杀虫气雾剂对家蝇及德国小蠊的驱避效果研究

研究了杀虫气雾剂对家蝇和德国小蠊的驱避效果.按GB/T 13917-2009试验方法测定五种不同配比的Es-生物烯丙菊酯·右旋苯醚菊酯对家蝇和德国小蠊的室内和模拟现场药效,结果表明配比为0.25％Es-生物烯丙菊酯·0.20％ 右旋苯醚菊酯对家蝇和德国小蠊室内及模拟现场药效为A级,优于其他4个含量,并达到显著水平.该配...     

山蒟(Piper hancei Maxim)杀虫活性初步研究

[目的]研究山蒟的杀虫活性,以丰富植物源农药的来源.[方法]采用胃毒法测定山蒟对家蝇的胃毒活性,浸渍法测定山蒟对致倦库蚊和白纹伊蚊的活性.[结果]结果显示:山药的石油醚萃取物表现较强的杀虫活性,石油醚提取物1 g/L处理家蝇12、24 h后,校正死亡率分别为86.66％、90％,处理家蝇12、24、36 h后的LC50值分别为1.4000、0.5000、0.2000 g/L,接近于处理36h后鱼藤酮的LC50值(0.08 g/L).石油醚提取物处理致倦库蚊和白纹伊蚊12h后的LC50值分别为2.4127、10.5163 mg/L,活性分别高于对照药物鱼藤酮的3.1727、21.5100 mg/L.[结论]山蒟具有较好杀虫活性,经检索未见相关文献曾报道山药的杀虫活性.     

方兴未艾的气雾剂

根据研制气雾剂的经验 ,结合其最新发展趋势 ,介绍了气雾剂的研制历史、基本组成 (尤其是抛射剂 ) ,气雾剂的应用 ,并在分析气雾剂工业现状的基础上指出国内的气雾剂工业具有良好的发展前景。     

鱼藤酮的薄层扫描定量分析研究

采用薄层扫描法对鱼藤酮进行了定量分析。该方法的标准偏差为0.24,变异系数为1.6％,回收率为96.9％～101.0％。     

鱼藤酮腙的合成及生物活性

用鱼藤酮和水合肼反应,得到新化合物鱼藤酮腙,其结构经^H NMR、^13C NMR和MS确认。杀虫活性测定结果表明,目标化合物对家蝇和黄曲条跳甲的活性与鱼藤酮相当。     

表鱼藤酮光稳定性的研究

采用HPLC法测定了5’β-表鱼藤酮、5’α-表鱼藤酮、鱼藤酮经365nm紫外光照射后的降解率,降解动力学方程分别为Cr=57．066e^-0.0537t、Ct=13．003e^-0.1748t、Ct=9.0851e^-0.3008t,其半衰期分别为12．9、4．0、2．3h。结果表明在相同时间内鱼藤酮的降解率最高,其次是5’α-表鱼藤酮．5’β-表鱼藤酮的降解率最低。     

鱼藤酮的应用现状及存在问题

鱼藤酮是一种天然的植物质杀虫剂和杀螨剂,主要从热带和亚热带的鱼藤属（Derris）、尖荚豆属（Lonchocarpus）和灰叶属（Tephrosia）植物中提取,其杀虫谱广,害虫不易产生抗药性,为无公害农产品生产推荐使用品种,具有广阔的应用前景。该文简要介绍了鱼藤酮的产品及应用范围、鱼藤酮的应用开发现状以及应用过程中出现的问题和解决方法,并对今后进一步开发应用鱼藤酮提出建议。     

鱼藤酮的高效液相色谱分析方法研究

介绍一种鱼藤酮的高效液相色谱定量分析方法。采用hypersil C18色谱柱,在以v(乙腈)∶v(水)=60∶40为流动相,流速为1.0 mL/m in,检测波长为294 nm的条件下,用外标法对鱼藤酮原药中的有效成分进行定量分析。方法的标准差为0.28,变异系数为0.39%,线性相关系数为0.9999,平均回收率为99.54%。     

气相色谱法分析鱼藤酮制剂的研究

研究了测定鱼藤酮制剂中的鱼藤酮含量的气相色谱方法。采用5％SE-30／Shimalite W(AW-DMCS)-80～100目固定相填充柱，270℃恒温分离，FID检测器测定。选择邻苯二甲酸二壬酯作为内标物内标法定量。方法回收率98.2％～102．9％，变异系数小于2％。也可以采用外标法定量。该分析方法操作简单，定量准确，与其他方法比较更易于推广应用，适应于产品的常规分析与质控研究。     

