山西省肿瘤研究所（０３００１３）文锦华史天良张华目前，癌症仍然是医学界面临的一大难题，世界各国投入了大量的人力物力，已有了很大的突破。研究表明，大多数致癌物均可损伤ＤＮＡ并由此导致细胞的突变和癌变。细胞突变机制有二种：第一，细胞中...     

抑癌基因与大肠癌

抑癌基因具有抑制原癌基因表达的作用。由于抑癌基因的突变或缺失 ,使抑癌基因失活 ,从而导致原癌基因活化或细胞增生失控而引起癌变。与大肠癌有关的抑癌基因有 ｐ5 3、ＡＰＣ/ＭＣＣ、ＤＣＣ、ｎｍ 2 3、ｐ16及一些新近发现的 ｐ73、ｐ2 1、ＨＳＵ17714等 ,现介绍如下。1　ｐ5 3ｐ5 3基因位于 17号染色体 (17ｐ5 3) ,其蛋白产物的分子量为 5 3ｋｄ ,故称 ｐ5 3。ｐ5 3分野生型和突变型。野生型 ｐ5 3保存期极短不易检测。而突变型ｐ5 3在细胞内保存期相对较长。在大肠癌中约 5 0 %～ 60 %有 ｐ5 3表达 ,明显高于正常组织及腺瘤[1] 。ｐ5 3…     

抑癌基因PTEN在肿瘤发生发展中的作用

近年来,肿瘤已成为危害人类健康最严重的一类疾病.各种环境和遗传因素可能以协同或序贯的方式引起细胞非致死性的DNA损害,从而激活原癌基因或(和)灭活肿瘤抑制基因,加上凋亡调节基因的改变,使细胞发生转化,导致肿瘤的发生.PTEN基因是继P53和Rb基因之后又一个重要的抑癌基因,也是迄今发现的第一个具有磷酸酶活性的抑癌基因,它在肿瘤的发生发展中具有重要作用.本文就PTEN和肿瘤的关系作一综述.     

乳腺癌癌基因及抑癌基因的研究新进展

随着细胞生物学和分子生物学理论和技术的发展,已认识到乳腺癌的发生发展是多种异常基因共同作用的结果。其中包括乳腺癌癌基因、抑癌基因、易感基因、细胞周期调控基因、细胞凋亡调控基因、多耐药基因、血管生成相关基因等。其中癌基因的激活和抑癌基因的失活是肿瘤发生的     

膀胱癌相关抑癌基因的研究进展

膀胱癌是泌尿外科最常见的恶性肿瘤,已证明膀胱癌与多种抑癌基因的异常表达有关,各种抑癌基因的抑癌机制和异常表达方式存在不同,近年来关于膀胱癌相关抑癌基因的研究取得了显著进展,这对膀胱癌的早期诊断及特异性靶向治疗具有重要意义。该文根据抑癌基因的主要的作用机制不同对膀胱癌相关抑癌基因做一综述。     

抑癌基因PTEN与泌尿系肿瘤

PTEN是继p53基因之后发现的人类肿瘤中最常发生突变的抑癌基因,美国有3家实验室于1997年几乎同时发现该基因[1].许多研究均已提示在多种类型的人类肿瘤细胞中,PTEN基因的突变或者缺失与之有着密切关系.动物实验同样证实了PTEN基因的缺失在多种肿瘤发生中发挥了重要的作用[2].PTEN基因在人类肿瘤发生发展中起着如此重要的作用,使其成为肿瘤研究中的热点.     

癌基因、抑癌基因、环境化学致癌的分子生物学基础

癌基因、抑癌基因、环境化学致癌的分子生物学基础李学明致癌作用是一个复杂的多阶段过程，大致可以分为启动、促癌、进展和转移几个阶段。多年来化学致癌理论偏重于体细胞突变学说，大量的实验肯定了肿瘤的发生和发展与ＤＮＡ损伤以及由于ＤＮＡ损伤导致的细胞突变有密切...     

