牛病毒性腹泻病毒RNA的cDNA合成及其分子杂交的研究

BVDV(牛病毒性腹泻病毒)是一类有重要经济价值的病毒,其核酸为单链RNA。该病毒提纯以后.用苯酚-氯仿-异戊醇提取RNA.在提取的BVDy RNA中所含的DNA杂质用DNase I降解除去,然后进一步用oligo dT纤维素拄亲和层析,琼脂糖凝胶电泳等方法纯化。纯化的BVDV RNA在E.coli,poly A聚合酶的催化作用下,在3’羟基末端聚腺化。cDNA在逆向转录酶的作用下,用polyA接尾的BVDV RNA作模板,oligodT_12—18作引物合成。琼脂糖凝胶电泳结果说明它与BVDV RNA相似。该cDNA的探针用斑点杂交方法与BVDV RNA,HCV RNA和酵母tRNA杂交,BVDV RNA和HCVRNA显阳性反应,酵母tRNA显阴性反应,结果说明合成的cDNA为BVDV RNA的cDNA。BVDV和HCV同为披盖科疫病毒属成员,它们具有部分相同的抗原,因此编码病毒蛋白的RNA序列具有同源序列,本研究证实了这种假设。     

吉林省杨树蛀干害虫的三种姬小蜂天敌(膜翅目:小蜂总科, 姬小蜂科)

1986年,原吉林省林业生防中心站(现为吉林省林业科学研究所)同中国科学院动物研究所合作,对吉林省杨树蛀千害虫的寄生蜂资源进行了开发利用研究。本文是该项研究成果的第一篇报道,记述了三种姬小蜂天敌,包括寄生白杨透翅蛾的透翅蛾黑姬小蜂Elachertus nigritulus(Zett.)和寄生杨窄吉丁的一新种丽凹面姬小蜂 Eniedon epicharisHuang及一新记录种 Eniedon zanara Walker。其它研究成果将陆续报道。     

国槐尺蠖性信息素的生物学研究

国槐尺蠖(semiothisa cinerearia Bremer et Grey)的性信息素腺体位置通过触角电位、扫描电镜和组织学三种研究技术进行了检查。触角电位证明性信息素腺体位于产卵器。扫描电镜确定在雌蛾腹部第Ⅷ和Ⅸ—Ⅹ节之间的节间膜背面有一囊状结构。触角电位进一步证明这一囊状结构为性信息素腺体。腺体横切显示性信息素腺体细胞特征为核大,细胞体呈柱状,细胞质内有小空泡。触角电位证明雌蛾在暗周期(20:00,21:00和22:00)产生的性信息素比在光周期(8:00、9:00和10:00)多。风洞试验显示雄蛾在暗周期(21:00)比在光周期(9:00)对性信息素提取物的行为反应强烈。田间试验证明性信息素腺体提取物具有诱蛾活性。上述结果为国槐尺蠖性信息素的化学分离和鉴定提供了基础。     

中国灵芝科真菌资源与分布

中国灵芝科资源十分丰富。许多种类具有重要的经济价值。现在已知灵芝种类有88种。本文概述了灵芝对国民经济的重要性,中国古籍中有关灵芝的记载,灵芝的化学成分与制剂,灵芝的临床应用,灵芝的人工培养,灵芝的生态习性与分布。     

5,6-二氯-吲哚乙酸对烟草愈伤组织衰老的延缓作用

5,6-二氯-吲哚乙酸对革新烟草愈伤组织生长有影响。当愈伤组织在MS_0(对照)和MS 2,4-D培养基上培养22d时,生长停滞,细胞已呈空泡状,正常的超微结构完全破坏,细胞器不复存在,愈伤组织明显褐化。但在MS 5,6-Gl_2-IAA培养基上的愈伤组织仍能正常生长,鲜重和干重下降亦明显延缓,细胞含有原生质内含物,各种细胞器的超微结构仍保持正常。此外,后者的SOD同工酶也明显不同于其它培养基上的愈伤组织,暗示5,6-Gl_2-IAA对烟草愈伤组织衰老的延缓作用可能与SOD同工酶的调节作用有关。     

Chronic Exposure to Diquat Causes Reproductive Toxicity in Female Mice

Diquat is a bipyridyl herbicide that has been widely used as a model chemical for in vivo studies of oxidative stress due to its generation of superoxide anions, and cytotoxic effects. There is little information regarding the toxic effects of diquat on the female reproductive system, particularly ovarian function. Thus, we investigated the reproductive toxic effects of diquat on female mice. Chronic exposure to diquat reduced ovary weights, induced ovarian oxidative stress, resulted in granulosa cell apoptosis, and disrupted oocyte developmental competence, as shown by reactive oxygen species (ROS) accumulation, decreased polar body extrusion rates and increased apoptosis-related genes expression. Additionally, after diquat treatment, the numbers of fetal mice and litter sizes were significantly reduced compared to those of control mice. Thus, our results indicated that chronic exposure to diquat induced reproductive toxicity in female mice by promoting the ROS production of gruanousa cells and ooctyes, impairing follicle development, inducing apoptosis, and reducing oocyte quality. In conclusion, our findings indicate that diquat can be used as a potent and efficient chemical for in vivo studies of female reproductive toxicity induced by oxidative stress. Moreover, the findings from this study will further enlarge imitative research investigating the effect of ovarian damage induced by oxidative stress on reproductive performance and possible mechanisms of action in large domestic animals.     

LINC01128 regulates the development of osteosarcoma by sponging miR‐299‐3p to mediate MMP2 expression and activating Wnt/β‐catenin signalling pathway

Osteosarcoma (OS) is one of the most common metastatic bone cancers, which results in significant morbidity and mortality. The important role of long non‐coding RNAs (lncRNAs) in the biological processes of OS has been demonstrated through several studies. In the current study, we evaluated the role of the lncRNA, LINC01128, in OS. We analysed the expression of LINC01128 in three OS gene expression omnibus (GEO) data sets {"type":"entrez-geo","attrs":{"text":"GSE21257","term_id":"21257"}}GSE21257, {"type":"entrez-geo","attrs":{"text":"GSE36001","term_id":"36001"}}GSE36001 and {"type":"entrez-geo","attrs":{"text":"GSE42352","term_id":"42352"}}GSE42352. The expression of LINC01128 in OS tissues and matched non‐tumour tissues obtained from 50 OS patients was detected using qRT‐PCR. The association between LINC01128 expression and overall survival of OS patients was evaluated using the Kaplan‐Meier method. The effects of LINC01128 knockdown and overexpression were evaluated through in vitro and in vivo assays. The LINC01128/miR‐299‐3p/ MMP2 axis was verified using dual‐luciferase reporter assay and qRT‐PCR assays. GEO data sets analysis revealed that the expression of LINC01128 was increased in OS. Elevated LINC01128 expression was accompanied by shorter overall survival in OS patients. Functional studies revealed that LINC01128 knockdown reduced the proliferation, migration and invasion of OS cells both in vitro and in vivo. Mechanistically, LINC01128 sponged miR‐299‐3p to increase MMP2 expression. Rescue assays determined the role of the LINC01128/miR‐299‐3p/MMP2 axis in the proliferation, migration and invasion of OS cells. Additionally, the Wnt/β‐catenin signalling pathway was activated by LINC01128 and MMP2 in OS cell lines. In summary, this study demonstrates that LINC01128 facilitates OS by functioning as a sponge of miR‐299‐3p, thus promoting MMP2 expression and activating the Wnt/β‐catenin signalling pathway.