稻田高活性杀稗剂苯噻草胺的开发与使用

本文评述了苯噻草胺的开发,特性,生物活性及其在中国的应用前景。     

苯噻草胺的分析方法

采用高效液相色谱法,使用反相谱柱和紫外检测器,用外标法对苯噻草胺进行定量分析。方法的标准偏差０．２４,变异系数０．２５％,线性相关系数０．９９９９,回收率９９．３％－１００．２％。     

苯噻草胺的合成

综述了苯噻草胺的合成方法及国内外研究状况.     

苯噻草胺的合成

综述了苯噻草胺的合成方法及国内外研究状况。     

除草剂苯噻草胺的合成

介绍了苯噻草胺及相关中间体的合成方法,其中苯噻草胺的合成采用２－氯代苯并噻唑与２－羟基－Ｎ－甲基乙酰胺反应来制备为宜,２－氯代苯并噻唑的合成采用２－在苯并噻唑氯化法为宜,２－羟基－Ｎ－甲基乙苯胺的合成采用氯乙酰氯法为宜。     

苯噻草胺的生物活性与应用技术研究

本文在温室条件下,采用盆栽试验方法,研究了苯噻草胺对稗草的生物活性以及对水稻的安全性,试验结果表明,苯噻草胺对１￣３叶期稗草有较高的生物活性,保水与否以及保水时间对其生物活性有明显的影响;苯噻草胺对移栽水稻,抛秧水稻较为安全,对１叶期直播水稻则有抑制作用,不宜使用。多点田间药效试验结果亦表明,苯噻草胺是一个安全,高效,施药适期较长的移栽稻田除稗剂。     

除草剂苯噻草胺的RP-HPLG测定

采用高效液相色谱法,以甲醇和水(含0.3%冰醋酸)为流动相,使用反相色谱柱和紫外检测器对除草剂苯噻草胺进行测定.方法的标准偏差0.29,变异系数0.79%(n=6),线性关系决定系数R2=0.9998,添加回收率100.9%～107.1%,检测限0.1mg·L-1,结果令人满意.     

苯噻草胺的合成

苯噻草胺的合成李树人（江苏省农药研究所，南京２１００３６）苯噻草胺￣［１．２］，通用名称ｍｅｆｅｎａｓｔ，化学名称２－ｂｅｎｚｏｔｈｉａｚｏ－２－ｙｌｏｘｙ－Ｎ－ｍｅｔｈｙｌａｃｅｔａｎｉｌｉｄｅ。德国拜耳公司、日本特殊农药公司１９８０年开发。该除草...     

除草剂苯噻草胺合成的技术经济评价

概述了苯噻草胺产品的用途、市场需求及合成方法 ,采用静态法和动态法对 2 -氯代苯并噻唑路线制备苯噻草胺进行了技术经济评价 ,认为该工艺条件简单 ,反应条件温和 ,操作方便 ,经济效益明显     

苯噻酰草胺的填充柱气相色谱分析

对苯噻酰草胺进行填充柱气相色谱分析方法研究。经试验,采用5%SE-30/Chromosorb w aw DMCS为固定相的填充柱,磷酸三苯酯为内标,成功地进行苯噻酰草胺气相色谱分析,并与行标HG3719-2003、HG3720-2003的液相色谱法、毛细管气相色谱法进行比较,取得一致结果。     

5种水田除草剂对稻稗和稗草的生物活性研究

室内生测结果表明,供试的5种水田除草剂中,丙草胺对稗草的活性最高,苯噻草胺对稗草的活性最低,莎稗磷、二甲戊灵和丁草胺居中,且三者对稗草的活性相当;二甲戊灵对稻稗的活性最高,丁草胺对稻稗的活性最低,莎稗磷、苯噻草胺和丙草胺对稻稗有较好的防除效果。     

