黑杨无性系日CO2固定总量的测定及与苗木生产潜势的相关性研究

通过对不同基因型黑杨无性系植株净光合速率日变化曲线与光合主体叶面积在时间和光强上进行累计积分来计算植株日CO2固定总量P。由于净光合速率日变化曲线不易准确测得，故以光响应曲线和光强的日变化来推测净光合速率日变化。对P值和生物量的相关性研究表明，二者的相关性很高。且认为可以用计算出的P值作为评估苗木生产潜势的指标之一，这为育种中生产力的早期选择提供了有力的证据。     

60Co辐射诱变姬松茸突变株J3子实体不同部位的氨基酸分析研究

测定并比较了60Co辐射诱变姬松茸突变株J3与原菌株J1子实体不同部位的氨基酸含量.结果表明,除菌柄和盖皮外,姬松茸突变株J3子实体其它部位的必需氨基酸、儿童氨基酸、硫氨酸、支链氨基酸、鲜味氨基酸、芳香族氨基酸和甜味氨基酸均高于原菌株J1.姬松茸突变株J3子实体中谷氨酸含量占氨基酸总量的比例分别比原菌株J1、α-酪蛋白和卵清蛋白提高34.88%、56.68%和122.32%.     

Bcl-2 antisense oligodeoxynucleotide increases the sensitivity of HL60 and K562 cells to daunorubicin

AIM:To investigate whether the bcl-2 antisense oligonucleotide increases the sensitivity of HL60 and K562 cell lines to daunorubicin.METHODS:IC50 for HL60 and K562 was determined with MTT method, the expression levels of Bcl-2 protein were assayed by immunofluorescence using fluoresce isothiocyanate labeling. In addition, apoptosis was detected by morphological observation and flow cytometric analysis of DNA fragmentation.RESULTS:It was found that the two oligonucleotides directed against the coding region and the translation initiation of bcl-2 mRNA, combined respectively with daunorubicin, inhibited expression of bcl-2 protein, increased apoptosis in HL60 and K562 cells, and decreased IC50 of daunorubicin significantly (P＜0.05). Compared to the antisense oligonucleotide directed against the translation initiation of bcl-2 mRNA, the antisense oligonucleotide directed against the coding region showed stronger effects in the aspects of increasing the sensitivity of HL60 cells to daunorubicin (P＜0.05).CONCLUSIONS:These two antisense sequences in the translation initiation and the coding region of bcl-2 mRNA increased the sensitivity of HL60 and K562 cell lines to daunorubicin in a sequence-specific manner.     

苹果柱型基因Co的一个AFLP 标记的SCAR转换

 将苹果柱型基因的一个AFLP 标记成功地转换成了简单实用的SCAR 标记。首先对AFLP 标记片段进行序列测定, 然后根据序列特点设计了两对特异引物CoA1/ CoA2 和CoA1/ CoA3 , 每条引物长20 bp。PCR 结果表明CoA1/ CoA2 可以扩增出216 bp 和148 bp 两条带, 其中216 bp 的为柱型性状的特征带; CoA1/CoA3 可以扩增出273 bp 和205 bp 的两条带, 其中273 bp 的为柱型性状的特征带。两对引物在杂交后代中扩增出的特征带与柱型性状的分离重组率都很低(CoA1/ CoA2 为6. 3 % ±2. 5 %; CoA1/ CoA3 为7. 3 % ±2. 6 %) , 所以它们都可以作为该SCAR 标记的特异引物所用。     

The mechanism of apoptosis induced by homoharringtonine in HL-60 cells

AIM: To study the signal transduction pathway of apoptosis initiation induced by homoharringtonine in HL-60 cells. METHODS: After establishing the model of apoptosis initiation induced by homoharringtonine in HL-60 cells, at the point of apoptosis initiation, molecular caspase-3, Bcl-2, Bax and Fas/FasL were measured with flow cytometry and transmission electron microscope. ERK2 and P38 expression in HL-60 cells were detected by using immunohistochemistry. RESULTS: The model of apoptosis initiation induced by homoharringtonine was established in HL-60 cells. At the point of apoptosis initiation, upregulation of caspase-3 and decrease in Bcl-2/Bax were observed. However, the expression of Fas/FasL did not significantly change. ERK2 expression decreased and P38 expression increased. CONCLUSIONS: Caspase-3, Bcl-2, Bax and mitogen activated protein kinase pathways were involved in signal transduction of apoptosis initiation induced by homoharringtonine in HL-60 cells.     

