PrP106—126诱导小胶质细胞BV-2抗氧化性能的变化

小胶质细胞活化是朊病的病理学特征之一。朊蛋白多肽PrP106—126具神经毒性,是研究异常腕蛋白（PrPSc）的理想工具。为探讨PrP106—126对小胶质细胞氧化压力的影响。本研究以小胶质细胞BV-2为细胞模型,PrP106—126作用48h,应用MTT和流式细胞仪检测细胞的活化情况,应用分子探针技术对细胞的氧化压力（reactiveoxygenspecies,ROs）进行检测,并通过荧光定量RT—PCR对与R0s相关的酶的mRNA表达进行了测定。结果表明PrPl06—126显著促进小胶质细胞BV-2的活化,并提高胞内的ROS水平;定量RT—PCR显示,PrP106—126显著降低细胞S0D-1（P〈0．01）表达水平、提高胞内Cat（P〈0．01）的表达水平;对Grx、Trx-1、和Trx-2mRNA的表达水平有升高的趋势,但未达到显著水平（P〉0．05）,对SOd-2、GPx、GR无显著性影响（P〉0．05）。从分子水平初步阐明小胶质细胞ROS升高的机理。     

籼稻恢复系桂R106对稻瘟病的抗性评价及遗传分析

通过与‘丽江新团黑谷’及13个已知抗性基因品种杂交和接种广西稻瘟病菌系鉴定,研究了籼稻恢复系‘桂R106’对稻瘟病的抗性及遗传。结果表明,‘桂R106’对广西565个稻瘟病菌系的抗谱达98.11%,对广西6个主要优势菌系表现全抗,对菌系03E-11和03E-23的抗性均受一对显性基因控制。等位性分析确认,‘桂R106’中抗菌系03E-11的抗病基因与Pi-ta、Pi-12(t)、Pi-3、Pi-5、Pi-7、Pi-a、Pi-at、Pi-sh、Pi-i、Pi-km、Pi-19(t)、Pi-ks、Pi-b这13个已知基因不等位,认为它可能是一个未知的新基因。     

实时荧光定量PCR构建朊病相关细胞因子标准品质粒和标准曲线

为能够用实时荧光定量PCR检测PrP106-126作用的鼠巨噬细胞细胞因子的表达水平,构建目的基因IL-1β、TNF-α、IL-6和内参基因β-actin的标准品质粒和标准曲线。根据GenBank中鼠基因编码区保守序列,设计特异性引物;细胞经PrP106-126作用后,提取总RNA。经反转录、PCR扩增、纯化、连接和转化后,提取质粒并测序鉴定,获得IL-1β、TNFα-、IL-6和β-actin质粒;将质粒梯度稀释,进行荧光定量PCR,获得标准曲线及回归方程。结果显示,产物溶解曲线峰值单一,引物特异性高;标准曲线相关系数r2=0.999,表明线性关系好,成功构建了目的基因和内参基因的标准品质粒和标准曲线。     

高产优质多抗玉米新品种"吉玉106"选育报告

"吉玉106"是吉林农业大学于2001年组配而成的玉米杂交种。在吉林省2004—2005年区域试验中平均产量10 255.2 kg/hm2,比对照品种"登海9"增产8.1%。2005年生产试验中平均产量8 498.8 kg/hm2,比对照品种"登海9"增产12.0%。该品种具有产量高、品质好、抗性强等特点。2006年通过吉林省农作物品种审定委员会审定,正式定名为"吉玉106"。该品种适宜吉林省晚熟、中晚熟区域种植。四平西部、长春北部、松原地区、吉林地区、白城部分地区和内蒙古等地亦可种植。     

miR-106b-5p靶向KLF4调控山羊肌内前体脂肪细胞分化

旨在明确miR-106b-5p对山羊肌内前体脂肪细胞分化的影响，并确定这种作用是通过靶向KLF4来实现的。本研究利用实时荧光定量PCR （quantitative real-time PCR，qRT-PCR）技术检测miR-106b-5p在山羊肌内前体脂肪细胞分化过程中的表达模式，通过脂质体转染技术将miR-106b-5p mimic和miR-106b-5p inhibitor转入体外培养的山羊肌内前体脂肪细胞，油红O染色法从形态学验证miR-106b-5p对脂肪细胞中脂滴积聚的影响，qRT-PCR检测预测的靶标基因KLF4和脂肪分化标志基因的表达情况，利用双荧光素酶报告系统鉴定miR-106b-5p与KLF4的靶标关系。qRT-PCR结果显示，miR-106b-5p在山羊肌内前体脂肪细胞诱导分化第3天时表达量最高。在山羊肌内脂肪细胞中干扰miR-106b-5p后油红O染色显示脂滴聚积减少，过表达miR-106b-5p后脂滴聚积增加。在山羊肌内前体脂肪细胞中转染miR-106b-5p inhibitor后PPARγ表达量显著降低（P<0.05），而KLF4表达量极显著升高（P<0.01）；转染miR-106b-5p mimic后LPL和PPARγ表达量极显著升高（P<0.01）。荧光素酶活性试验结果显示，过表达miR-106b-5p可显著抑制KLF4荧光活性。miR-106b-5p通过靶向并负调节KLF4的表达促进山羊肌内脂肪细胞分化。     

Spatial-temporal Patterns of Land-use Change in Typical Transect Area Along China National Highway 106 During 1996-2008