新的抑癌基因PDCD4最新研究进展

目的:程序性细胞死亡4(PDCD4)是一种新的细胞凋亡相关基因,最近来自动物和人类肿瘤的研究显示 PDCD4可能是一种新的抑癌基因,在肿瘤的发生、发展中可能发挥重要作用。本文从该基因的发现、生物学特点以及与肿瘤发生、发展的关系进行了综述。     

7,8-二羟基黄酮及其稀土配合物的合成与表征

目的 寻找具有抗炎、镇痛、抗凝血作用的黄酮金属配合物药物，充分利用内蒙古地区丰富的稀土资源。方法 采用Baker-Venkataraman反应，合成了7，8-二羟基黄酮，该化合物再与几种稀土配合。结果 合成5种未见文献报道的稀土配合物。结论 用改进工艺后的方法合成黄酮，使重排反应收率提高，溶剂成本降低；而且利用具邻苯二酚结构的黄酮作配体合成配合物，为今后开发研制此类化合物提供了参考。     

芦荟抗肿瘤作用研究

目的：研究不同品种芦荟抗肿瘤作用，方法：健康小鼠接种S180肉瘤及H22肝癌腹水瘤，观察其抗肿瘤作用，结果：各品种的芦荟对S180肿瘤均有抑制作用，均能延长荷瘤H22小鼠的生命率。结论：各品种的芦荟均有抗肿瘤作用。     

Extraction of rare earth elements via electric field assisted mining applying deep eutectic solvents

Rare earth elements play an important role in our society, as they are used in green energy technologies. However, they are considered critical raw materials. For this reason, there is a concern for obtaining alternative and complementary sources for conventional mining. In light of this view, electric field assisted mining arises as a technique to extract species from soils using green electrolytes to help in the extraction of metals. The aim of this paper was to evaluate the effect of different types of biodegradable electrolytes, including the use of deep eutectic solvents, in the electromining process. Six experiments were conducted applying an electric field of 1.0 V cm^?1, and all electrolytes were used at a concentration of 0.1 mol L^?1. The results showed that different electrolytes achieved different selectivities. The maximum efficiency using acetic acid resulted in 69.1% of Ce⁴⁺, citric acid removed 62.3% of La³⁺, and oxalic acid extracted 21.5% of La³⁺. The electromining efficiencies using deep eutectic solvents presented minor results. Therefore, considering the biodegradability and selectivity of the organic acids used, electromining showed to be a promising eco-friendly alternative for preferential extraction of metal species from soils.     

抑癌基因PTEN与肿瘤血管生成研究进展

PTEN是具有磷酸脂酶活性的抑癌基因,是双特异蛋白磷酸酶家族(DSPs)的成员,同时具有脂质磷酸酶和蛋白酪氨酸磷酸酶活性。而在肿瘤增殖,侵袭,迁移的过程中,肿瘤血管生成作为肿瘤发生发展中一个关键因素已越来越受到人们的关注。抑癌基因PTEN可以参与PI3K/Akt信号通路,调控缺氧诱导因子1,基质金属蛋白酶,血管内皮生长因子,钠氢交换调控因子1等血管生成相关信号以及一些机体氧化产物来影响肿瘤血管生成。根据近年来PTEN基因与肿瘤血管生成关系最新研究信息,该文综述了其目前的研究现状。     

整合素在肿瘤转移中的作用机制研究进展

机体重要的黏附分子整合素(Integrins)在细胞与细胞外基质间及细胞与细胞间的黏附作用已为人共知。以往的研究证实整合素与肿瘤转移有着密切关系,文献分析表明,这一研究领域一直是肿瘤转移方面的研究热点,该文着重概述近5年国际上关于整合素在肿瘤转移的作用机制方面的研究进展,表明整合素介导了大量的非配体依赖的信号转导通路促进了肿瘤转移。这使得整合素在肿瘤转移中的作用机制更加明确和深入,也为整合素抑制剂的开发带来了光明的前景。     

