杉木人工林胸径的Weibull分布及其最优拟合研究

运用遗传算法最优拟合Ｗｅｉｂｕｌ分布,研究杉木人工林胸径分布规律。结果表明,最优拟合的Ｗｅｉｂｕｌ模型拟合杉木人工林胸径分布的接受率达８０％以上,证明遗传算法是非线性模型的一种有效拟合方法。     

利用cDNA-AFLP技术分析白菜核雄性不育两用系的表达差异

 利用cDNA AFLP技术 ,对白菜核雄性不育两用系可育株群和不育株群分析显示 :花蕾之间基因表达存在差异 ;莲座期叶片之间、开花期叶片之间和花茎之间基因表达无差异 ;叶片、花茎和花蕾之间基因表达存在差异。对开花期的小蕾、中蕾和大蕾分析显示 :10对引物中 ,1对在可育株中蕾和大蕾中扩增出 1条特异带 ,另 1对扩增出 1条在可育株中蕾中表达丰度高于不育株中蕾的条带 ,其余 8对未发现差异条带。对上述表达丰度有差异的基因进行Northern验证 ,结果与之一致 ,表明cDNA AFLP技术可以用于植物雄性不育基因表达差异的研究。     

特早熟双低甘蓝型油菜杂交种的选育

采用优质早熟甘蓝型品种与特早熟白菜型油菜品种门源小油菜进行甘白种间杂交的方法,创造出了一批优质特早熟甘蓝型遗传资源,用这些资源作为亲本转育出了3个优质波里马细胞质雄性不育系和1个恢复系,在这些不育系和恢复系配置的杂种中E144表现最突出,它不仅能在海拔2800～3000m的白菜型产区正常成熟,而且芥酸含量小于1%、硫甙含量小于30μmol/g,产量比白菜型油菜主栽品种青油241高30%以上。     

白浆土土体构型改造的研究

 三年盆栽和田间试验表明：⒈淀积层混拌白浆层最适宜比例为1∶1和0.5∶1，增产率为12-52%。⒉改土增产机理在于：混拌以后，打破了紧实、板结的白浆层，土壤机械组成两层性和砂粘比发生了明显变化，白浆层复原性降低，土壤总孔隙和非毛管孔隙增加，土壤水分性质得到改善，混拌土层自身调节水分的能力得到提高，进而增强了土壤抗旱、抗涝性；活土层增厚到60厘米，增加了土壤库容，扩大了作物根系生活领域，根系可免受白浆层影响。     

ICPS-7500光谱仪同时测定橡胶树叶片硼、钼含量

橡胶树叶片样品用干灰化法,稀盐酸溶解灰分,以ICPS-7500光谱仪同时测定样品中硼、钼含量,回收率在96.4%～107.7%,操作简单,精密度高,与其它方法比较差异小,快速、准确,可用于同时测定橡胶树叶片中硼、钼。     

基于B/S架构及物联网模式下的黑玫瑰组培快繁应用技术研究

试验探索外植体采集、不定芽诱导分化增殖、生根培养、试管苗驯化移栽等黑玫瑰组织培养快繁技术,培养出无病毒的优质种质,旨在提高黑玫瑰的产量和品质,同时借助温室大棚物联网智能控制系统,缩短黑玫瑰生产周期,提高经济效益。     

针叶中紫外吸收物质含量的测定

风干处理对常见针叶植物叶中紫外吸收物质含量没有影响,60℃水浴提取1h或浸泡7天的方法都能有效提取出针叶中的紫外吸收物质;针叶中紫外吸收物质的含量可用A300·L·g-1FW来表示。     

