通过花粉管通道导入外源DNA创造抗白粉病小麦新种质

 小麦品种复壮 3 0和小白冬麦的白粉病抗性表现突出 ,是 2个抗性持久、抗谱广泛的优良白粉病抗源。但由于农艺性状欠佳 ,不适于直接作为亲本用于常规育种。为此 ,采用花粉管通道法将复壮 3 0和小白冬麦的基因组DNA导入农艺性状较好的小麦品种北农 6号 ,旨在转移复壮 3 0和小白冬麦的抗白粉病基因 ,创造抗白粉病小麦新种质。本文总结 3年来所得到的研究结果 ,阐述采用花粉管通道法导入外源DNA创造新种质的可行性     

瓯江彩鲤线粒体DNA的限制性内切酶分析

用 13种限制性内切酶对瓯江彩鲤的线粒体DNA(mtDNA)进行RFLP分析 ,结果表明 :(1)共产生 18种限制性态型 ,其中 5种酶产生限制性片段长度多态性 (RFLPs) ,归结为 5种基因单倍型。 (2 )瓯江彩鲤mtDNA大小为 16 .6 0± 0 .15kb ,单倍型间的基因多样性指数和群体核苷酸多样性指数分别为 0 .75 17、0 .0 2 86 ,遗传多样性较丰富     

蔗糖离心法分离土壤线虫的最佳条件筛选

采用单因素试验和二因素组合试验,对蔗糖离心法分离线虫的效果进行研究。分别对在蔗糖液中的离心时间、离心转速和蔗糖的浓度进行了单因素试验,并对效果较好的离心时间和离心转速进行了二因素组合设计试验。试验结果表明:离心时间和离心速度对线虫的分离有影响,但蔗糖浓度对分离结果影响不显著。经蔗糖离心30s后,所获得的线虫数量最多;离心2000r.min-1(离心力447×g)时,效果显著高于其他4个离心转速处理;在离心时间和离心转速的二因素组合试验中,以30s、2000r.min-1的分离效果为最优。     

Carbon-based supercapacitors produced by activation of graphene

Supercapacitors, also called ultracapacitors or electrochemical capacitors, store electrical charge on high-surface-area conducting materials. Their widespread use is limited by their low energy storage density and relatively high effective series resistance. Using chemical activation of exfoliated graphite oxide, we synthesized a porous carbon with a Brunauer-Emmett-Teller surface area of up to 3100 square meters per gram, a high electrical conductivity, and a low oxygen and hydrogen content. This sp(2)-bonded carbon has a continuous three-dimensional network of highly curved, atom-thick walls that form primarily 0.6- to 5-nanometer-width pores. Two-electrode supercapacitor cells constructed with this carbon yielded high values of gravimetric capacitance and energy density with organic and ionic liquid electrolytes. The processes used to make this carbon are readily scalable to industrial levels.     

以太网中的网络监听的检测

网络监听的重要性，以及在广播式以太网和交换式以太网中的网络监听工作的原理和几种常用的防范网络监听的方法。     

烟草品种对TMV病害苗期抗病性鉴定研究

 采用大田病圃人工诱发鉴定和温室人工苗期诱发鉴定的方法,对60个品种进行了TMV病害的抗病性鉴定。结果表明:可以用温室人工苗期诱发鉴定结果代替大田病圃人工诱发鉴定结果,接种的最佳时期为大十字至猫耳期,接种的最佳浓度为2%.     

一种分析边坡稳定性的新型方法

本文对人工神经网络即BP模型做了简要的介绍，并用BP网络的非线性映射能力计算了边坡稳定性的安全系数。结果表明利用BP网络求得的安全系数满足工程要求，并且其方法是合理、简单、可行的，值得推广。     

