小麦化感作用物的提取,分离及其对白茅的杀除效果

小麦颖壳提取物经3520树脂分离后,对所得甲醇洗脱物离心,分得油类似物、上清液及沉淀物。前两个组分在300mg/L的浓度下,对白茅生长抑制率分别为100％和98％。上清液经硅胶柱分离,得7个亚组分,其中第1、3和7号亚组分在500mg/L浓度下对白茅生长的抑制率分别为95％、91％和95％。第3亚组分经葡聚糖凝胶柱分离,又分得A、B、C 3个组分,褐色粉末状的B组分在1000mg/L浓度下使白茅的生长量下降81％。从而证明小麦颖壳对白茅的化感作用是由多个化感物共同作用的结果。室内和温室及大田的测定结果表明,小麦颖壳中的甲醇洗脱物在24mg/株的剂量下对白茅生长的抑制率可达90％以上。这暗示,小麦颖壳中的甲醇可溶物可望开发成为防治白茅的生物除草剂。     

华北地区夏玉米田马唐治理的生态经济杀除阈期研究

作者于1992～1994年研究夏玉米田马唐(Digitaria sanguinalis L.)治理的生态经济阈期,借助计算机进行数学模拟,建立夏玉米的相对产量与马唐的相对干扰生长时间、相对出苗时间的函数关系。苗后马唐干扰生长的相对时间即相对天数(Xu)与夏玉米相对产量(Yu)的关系式为: Yu=101.5/{1.0 0.01756EXP[—(—0.0876Xu 0.0004888Xu~2)]}…………(1)苗后马唐出苗的相对时间与玉米相对产量的关系式为: Yd=100.73/{1.0 0.96EXP[—(0.06346Xd-0.00006859Xd~2)]}……………(2) 根据生态经济杀除阈期的定义和(1)、(2)两公式计算可知:夏玉米田马唐防除的生态经济杀除阈期的始期应从夏玉米苗后生育期总天数的11.8％开始,结束于夏玉米苗后生育期总天数的53.9％。例如华北地区夏玉米全生育期总天数一般是95天,夏玉米苗后生育期总天数(T)约为88天,故夏玉米田马唐防除的生态经济杀除阈期约在夏玉米苗后10.6—47.5天之间。     

非自然越夏区小麦白粉病模拟鉴定病圃

作者于1990～1995年根据陕西省关中麦区小麦白粉病侵染循环特点,人工模拟自然发病条件,在非自然越夏区杨陵(省农科院试验地)成功地建立起白粉病菌可周年存活,且秋、春季均能充分诱发感染的混合菌系病圃,宜对小麦种质材料进行全生育期抗白粉病鉴定。利用该病圃已对陕西省1000余份小麦品种(系)及部分国内外抗源亲本材料做了抗病性鉴定和利用评价。     

蜗牛液对不同果蔬病原菌的抑制及其细胞的溶解

蜗牛(Bradybaena kiangsinensis Martens)是我国的特有种群,它的腺体中含有多种生物活性物质。由于蜗牛在农业生产中具有一定的危害性,而忽视了其在生防中的作用。为探索蜗牛用于生防的可能性,作者对蜗牛提取液的抑菌和溶菌效果进行了研究。 1 材料与方法蜗牛液采用活体提取法,以无菌水作提取介质,用量为蜗牛量的30％,常温下浸提1h,然后过滤备用,以无菌水作提取液对照。抑菌试验采用含毒介质法,即取9ml PDA培     

百合组培中鳞片处理及其颜色变化与鳞茎形成的关系

 研究了百合鳞片发育程度、切割段数、形态及生理变化、培养基的P 和K含量与鳞茎形成的关系。结果表明: 取中层鳞片、每片横切6 段的繁殖系数最高, 基部鳞片结鳞茎数最多, 且鳞茎发生最早。鳞片由基部向顶部繁殖系数递减。培养过程中鳞片颜色和形态变化依次为乳白色、浅黄、浅紫色、绿紫、鳞片干枯、鳞茎增大, 鳞片由浅黄变为绿紫色过程中叶绿素含量增加, 淀粉和可溶性糖含量下降。适当增加培养基中P、K的含量可提高鳞茎形成的数量和质量。     

