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1.
NEW MURID RODENTS FROM THE LATE CENOZOIC OF YUSHE BASIN, SHANXI 总被引:8,自引:8,他引:0
Lawrence J.Flynn 《古脊椎动物学报》1992,(1)
<正> As scientific collaborators of the Chinese-American joint project "Neogene Rocks and Faunas, Yushe Basin, Shanxi, PRC", the present authors, with William R. Downs, Northern Arizona University, sampled the Yushe microfauna in the fall of 1987 and 1988. The fossil temains were retrieved by surface collection and by wet-sieving bulk quantities of sediment. 相似文献
2.
枝跗瘿蜂科(Ibahidae)是个小科,所有种类均寄生蛀干害虫树蜂科(Siricidae)的幼虫。我国大陆的本科种类由杨忠岐1991年首次作了报道。现记述采自祁连山林区的另1新种。该种寄生于为害青海云杉(Picea crassifolia Kom.)的黄肩长尾树蜂(Xeris spec-trum spectrum)等树蜂的幼虫。新种的模式标本保存于西北林学院天敌昆虫研究室。至此,我国大陆共有本科种类3种,加上台湾的1个种,我国共有4种: 相似文献
3.
本文记述了我国南方姬小峰科红眼姬小蜂属Mangocharis一新种,荔枝瘿蚊红眼姬小蜂M.litchiiYang et Luo.该种单个内寄生于严重危害荔枝叶片的荔枝叶瘿蚊Mayetiola sp.幼虫或跨期寄生于该害虫的卵—幼虫期,在自然控制这种害虫上具有重要作用.红眼姬小蜂属在我国首次发现. 相似文献
4.
为了解湖南高望界国家级自然保护区蝶类多样性本底及其影响因素, 2016年5月至2018年10月, 我们采用样线法对保护区内外的6种生境(保护区内4种, 区外2种)开展了20次蝶类多样性调查。共记录蝴蝶个体13,956只, 依照五科分类系统, 隶属5科113属239种, 其中湖南省蝶类新记录17种。区系成分以东洋种为主(139种, 占58.1%), 广布种次之(97种, 占40.6%), 古北种最少(3种, 占1.3%)。对不同生境的蝶类群落多样性指数进行分析后发现, 人为干扰程度和生境异质性共同影响蝶类多样性。不同生境相似性分析结果表明, 蝶类群落的相似度与人为干扰程度和植被类型差异密切相关。3年间, 蝶类多样性指数月度变化基本一致, 蝶类物种数、多样性指数与月均温间呈显著正相关, 与月降水量无相关性。综上, 蝶类多样性受到人为干扰程度和气象因子的影响。为保护蝶类资源, 建议保护好蝶类栖息地, 减少人为干扰。 相似文献
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6.
Xiangjing Fu Xiaolong Gao Shengfang He Di Huang Peng Zhang Xinglong Wang Shuxia Zhang Ruyi Dang Shuanghui Yin Enqi Du Zengqi Yang 《PloS one》2013,8(3)
Nanobodies (or variable domain of the heavy chain of the heavy-chain antibodies, VHHs) are single-domain antigen-binding fragments derived from camelid heavy chain antibodies. Their comparatively small size, monomeric behavior, high stability, high solubility, and ability to bind epitopes inaccessible to conventional antibodies make them especially suitable for many therapeutic and biotechnological applications. In this paper, for the first time, we created the immunized Camelus Bactrianus VHH yeast two-hybrid (Y2H) library according to the Clontech Mate & Plate library construction system. The transformation efficiency and titer of the VHH Y2H library were 7.26×106 cfu/3 µg and 2×109 cfu/ml, which met the demand for Y2H library screening. Using as an example the porcine circovirus type 2 (PCV2) Cap protein as bait, we screened 21 positive Cap-specific VHH sequences. Among these sequences, 7 of 9 randomly selected clones were strongly positive as indicated by enzyme-linked immunosorbent assay, either using PCV2 viral lysis or purified Cap protein as coated antigen. Additionally, the immunocytochemistry results further indicated that the screened VHHs could specifically detected PCV2 in the infected cells. All this suggests the feasibility of in vivo VHH throughput screening based on Y2H strategy. 相似文献
7.
