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排序方式: 共有325条查询结果,搜索用时 15 毫秒
1.
吸附法治理汞废气的机理研究 总被引:4,自引:0,他引:4
该文对载银活性炭吸附汞蒸气的机理进行了探讨 ,通过电子探针和扫描电镜对载银活性炭及被汞“饱和”的载银活性炭进行微观结构分析 ,结果显示 ,银在活性炭中主要分布于活性炭的凸面处 ,汞只在有银存在的地方出现 ,表明普通活性炭不具备吸附汞的能力 ,载银活性炭吸附汞属于以银为核心的多分子物理吸附 ,工业上的“饱和”载银活性炭仍具有一定的吸附汞蒸气的能力 ,为交替式吸附床的结构设计提供了技术依据 . 相似文献
2.
Rui M Costa Nikolai B Federov Jeff H Kogan Geoffrey G Murphy Joel Stern Masuo Ohno Raju Kucherlapati Tyler Jacks Alcino J Silva 《Nature》2002,415(6871):526-530
Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1. 相似文献
3.
一种基于最小熵准则的SAR图像自聚焦算法 总被引:11,自引:2,他引:11
研究了一种新颖的SAR图像自聚焦算法。该方法从复图像域出发 ,利用最小熵准则盲解卷积原理 ,通过多维搜索完成相位误差校正。同相位梯度自聚焦算法相比 ,最小熵算法无需在图像域分离出强点目标 ,因而特别适用于无任何明显特征的图像。仿真及实测数据处理结果证明了该方法的有效性 相似文献
4.
王宏达 《科技情报开发与经济》2003,13(6):207-209
通过对天津市国有大中型工业企业的调查,揭示了国有大中型工业企业技术创新中存在的问题,并对提高国有企业技术创新能力提出了建议。 相似文献
5.
在导致英语写作时出现言语错误的各因素中母语的影响居为首位。而汉语对英语写作的干扰中以汉语的词语及句法的干扰较为突出。应使学生主动适应英语思维,有意识地避免母语的负迁移,不断提高英语写作能力。 相似文献
6.
为了寻找花 -格管线腐蚀穿孔的原因 ,对西起柴达木盆地西部的油沙山 ,东至其东部格尔木 ,全长 435.7km的花 -格管线运行以来的腐蚀穿孔次数进行统计分析和相关性计算 ,得出腐蚀穿孔累积数对数和运行时间的线性关系、腐蚀穿孔累积数和运行时间的指数关系 .模型表明腐蚀穿孔失效呈加速态势 ,其腐蚀失效机理是管道防腐层下电屏蔽的电化学自催化腐蚀和管道保温层中干湿交界处氧浓差腐蚀 . 相似文献
7.
在拓朴向量空间中,引进映射的几个锥广义凸概念,对于目标映射约束映射为Gateaux可导的情况,建立了拓朴向量空间多目标规划问题锥有效解和锥弱有效解在锥广义凸条件下的几个最优性充分条件。 相似文献
8.
Angiotensin-converting enzyme 2 is an essential regulator of heart function 总被引:131,自引:0,他引:131
Crackower MA Sarao R Oudit GY Yagil C Kozieradzki I Scanga SE Oliveira-dos-Santos AJ da Costa J Zhang L Pei Y Scholey J Ferrario CM Manoukian AS Chappell MC Backx PH Yagil Y Penninger JM 《Nature》2002,417(6891):822-828
Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo. 相似文献
9.
Nussbaum JM Schilling S Cynis H Silva A Swanson E Wangsanut T Tayler K Wiltgen B Hatami A Rönicke R Reymann K Hutter-Paier B Alexandru A Jagla W Graubner S Glabe CG Demuth HU Bloom GS 《Nature》2012,485(7400):651-655
Extracellular plaques of amyloid-β and intraneuronal neurofibrillary tangles made from tau are the histopathological signatures of Alzheimer's disease. Plaques comprise amyloid-β fibrils that assemble from monomeric and oligomeric intermediates, and are prognostic indicators of Alzheimer's disease. Despite the importance of plaques to Alzheimer's disease, oligomers are considered to be the principal toxic forms of amyloid-β. Interestingly, many adverse responses to amyloid-β, such as cytotoxicity, microtubule loss, impaired memory and learning, and neuritic degeneration, are greatly amplified by tau expression. Amino-terminally truncated, pyroglutamylated (pE) forms of amyloid-β are strongly associated with Alzheimer's disease, are more toxic than amyloid-β, residues 1-42 (Aβ(1-42)) and Aβ(1-40), and have been proposed as initiators of Alzheimer's disease pathogenesis. Here we report a mechanism by which pE-Aβ may trigger Alzheimer's disease. Aβ(3(pE)-42) co-oligomerizes with excess Aβ(1-42) to form metastable low-n oligomers (LNOs) that are structurally distinct and far more cytotoxic to cultured neurons than comparable LNOs made from Aβ(1-42) alone. Tau is required for cytotoxicity, and LNOs comprising 5% Aβ(3(pE)-42) plus 95% Aβ(1-42) (5% pE-Aβ) seed new cytotoxic LNOs through multiple serial dilutions into Aβ(1-42) monomers in the absence of additional Aβ(3(pE)-42). LNOs isolated from human Alzheimer's disease brain contained Aβ(3(pE)-42), and enhanced Aβ(3(pE)-42) formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background. We conclude that Aβ(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Aβ(1-42) into structurally distinct LNOs that propagate by a prion-like mechanism. Our results raise the possibility that Aβ(3(pE)-42) acts similarly at a primary step in Alzheimer's disease pathogenesis. 相似文献
10.
从中国石龙子(Eumeceschinensis)胃、小肠和大肠中分离出的细菌包括枸橼酸杆菌属的弗劳地枸橼酸杆菌(Cirrobacterfreundii)和异型构枸橼酸杆菌(Citrobacterdiversus)、变形杆菌属的奇异变形杆菌(Proteusmiralelis)、肠杆菌属的阴沟肠杆菌(Enterobactercloacae)、芽孢杆菌属的枯草芽孢杆菌(Bacillussubtilis)、葡萄球菌属的表皮葡萄球菌(Staphylococcusepidermidis)和类杆菌属普通类杆菌(Bacteroidesvulqatus).细菌在胃、小肠和大肠中分布数量为3.42×106、2.04×106和1.11×109.弗劳地枸橼酸杆菌为优势菌群.分离出的霉菌属于青霉属(Pencillium)、曲霉属(Aspergillus)和毛孢子菌属(Trichosporon),主要是青霉属.在胃、小肠和大肠中霉菌的数量分别是2.19×104、1.67×104和1.61×104,酵母菌和放线菌都未发现. 相似文献