玉米螟赤眼蜂对亚洲玉米螟种群的控制作用

为了解决深圳特区甜玉米产区日趋严重的农药污染问题,笔者在深圳龙岗生态示范农场甜玉米地研究了玉米螟赤眼蜂Trichogramma ostriniae的应用技术,分析了玉米螟赤眼蜂释放量、释放次数对亚洲玉米螟Ostrinia furnacalis Guen6e控制作用的关系,提出了最件释放方法.     

钙及其拮抗剂对苹果果肉质膜透性的调节作用

采用培养果肉圆片的方法,研究了Ca2+及其拮抗剂对苹果果肉质膜透性的调节作用。结果表明,CaCl2(1、10mmol/L)降低果肉膜透性和溶质外渗速率(Js);细胞膜Ca2+通道阻塞剂Verapamil(100μmol/L)的影响不显著;细胞外Ca2+螯合剂EGTA(5mmol/L)、CaM的拮抗剂CPZ、TFP(100μmol/L)明显提高果肉膜透性和细胞溶质外渗速率。培养24h时,CaCl2能明显维持较高的SOD活性和ACC向乙烯的转化能力,EGTA、Verapamail、CPZ和TFP的作用相反。这些说明Ca2+对果肉细胞膜具有保护作用,而减少细胞外Ca2+和抑制细胞内Ca2+-CaM功能对果肉细胞膜具有伤害作用。     

早熟油桃‘玫瑰红’选育

玫瑰红油桃是1992年以京玉为母本,五月火为父本进行杂交培育的早熟油桃品种。该品种在郑州6月下旬成熟,果实发育期85d左右;果面75%～100%着玫瑰红色,不裂果;平均单果重150g,最大250g;果肉乳白色,肉质硬溶,果实风味甜,可溶性固形物11%,半离核;需冷量700h,早期丰产性强,极丰产。     

Expression of cyclooxygenase-2 in IL-1β-stimulated mesangial cells is medicated by NF-κB/IκB signal pathway

AIM: To investigate the role of NF-κB/IκB signal pathway in the regulation of cyclooxygenase-2 (COX-2) expression in human mesangial cells (HMC). METHODS: The PGE₂ concentration in supernatants of HMC was measured by radioimmunoassay. COX-2 mRNA and protein expression were determined by RT-PCR and Western blot. Electrophoretic mobility shift assay (EMSA) and Western blot were used to detect the activity of NF-κB and degradation of IκB. RESULTS: IL-1β significantly upregulated COX-2 expression and PGE₂ production in HMC. Significant up-regulation of NF-κB activation, nuclear translocation of p65 subunit, and degradation of IκB α and IκB β were observed in IL-1β-induced HMC. CONCLUSION: Expression of COX-2 in IL-1β-induced HMC is mediated by NF-κB/IκB signal pathway.     

Inhibition of K562 cell growth by antisense drug targeting with VEGF mRNA in vitro

AIM: To investigate inhibition of K562 cell growth by antisense drug targeted VEGF mRNA. METHODS: X7, 20-mer antisense sequences were selected, synthesized and modified with phosphorothioate. The drug was transfected into K562 cells in the present of lipofection. Cell growth was assayed by trypan blue dye exclusion assay and MTT. The level of VEGF protein in the media was determined by ELISA. The morphology of apoptotic cells were observed by Giemsa staining, and the propotion of apoptotic cells was detected by flow cytometry. RESULTS: The antisense drug inhibited growth of K562 and downregulated expression of VEGF protein significantly, compared with Scrambed control group and showed dose-dependent relation. Signs of apoptosis of K562 cells were not observed. CONCLUSION: Inhibition of K562 cell proliferation, but not cells apoptosis induction is the mechanism of inhibing growth of K562 cells by antisense drug targeted VEGF mRNA. At same time, VEGF has function of promoting K562 cell proliferation, and VEGF mRNA may be a new target attached by drugs.