三氯化铝催化鱼藤酮异构化制备异鱼藤酮

为了优化鱼藤酮异构化制备异鱼藤酮的工艺。采用三氯化铝催化下异构化。合成收率高达90.5%,较文献提高56%。目标产物经核磁共振谱确证。实验结果表明,三氯化铝催化鱼藤酮异构化的方法可行,反应条件温和。     

广州大气颗粒物与酸沉降的关系研究

本文研究了大气颗粒物的酸度和酸缓冲能力,实验证实广州大气颗粒物中存在着游离的硫酸,其水溶性离子中SO4^2-及NO3^-占很大的比例。颗粒物中的碱性成分含量大于酸性成分,对酸性降水有一定的缓冲能力。气溶胶中细颗粒物的酸性大于粗颗粒物,且酸缓冲能力远低于粗颗粒物。     

Intranasal Administration of Rotenone Reduces GABAergic Inhibition in the Mouse Insular Cortex Leading to Impairment of LTD and Conditioned Taste Aversion Memory

The pesticide rotenone inhibits mitochondrial complex I and is thought to cause neurological disorders such as Parkinson’s disease and cognitive disorders. However, little is known about the effects of rotenone on conditioned taste aversion memory. In the present study, we investigated whether intranasal administration of rotenone affects conditioned taste aversion memory in mice. We also examined how the intranasal administration of rotenone modulates synaptic transmission and plasticity in layer V pyramidal neurons of the mouse insular cortex that is critical for conditioned taste aversion memory. We found that the intranasal administration of rotenone impaired conditioned taste aversion memory to bitter taste. Regarding its cellular mechanisms, long-term depression (LTD) but not long-term potentiation (LTP) was impaired in rotenone-treated mice. Furthermore, spontaneous inhibitory synaptic currents and tonic GABA currents were decreased in layer V pyramidal neurons of rotenone-treated mice compared to the control mice. The impaired LTD observed in pyramidal neurons of rotenone-treated mice was restored by a GABA_A receptor agonist muscimol. These results suggest that intranasal administration of rotenone decreases GABAergic synaptic transmission in layer V pyramidal neurons of the mouse insular cortex, the result of which leads to impairment of LTD and conditioned taste aversion memory.     

Non-Reproducibility of Oral Rotenone as a Model for Parkinson’s Disease in Mice

Oral rotenone has been proposed as a model for Parkinson’s disease (PD) in mice. To establish the model in our lab and study complex behavior we followed a published treatment regimen. C57BL/6 mice received 30 mg/kg body weight of rotenone once daily via oral administration for 4 and 8 weeks. Motor functions were assessed by RotaRod running. Immunofluorescence studies were used to analyze the morphology of dopaminergic neurons, the expression of alpha-Synuclein (α-Syn), and inflammatory gliosis or infiltration in the substantia nigra. Rotenone-treated mice did not gain body weight during treatment compared with about 4 g in vehicle-treated mice, which was however the only robust manifestation of drug treatment and suggested local gut damage. Rotenone-treated mice had no deficits in motor behavior, no loss or sign of degeneration of dopaminergic neurons, no α-Syn accumulation, and only mild microgliosis, the latter likely an indirect remote effect of rotenone-evoked gut dysbiosis. Searching for explanations for the model failure, we analyzed rotenone plasma concentrations via LC-MS/MS 2 h after administration of the last dose to assess bioavailability. Rotenone was not detectable in plasma at a lower limit of quantification of 2 ng/mL (5 nM), showing that oral rotenone had insufficient bioavailability to achieve sustained systemic drug levels in mice. Hence, oral rotenone caused local gastrointestinal toxicity evident as lack of weight gain but failed to evoke behavioral or biological correlates of PD within 8 weeks.     

固相萃取-高效液相色谱法检测上海青(Brassica chinensis L.)中鱼藤酮的残留动态

[目的]建立固相萃取-高效液相色谱-紫外(SPE-HPLC-UV)检测上海青中鱼藤酮的分析方法,对上海青中鱼藤酮的含量进行动态分析.[方法]样品先经乙腈提取,随后在乙腈提取液中加入氯化钠,盐析后过Florisil固相萃取柱富集净化,再用正己烷-乙醚(体积比3∶7)洗脱,最后以乙腈-水(体积比6∶4)为流动相,在290 nm下用高效液相色谱检测分析上海青中鱼藤酮的含量.[结果]该方法稳定可靠,检测物在0.05～10 mg/L范围内线性关系良好.在0.5～5 mg/kg范围内,平均加标回收率为85.9％～86.3％,检出限为0.05 mg/kg.田间推荐剂量和2倍推荐剂量分别施药,鱼藤酮在上海青中的原始沉积量分别为6.26、18.34 mg/kg.[结论]该化合物在田间降解速率快,在上海青中的半衰期分别为11.2、11.1h.