目的 比较氯胺酮、舒泰、速眠新Ⅱ、戊巴比妥钠等4种全身麻醉药或其组合对非人灵长类的麻醉效果,探寻能替代或者减少氯胺酮使用的个性化麻醉方案。方法 以单独使用氯胺酮麻醉的方案作为对照,另设单独使用舒泰、氯胺酮复合速眠新Ⅱ、舒泰复合速眠新Ⅱ和戊巴比妥钠复合速眠新Ⅱ等麻醉4个实验组,每组选取5只食蟹猴进行实验,记录麻醉后的心率、体温、血氧饱和度、以及麻醉诱导时间和维持时间,以比较各方案的麻醉效果。结果 与单独使用氯胺酮麻醉比较,其他四种麻醉方案在心率、体温、血氧饱和度和麻醉诱导时间上均无显著性差异,不同方案麻醉维持时间分布在30~200min之间。在非人灵长类的全身麻醉中,舒泰可以很好地替代氯胺酮;氯胺酮复合速眠新Ⅱ麻醉可取得较长的麻醉维持时间,并减少氯胺酮的使用量;舒泰与速眠新Ⅱ联用、戊巴比妥钠与速眠新Ⅱ联用的方案也可替代氯胺酮,且麻醉维持时间较长。结论 在一定的麻醉时间内,联合用药可以降低氯胺酮的使用量,不同麻醉方案灵活运用可满足不同实验对麻醉维持时间的需求。 相似文献
8.
Wang X Liu L Liu S Sun X Deng Z Pi Y Sun X Tang K 《Journal of biochemistry and molecular biology》2004,37(5):538-545
A new CRT binding factor (CBF) gene designated Cbcbf25 was cloned from Capsella bursa-pastoris, a wild grass, by the rapid amplification of cDNA ends (RACE). The full-length cDNA of Cbcbf25 was 898 bp with a 669 bp open reading frame (ORF) encoding a putative DRE/CRT (LTRE)-binding protein of 223 amino acids. The predicted CbCBF25 protein contained a potential nuclear localization signal (NLS) in its N-terminal region followed by an AP2 DNA-binding motif and a possible acidic activation domain in the C-terminal region. Bioinformatic analysis revealed that Cbcbf25 has a high level of similarity with other CBF genes like cbf1, cbf2, and cbf3 from Arabidopsis thaliana, and Bncbf5, Bncbf7, Bncbf16, and Bncbf17 from Brassica napus. A cold acclimation assay showed that Cbcbf25 was expressed immediately after cold triggering, but this expression was transient, suggesting that it concerns cold acclimation. Our study implies that Cbcbf25 is an analogue of other CBF genes and may participate in cold-response, by for example, controlling the expression of cold-regulated genes or increasing the freezing tolerance of plants. 相似文献
9.
Expressionofmilkproteingenesisinvolvedinahugenetworkofregulatorycircuitswhicharelinkedtotheintactdevelopingmammarygland,andhomeostasisduringpuberty,pregnancy,lactationandinvolution.Analysisofputativeregulatoryelementsandhybridgeneintissueculturesystems… 相似文献
10.
Wenzhang Wang Fan Zhang Li Li Fangqiang Tang Sandra L. Siedlak Hisashi Fujioka Yingchao Liu Bo Su Yan Pi Xinglong Wang 《The Journal of biological chemistry》2015,290(1):168-182
Mitochondrial dysfunction plays a central role in glutamate-evoked neuronal excitotoxicity, and mitochondrial fission/fusion dynamics are essential for mitochondrial morphology and function. Here, we establish a novel mechanistic linker among glutamate excitotoxicity, mitochondrial dynamics, and mitochondrial dysfunction in spinal cord motor neurons. Ca2+-dependent activation of the cysteine protease calpain in response to glutamate results in the degradation of a key mitochondrial outer membrane fusion regulator, mitofusin 2 (MFN2), and leads to MFN2-mediated mitochondrial fragmentation preceding glutamate-induced neuronal death. MFN2 deficiency impairs mitochondrial function, induces motor neuronal death, and renders motor neurons vulnerable to glutamate excitotoxicity. Conversely, MFN2 overexpression blocks glutamate-induced mitochondrial fragmentation, mitochondrial dysfunction, and/or neuronal death in spinal cord motor neurons both in vitro and in mice. The inhibition of calpain activation also alleviates glutamate-induced excitotoxicity of mitochondria and neurons. Overall, these results suggest that glutamate excitotoxicity causes mitochondrial dysfunction by impairing mitochondrial dynamics via calpain-mediated MFN2 degradation in motor neurons and thus present a molecular mechanism coupling glutamate excitotoxicity and mitochondrial dysfunction. 相似文献