Based on land-use database updated with the survey of 1996, 2000, 2004 and 2008, this paper analyzed the land-use changes in the typical transect area along National Highway 106 with the aid of GIS technology and quantitative models. The results showed that arable land had been continuously decreased from 1996 to 2008, with a loss of 65.85× 10^3 hm2 and an average decrement of 5.49×10^3 hm^2 per year, and the loss in northern areas was larger; garden land and woodland were gradually centralized to the predominance area with an increment of 25.73×10^3 hm2 and 22.37×10^3 hm2, respectively; residential and industrial land increased year after year, and the transportation land showed the equalized developing spatial pattern; the increment of construction land and encroachment on arable land in the area were deeply influenced by the national macroscopic land-use policies, the rapid advance of urbanization and the development level of the regional economy. Through this case study, it is suggested that differential land- use policies should be adopted to create good environmental conditions to guarantee food security and to promote the economic development.     

灌浆期干旱胁迫对小麦西农106部分生理指标、产量及品质的影响

为了解小麦品种‘西农106’灌浆期的抗旱性,以小麦品种‘周麦18’为对照,通过盆栽称重控水模拟干旱环境,比较分析正常供水、中度干旱胁迫和重度干旱胁迫处理下小麦的旗叶面积、SPAD值、荧光、抗氧化酶活性等抗旱生理指标及产量和品质的差异。结果表明,与正常供水处理相比,在重度干旱处理下两个品种的旗叶面积、SPAD值、荧光参数（F_v/F_m、Φ_PSⅡ和qP）均显著降低,其中‘西农106’的Φ_PSⅡ和qP降低幅度更小;在重度干旱处理下,两个品种旗叶MDA含量、抗氧化酶活性、可溶性糖含量和可溶性蛋白含量均显著升高。重度干旱胁迫后,‘周麦18’和‘西农106’的千粒质量和产量均显著下降,其中千粒质量降幅分别为 41.96%和35.33%,产量降幅分别为40.43%和42.53%。重度干旱胁迫显著降低小麦籽粒淀粉含量和吸水率,显著提高籽粒蛋白含量、湿面筋含量、体积质量、稳定时间和沉降值。中度干旱胁迫对两个品种生理、产量和品质的影响较小,以上指标变化基本上表现不显著。综合来看,在荧光特性和产量性状方面‘西农106’品种表现出较好的抗旱性。     

双季晚稻新组合新两优106黄山市示范表现及其高产栽培技术

在阐述高产优质抗倒杂交稻新组合新两优106在安徽黄山大面积示范表现的基础上,从播种育秧、栽植、肥水管理及病虫害防治等方面总结了新两优106实现高产、稳产、抗倒的栽培关键技术,为其大面积推广提供了技术参考。     

Combined targeting blockage of miR-29b/92b/106b inhibits gastric can-cer cell growth and migration

AIM: To investigate the metastasis-associated microRNAs (miRNAs, miR) in gastric cancer, and to determine their biological and therapeutic roles in this malignancy. METHODS: The tumor tissue samples from gastric cancer patients with or without lymph node metastasis were collected (n=3 each). miRNA microarray was used to determine the metastasis-associated miRNAs. Gastic cancer cell line BGC-823 was transfected with locked nucleic acidmodified antisense oligonucleotides of candidate miRNAs and subsequently used for functional assays including CCK-8 assay, flow cytometry, wound healing assay and Transwell migration assay. Furthermore, the in vivo xenograft mice were used to evaluate the tumor suppressive effect of collaborative inhibition of the candidate miRNAs. RESULTS: miR-29b, miR-92b and miR-106b were up-regulated in the tumor tissues from the gastric cancer patients with lymph node metastasis. The functional assays showed that blockage of miR-29b, miR-92b and miR-106b by antisense oligonucleotides in the BGC-823 cells significantly inhibited cell growth and migration, and induced apoptosis. Furthermore, the collaborative inhibition of these triple miRNAs remarkably suppressed tumor growth in vivo. CONCLUSION: miR-29b, miR-92b and miR-106b are metastasis-associated miRNAs. These miRNAs may provide promising therapeutic targets in gastric cancer.     

Effect of oncogenic microRNA-106a on growth of normal gastric mucous epithelial cells and gastric cancer cells

AIM: To investigate the oncogenic effect of microRNA-106a (miR-106a) on normal gastric mucous epithelial cells and gastric cancer cells.METHODS: The miR-106a mimic was transfected into normal gastric mucous epithelial cell line GES-1 using liposome. The change of cell growth was measured by MTT assay. The miR-106a inhibitor was transfected into gastric cancer cell lines MGC-803 and SGC-7901 using liposome, and the changes of cell cycle distribution and cell cycle-related protein expression were measured by flow cytometry and Western blotting,respectively. The growth of gastric cancer was also observed using nude mouse xenograft model. RESULTS: The miR-106a mimic increased the growth of GES-1 cells in a dose-dependent manner. By decreasing the expression of cyclin-dependent kinase (CDK) 1 and CDK2, the miR-106a inhibitor arrested MGC-803 cells at G₀/G₁ and G₂/M phases. The miR-106a inhibitor also arrested SGC-7901 cells at G₂/M phase by decreasing the expression of CDK1. The results of animal experiments showed that the miR-106a inhibitor significantly suppressed the tumor growth in a dose-dependent manner.CONCLUSION: miR-106a may play an important role in the development of gastric cancer.