EMP3 as a candidate tumor suppressor gene for solid tumors

Background: Epithelial membrane protein 3 (EMP3), was recently reported to be a tumor suppressor gene for several solid tumors, and is drawing attention as a novel prognostic marker, since its expression level or hypermethylation of the promoter region is associated with clinical prognosis in neuroblastoma and esophageal cancer. However, some controversial data were also observed in gliomas and breast cancers, and there seems to be more than deletion/hypermethylation to its silencing mechanisms. Objective: To clarify the discrepancies in the biological behavior of EMP3 among the different organ-derived malignancies or histologies and validate the potential of EMP3 as a tumor suppressor for solid tumors. Methods: Literature dealing with EMP3 in the PubMed database was reviewed. Results/conclusions: EMP3 is a novel tumor suppressor gene in some kinds of malignancies, but not all, at the step of cellular immortalization rather than carcinogenesis. It may become a potent prognostic marker and a therapeutic target in such tumors.     

稀土元素铕对大黄愈伤组织生长及蒽醌类成分的影响

研究了稀土元素Eu3＋对药用植物大黄愈伤组织生长的影响，结果显示：在MS培养基中附加稀土元素可明显影响愈伤组织的生长；低浓度稀土促进生长，高浓度抑制生长；并对稀土的作用机理做了探讨以及对愈伤组织中的蒽醌类化合物进行了定性、定量分析。     

参麦注射液联合羟基喜树碱抑制肿瘤血管生成的作用机制

目的:研究参麦注射液联合羟基喜树碱对肿瘤血管生成的作用机制。方法:将人结肠癌细胞株CW-2细胞分4组:对照组,参麦组,羟基喜树碱组,参麦联合羟基喜树碱组。分组后的CW-2细胞培养24h后,用ELISA检测上清液中VEGF和bFGF的浓度,RT-PCR法检测VEGF和bFGF mRNA的量,Western-blot检测VEGF和bFGF的表达。结果:与空白对照组比较,3个实验组均能明显降低CW-2细胞上清液中VEGF和bFGF的含量,显著减少CW-2细胞VEGF和bFGF的mRNA合成及蛋白质表达,而参麦注射液联合羟基喜树碱则具有协同效应。结论:参麦注射液联合羟基喜树碱抑制肿瘤细胞VEGF和bFGF合成和分泌,是其抑制肿瘤血管生成的可能机制之一。     

The mechanism for cellular uptake,storage and release of daunorubicin: Studies on fibroblasts in culture

The mechanism for uptake, storage and release of daunorubicin have been studied in cultured fibroblasts. Analysis by high performance liquid chromatography of cells incubated with daunorubicin revealed that the major part of the accumulated drug did not undergo metabolic transformation. Small amounts of daunorubicinol and aglycone were formed. [³H]-daunorubicin was used to study membrane fluxes of the drug under different conditions. Metabolic inhibitors enhanced the influx of [³H]-dauno-rubicin and, under certain conditions, also reduced its efflux, indicating that the cells have an active mechanism for the outward transport of the drug. The very high intracellular drug accumulation is due to trapping in nuclei and lysosomes. Cell fractionation techniques have been used to study drug trapping under various conditions. Nuclear storage of daunorubicin is probably due to binding to DNA. Metabolic inhibitors, as well as lowering the incubation temperature, reduced the lysosomal trapping, supporting the hypothesis that the low pH in these organelles is maintained by a proton pump and that the drug is trapped in the protonated form. A hypothesis is presented, which by combining the mechanisms for membrane transport and intracellular storage of daunorubicin, gives also an explanation for the observed differences in the cellular accumulation and subcellular distribution of daunorubicin and its 14-hydroxy derivative, doxorubicin. Daunorubicin is more lipophilic than doxorubicin and will therefore diffuse faster through the cell membrane. Assuming that both substances have the same affinity for the proposed active outward transport mechanism, this will lead to a higher steady-state level of daunorubicin in the cytosol and as a consequence to a higher lysosomal storage level if the drug in the lysosomes is in equilibrium with that in the cytosol. The similarity in nuclear storage capacity for the two substances can be explained by saturation of the available storage sites.