苯噻草胺·苄嘧磺隆可湿性粉剂的分析

采用高效液相色谱法 ,以甲醇和水作流动相 ,同时测定苯噻草胺·苄嘧磺隆可湿性粉剂中苯噻草胺和苄嘧磺隆含量。方法的线性关系好 ,苯噻草胺和苄嘧磺隆的变异系数分别为 :0 8%、1 2 % ,平均回收率分别为 99 6%、99 0 %。     

HPLC法测定苯噻·苄·乙复配除草剂中的活性成份

报道了 30 %苯噻·苄·乙复酸除草剂的高效液相色谱分析方法 ,采用乙腈 +甲醇+水 =30 +4 0 +30 (V/V )为流动相 ,在C18柱上UV - 2 30nm下 ,同时测定了苯噻草胺、苄嘧磺隆和乙草胺的含量 ,标准偏差分别为 0 0 38、0 0 15和 0 0 16,变异系数分别为 0 16%,0 5 9%,0 63%,回收率在 98 10 %～ 10 2 2 8%之间。     

68%吡嘧·苯噻酰WP防除移栽水稻杂草试验总结

为探讨68%吡嘧·苯噻酰WP在水稻田的应用前景,于2007—2008年在湖南、浙江、河北、辽宁、黑龙江等地进行了两年布点登记试验。试验结果表明,68%吡嘧·苯噻酰WP具有安全、广谱、增产显著的特点,能有效防除水稻稗草、稻稗、三棱草、野荸荠、鸭舌草、水莎草等单双子叶杂草。     

循环伏安法验证有机碘试剂氧化下偶联反应的机理

利用循环伏安法测定了有机碘试剂作用下交叉偶联反应中两种反应底物的氧化还原电位,通过比较两种底物的氧化电位,确定了偶联反应机理的优势路径。     

稻田稗草对丁草胺和二氯喹啉酸抗药性的测定

[目的]为明确稻田稗草对丁草胺和二氯喹啉酸的抗药性水平,利用盆钵法测定了广东佛冈、韶关、梅州等地共14个点稻田稗草对丁草胺和二氯喹啉酸的抗药性.[结果]对于丁草胺,惠州龙门稗草ED50值最大,为757.33 g a.i./hm2,相对抗性指数(RI)为3.4,说明龙门点稗草对丁草胺已产生一定的抗药性;对于二氯喹啉酸,所测定的14个稗草生态型对其未表现出抗药性.[结论]稻田稗草对丁草胺已经产生不同程度的抗药性,其中惠州龙门点抗性最高;稻田稗草对二氯喹啉酸未产生抗药性.     

三核钼钨簇合物的循环伏安法研究

本文利用循环伏安法在铂电极上研究了三核钼钨簇合物（〔Ｍｏ３Ｌ〕２＋ ,〔Ｗ ３Ｌ〕２＋其中Ｌ＝ 〔（μ３－ Ｏ）２（μ－ ＣＨ３ＣＯＯ）６（Ｈ２Ｏ）３〕的电化学性质及其对电化学性质的影响因素。     

Inhibition of N-Acetyltransferase 10 Suppresses the Progression of Prostate Cancer through Regulation of DNA Replication