黄原胶-N-乙烯基吡咯烷酮辐射接枝共聚物的制备及结构特性研究

为提高黄原胶分子的应用性能,以60Co-γ为辐射源,对黄原胶和N-乙烯基吡咯烷酮进行共辐射接枝处理,制备黄原胶-N-乙烯基吡咯烷酮共聚物(XG-g-NVP),并研究反应条件对接枝率和单体利用率的影响及共聚物的结构表征。结果表明,当辐射吸收剂量为10k Gy,黄原胶浓度12g·L-1,NVP/XG质量比8∶1,4-甲氧基酚阻聚剂添加量为NVP单体质量的0.01%时,最佳接枝率为543.3%,单体利用率为67.9%。红外光谱表明接枝反应发生在NVP乙烯基部位,扫描电镜图显示共聚物形貌由片层状逐步过渡到颗粒状;XG-g-NVP的抗高温及抗剪切能力相比黄原胶有所提高,且黏度值在高温、高剪切力时仍保持恒定值,因此,改性后的黄原胶结构及热稳定性提高。通过对黄原胶分子接枝改性,使其具备了更多优良的性能,为改性黄原胶的进一步应用奠定了理论基础。     

椿树辐射诱变育种初报

以椿树种子为材料,用60Co γ射线进行了0、30、50、75、100、150和200Gy辐照处理,研究辐照对椿树种子发芽及幼苗生长的影响,以期获得耐盐突变体。结果表明：辐照抑制了种子的萌发,成苗率下降,幼苗生长受到抑制,且随着剂量的增加,抑制作用增强;椿树种子的半致死剂量为50Gy,适宜辐照剂量是50~75Gy。辐照后的植株经0.5% 的海盐筛选,共获得9株耐盐能力提高的变异株。     

苏云金芽胞杆菌Bt9875杀虫晶体蛋白可诱导Caspase和Bcl-2家族参与调控HL-60细胞凋亡

研究Caspase家族与Bcl-2家族参与调控苏云金芽胞杆菌(Bacillus thuringiensis,Bt)Bt9875杀虫晶体蛋白对人急性髓细胞性白血病细胞HL-60的影响.本实验采用MTT法检测了杀虫晶体蛋白诱导HL-60细胞凋亡后的Caspase家族的活性和Caspase凋亡酶抑制剂对杀虫晶体蛋白诱导HL-60细胞凋亡的影响;采用Western blot检测了杀虫晶体蛋白诱导多聚ADP-核糖聚合酶(PARP)降解、Bcl-2/Bax调控和细胞色素C的释放.研究结果表明,杀虫晶体蛋白作用HL-60细胞后,激活了Caspase-3、Caspase-8和Caspase-9,在48 h内Caspase家族抑制剂(Z-VAD-FMK)、Caspase-3抑制剂(z-DEVD-FMK)和Caspase-9抑制剂(Z-LEHD-FMK)均可显著抑制杀虫晶体蛋白诱导的细胞凋亡;杀虫晶体蛋白可明显上调促凋亡蛋白Bax的表达,同时下调抗凋亡蛋白BCl-2的表达,并观察到胞浆中细胞色素C的释放.初步证明了Bt9875杀虫晶体蛋白诱导的HL-60细胞凋亡是由Caspase家族和Bcl-2家族共同调控的,线粒体途径在诱导细胞凋亡过程中起着重要作用.