PI3K/Akt regulates endoplasmic reticulum stress-mediated GRP78 induction

AIM: To investigate the effect of PI3K/Akt pathway on endoplasmic reticulum (ER) stress-mediated glucose-regulated protein 78 (GRP78) induction in human embryonic kidney 293 cells (HEK293) cells.METHODS: PI3K inhibitor LY294002, dominant negative kinase-dead mutant vector for HA-Akt (K179M) and Akt1 siRNAs were used to block the PI3K/Akt pathway under ER stress. Constitutively active expression vectors for Akt (myr-HA-Akt) were used to up-regulate Akt activity under ER stress. The effects of PI3K/Akt on ER stress-mediated GRP78 induction in HEK293 cells were determined by Western blotting and RT-PCR. RESULTS: GRP78 induction was inhibited by LY294002, Akt1 (K179M) and Akt1 siRNA, but was increased by myr-Akt1 in dithiothreitol-and thapsigargin-treated HEK293 cells. However, both myr-Akt2/3 and Akt2/3 siRNA had no effect on GRP78 induction in HEK293 cells under ER stress. Furthermore, the PI3K/Akt pathway didnt regulated GRP78mRNA induction but increased GRP78 protein stability.CONCLUSION: PI3K/Akt promotes GRP78 accumulation through increasing the stability of GRP78 protein in HEK293 cells under ER stress.     

豆芽立枯病诊断与防治试验

模拟工厂化生产豆芽工艺培育黄豆芽,对培育过程中出现的烂芽病样进行病原菌的分离、纯化及鉴定,确定病原菌为立枯丝核菌（Rhizoctonia solani）;并测定了立枯丝核菌不同菌量对绿豆芽的致病性,结果显示：不同接种量引起绿豆芽的发病时间、发病率及生物产量均存在明显差异。接种量为2块菌饼配制5 mL和2块菌饼配制10 mL的菌丝悬浮液造成严重的烂芽,第5天发病率分别达46 %和25 %。不同处理防治豆芽立枯病的试验表明：40 ℃热力消毒、1 %石灰水和1/5 000高锰酸钾均有一定的防治作用,相对防治效果分别为91.30 %、54.35 %和50.00 %。     

Effect of ischemic post-conditioning on myocardial mitochondrial function in isolated rat heart

AIM: To investigate the protective effect of ischemic post-conditioning on isolated rat myocardial mitochondrial function during ischemia/reperfusion, and to study the role of mitochondrial ATP-sensitive potassium channel (mitoK_ATP) in myocardial protection. METHODS: Sprague-Dawley male rats were randomized into 4 groups (n=8 in each group): control group (C), model group (M), ischemic post-conditioning group (IPO) and 5-hydroxydecanoate plus IPO group (5-HD+IPO). The hearts isolated from the SD rats were mounted on a Langendorff apparatus and started with a 20-minute perfusion for equilibration. In C group, the hearts went on perfusion for another 70 min after equilibration. In M group, 4 ℃ St. Thomas cardioplegic solution was administered prior to ischemia, followed by ischemia for 40-minute, and reperfusion for another 30 min. In IPO group, the hearts underwent 40-minute global ischemia after equilibration, then perfusion for 10 s and ischemia for another 10 s. The procedure was repeated 6 times before 28-minute reperfusion. In 5-HD+IPO group, the hearts were perfused with 5-HD (100 μmol/L in K-H solution) and treated as that in IPO group, then reperfusion for 23 min. The reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and respiratory function of myocardial mitochondria were measured at the ends of equilibration and reperfusion. RESULTS: (1) Compared with the data collected at the end of equilibrium, the MMP was obviously decreased at the end of reperfusion in all groups, The highest in C group. MMP in 5-HD+IPO group was markedly higher than that in IPO group and M group. MMP in IPO group was higher than that in M group. (2) In contrast to that at the end of equilibrium, ROS was obviously increased at the end of reperfusion in all groups. However, ROS was observably higher in M group than that in the other 3 groups, and ROS in 5-HD+IPO group was markedly higher than that in IPO group and C group. ROS in IPO group was higher than that in C group. (3) The respiratory function of mitochondria was obviously injured at the end of reperfusion in all groups. The arrangement of the mitochondrial respiratory function from the best to the worse was C group > IPO group > 5-HD+IPO group > M group. CONCLUSION: Ischemic post-conditioning attenuates myocardial reperfusion injury by maintaining the stability of MMP, decreasing the generation of ROS and preserving the respiratory chain function of mitochondria. The mitoK_ATP antagonist 5-HD can not completely block the myocardial protective effect of ischemic post-conditioning. Myocardial protective effect of ischemic post-conditioning may achieve by activating mitoK_ATP, meanwhile the other factors may also take part in the myocardial protective processes.