Cancer suppression through the inhibition of N-acetyltransferase 10 (NAT10) by its specific inhibitor Remodelin has been demonstrated in a variety of human cancers. Here, we report the inhibitory effects of Remodelin on prostate cancer (PCa) cells and the possible associated mechanisms. The prostate cancer cell lines VCaP, LNCaP, PC3, and DU145 were used. The in vitro proliferation, migration, and invasion of cells were measured by a cell proliferation assay, colony formation, wound healing, and Transwell assays, respectively. In vivo tumor growth was analyzed by transplantation into nude mice. The inhibition of NAT10 by Remodelin not only suppressed growth, migration, and invasion in vitro, but also the in vivo cancer growth of prostate cancer cells. The involvement of NAT10 in DNA replication was assessed by EdU labeling, DNA spreading, iPOND, and ChIP-PCR assays. The inhibition of NAT10 by Remodelin slowed DNA replication. NAT10 was detected in the prereplication complex, and it could also bind to DNA replication origins. Furthermore, the interaction between NAT10 and CDC6 was analyzed by Co-IP. The altered expression of NAT10 was measured by immunofluorescence staining and Western blotting. Remodelin markedly reduced the levels of CDC6 and AR. The expression of NAT10 could be altered under either castration or noncastration conditions, and Remodelin still suppressed the growth of in vitro-induced castration-resistant prostate cancers. The analysis of a TCGA database revealed that the overexpression of NAT10, CDC6, and MCM7 in prostate cancers were correlated with the Gleason score and node metastasis. Our data demonstrated that Remodelin, an inhibitor of NAT10, effectively inhibits the growth of prostate cancer cells under either no castration or castration conditions, likely by impairing DNA replication.     

Complex Mechanisms of Antimony Genotoxicity in Budding Yeast Involves Replication and Topoisomerase I-Associated DNA Lesions,Telomere Dysfunction and Inhibition of DNA Repair

Antimony is a toxic metalloid with poorly understood mechanisms of toxicity and uncertain carcinogenic properties. By using a combination of genetic, biochemical and DNA damage assays, we investigated the genotoxic potential of trivalent antimony in the model organism Saccharomyces cerevisiae. We found that low doses of Sb(III) generate various forms of DNA damage including replication and topoisomerase I-dependent DNA lesions as well as oxidative stress and replication-independent DNA breaks accompanied by activation of DNA damage checkpoints and formation of recombination repair centers. At higher concentrations of Sb(III), moderately increased oxidative DNA damage is also observed. Consistently, base excision, DNA damage tolerance and homologous recombination repair pathways contribute to Sb(III) tolerance. In addition, we provided evidence suggesting that Sb(III) causes telomere dysfunction. Finally, we showed that Sb(III) negatively effects repair of double-strand DNA breaks and distorts actin and microtubule cytoskeleton. In sum, our results indicate that Sb(III) exhibits a significant genotoxic activity in budding yeast.     

Regulation of DNA Replication Licensing and Re-Replication by Cdt1

In eukaryotic cells, DNA replication licensing is precisely regulated to ensure that the initiation of genomic DNA replication in S phase occurs once and only once for each mitotic cell division. A key regulatory mechanism by which DNA re-replication is suppressed is the S phase-dependent proteolysis of Cdt1, an essential replication protein for licensing DNA replication origins by loading the Mcm2-7 replication helicase for DNA duplication in S phase. Cdt1 degradation is mediated by CRL4^Cdt2 ubiquitin E3 ligase, which further requires Cdt1 binding to proliferating cell nuclear antigen (PCNA) through a PIP box domain in Cdt1 during DNA synthesis. Recent studies found that Cdt2, the specific subunit of CRL4^Cdt2 ubiquitin E3 ligase that targets Cdt1 for degradation, also contains an evolutionarily conserved PIP box-like domain that mediates the interaction with PCNA. These findings suggest that the initiation and elongation of DNA replication or DNA damage-induced repair synthesis provide a novel mechanism by which Cdt1 and CRL4^Cdt2 are both recruited onto the trimeric PCNA clamp encircling the replicating DNA strands to promote the interaction between Cdt1 and CRL4^Cdt2. The proximity of PCNA-bound Cdt1 to CRL4^Cdt2 facilitates the destruction of Cdt1 in response to DNA damage or after DNA replication initiation to prevent DNA re-replication in the cell cycle. CRL4^Cdt2 ubiquitin E3 ligase may also regulate the degradation of other PIP box-containing proteins, such as CDK inhibitor p21 and histone methylase Set8, to regulate DNA replication licensing, cell cycle progression, DNA repair, and genome stability by directly interacting with PCNA during DNA replication and repair synthesis.