小麦芒长抑制基因B2的精细定位与候选基因分析

芒是小麦重要的穗部器官和形态特征,是小麦长期进化和适应环境的结果,对产量和抗旱性等具有重要影响。目前,对麦芒的遗传与发育还缺乏系统的研究,相关基因克隆或精细定位的研究尚未见报道。本试验利用短芒材料‘六柱头’与长芒材料‘石矮1号’构建的F2群体(SL-F2)对芒的遗传与发育进行了研究。细胞学观察表明,短芒主要是由细胞长度变短引起;遗传分析表明,‘六柱头’的短芒由显性单基因控制;借助Wheat660K SNP芯片的BSA分析和SL-F2群体的精细定位,确定‘六柱头’的芒长抑制基因是前人报道的B2位点,并将其定位到6B染色体4.84Mb的物理区间(471.28～476.12 Mb)内,该区段在中国春与矮抗58间具有良好的共线性。在B2定位区间共有61个基因,其中5个在中国春穗部特异表达,TraesCS6B02G264400在中国春和Azhurnaya幼穗表达差异显著。这些研究结果为B2基因的克隆、小麦芒形成机理的解析及育种中的应用奠定了基础。     

FAM3C activates Akt to promote viability of oral squamous-cell carcinoma cells

AIM: To investigate the expression and roles of family with sequence similarity 3, member C (FAM3C) in oral squamous-cell carcinoma cells. METHODS: The mRNA and protein expression levels of FAM3C in dysplastic oral keratinocyte (DOK) and oral squamous-cell carcinoma WSU-HN6 cells were detected by RT-qPCR and Western blot. The WSU-HN6 cells were treated with siFAM3C or FAM3C antibody. After 24, 48 and 72 h, the viability of WSU-HN6 cells was measured by CCK-8 assay, and the activation of protein kinase B (Akt) was detected by Western blot. Adenovirus was used to mediate over-expression of FAM3C in the DOK cells. The DOK cell viability was measured by CCK-8 assay after adenovirus infection for 24, 48 and 72 h, and the activation of Akt was detected by Western blot. RESULTS: Compared with the DOK cells, the mRNA and protein levels of FAM3C were significantly increased in the WSU-HN6 cells (P<0.05). The viability of WSU-HN6 cells transfected with siFAM3C was significantly inhibited at 48 h and 72 h (P<0.05). siFAM3C treatment inhibited the activation of Akt (P<0.05). FAM3C antibody treatment also suppressed the viability of the WSU-HN6 cells at 48 h and 72 h and the activation of Akt (P<0.05). Over-expression of FAM3C in the DOK cells promoted the cell viability at 48 h and 72 h and activated Akt (P<0.05). CONCLUSION: FAM3C might promote oral squamous-cell carcinoma cell growth by activating Akt.     

Role of TLR4-TRPC6 in LPS-induced NF-κB P65 expression and nuclear translocation in airway epithelial 16HBE cells

AIM: To investigate the role of Toll-like receptor 4 (TLR4) and transient receptor potential channel 6 (TRPC6) signaling pathway in lipopolysaccharide (LPS)-induced nuclear factor-κB (NF-κB) P65 expression and nuclear translocation in airway epithelial cells (16HBE) for supplementing the mechanism for airway inflammation. METHODS: After stimulating the 16HBE cells with LPS at 1 mg/L for 0, 0.5, 2, 6, 12 and 24 h, the expression of NF-κB P65 at mRNA and protein levels in the 16HBE cells were determined by RT-PCR and Western blot respectively, and the nuclear translocation of NF-κB P65 was detected by immunocytochemical staining method. The effects of TLR4 inhibitor CLI-095 at 5 μmol/L and TRPC6 agonist Hyp9 at 10 μmol/L on LPS (1 mg/L)-induced NF-κB P65 expression and nuclear translocation in the 16HBE cells were determined by RT-PCR, Western blot and immunocytochemical staining. RESULTS: LPS increased the mRNA and protein expression of NF-κB P65 and nuclear translocation in the 16HBE cells(P<0.05). TLR4 inhibitor CLI-095 reduced the mRNA and protein expression of NF-κB P65 and nuclear translocation induced by LPS, while Hyp9 enhanced the mRNA and protein expression of NF-κB P65 and nuclear translocation induced by LPS in the 16HBE cells(P<0.05). CONCLUSION: LPS induces the expression and nuclear translocation of NF-κB P65 in the 16HBE cells via TLR4-TRPC6 signaling pathway.