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排序方式: 共有94条查询结果,搜索用时 31 毫秒
41.
通过微电子加工工艺,制备出具有ITO/TaO_x/AlO_x/Ti结构的双介质层阻变存储器.器件中引入的氧化铝介质层有效地减小了器件的运行电流,降低了高/低阻态间切换所需的功耗,并增大了高/低阻态电阻比值.研究表明,器件的高低态电阻与其切换电压均有良好的稳定性和均匀性,且器件表现出可靠的擦写性能与保持性能.进一步研究表明,器件高阻态导电受肖特基发射机制主导,低阻态导电受空间电荷限制机制主导.器件还具有连续可调的电阻渐变行为,利用反复电脉冲刺激下的器件电阻变化来表征突触的权值,可以模拟突触行为. 相似文献
42.
将基于复数编码的遗传算法引入竞争性协进化的理论研究中,提出一种竞争性协进化的新策略,即:在仿真实验中,采用2个基于神经网络结构控制的移动机器人,并将它们投入到一个陌生的环境中.其中,一个机器人扮演猎手,另一个扮演猎物,猎手对猎物进行捕捉,最终得到每一代的最好猎手机器人和最好猎物机器人以及它们的适应度曲线.在这个竞争性协进化系统中,基于复数编码的遗传算法主要用于对机器人控制系统的神经网络进行进化.计算机仿真结果表明,与基本遗传算法相比,基于复数编码的遗传算法具有更强的进化能力. 相似文献
43.
吕继华 《高技术通讯(英文版)》2009,15(1):101-107
Lipid rafts are cholesterol-enriched microdomains and implicated in many essential physiological activities such as the neurotransmitter release. Many studies have been carried out on the function of rafts in the plasma membranes, whereas little is known about the information of such microdomains in subcellular compartments especially synaptic vesicles (SVs). In the well-studied plasma membranes, several proteins have been recognized as raft markers, which are used to label or trace rafts. But the raft marker protein on SVs has not been identified yet. Although some SV proteins, including VAMP and CPE, have been found in raft fractions, they cannot be used as markers due to their low abundance in rafts. In this work, we designed several chimera proteins and tested their characteristics for using as SV raft makers. First, we detected whether they located in SVs, and then the chimeras exhibiting the better localization in SVs were further examined for their enrichment in raft using detergent treatment and gradient density floatation analysis. Our results indicate that one of the chimeric proteins is primarily located in SVs and distributed in raft microdomains, which strongly suggests that it could be served as a raft marker for SVs. 相似文献
44.
Huntington’s disease (HD) is caused by a polyglutamine expansion in the protein huntingtin and is characterized by intraneuronal inclusions and widespread neuronal death at the late stage of the disease. In research, most of the emphasis has been on understanding the cell death and its mechanisms. Until recently, it was believed that the vast majority, if not all, of the symptoms in HD are a direct consequence of neurodegeneration. However, increasing evidence shows that subtle alterations in synaptic function could underlie the early symptoms. It is of particular interest to understand the nature of this neuronal dysfunction. Normal huntingtin interacts with various cytoskeletal and synaptic vesicle proteins that are essential for exocytosis and endocytosis. Altered interactions of mutant huntingtin with its associated partners could contribute to abnormal synaptic transmission in HD. This review describes recent advances in understanding synaptic dysfunction in HD.Received 2 March 2005; received after revision 13 April 2005; accepted 19 April 2005 相似文献
45.
神经元通过钠.钾泵(Na+,K+-AT.Pase)在细胞浆中富集钾离子并排出细胞内的钠离子,从而维持细胞膜内外的钠和钾离子浓度梯度,调控细胞膜电位和兴奋性,该过程对调节神经元功能起到十分重要的作用。但是,人们一直不清楚除了ATP、钠和钾离子对钠.钾泵的驱动作用以及一些神经递质、激素通过它们的受体间接地调节钠一钾泵活性以外,身体内是否存在可以直接激动钠一钾泵的物质,并对神经系统功能进行调节。我们的研究发现传导痛觉的背根节神经元高表达滤泡素抑制素样蛋白1(follistatin.1ike 1,FSTL1),并通过清亮小泡将FSTL1运输至脊髓内的传入神经终末释放,直接与位于感觉传入神经终末突触前膜上的钠一钾泵仪1亚基相结合,增强钠.钾泵活性,使细胞膜超极化,从而对感觉传入神经终末的兴奋性突触传递起抑制性调控作用。我们与南京大学模式动物研究所高翔研究组密切合作,制备了国内第一例条件式敲除小鼠,在背根节神经元中特异性敲除了FSTL1的基因。研究发现FSTL1条件式敲除小鼠兴奋性突触传递增强.痛觉敏感度提高。因此,FSTL1作为第一个被发现的内源性钠。钾泵激动剂,对于保持正常的躯体感觉是必需的,FSTL1减少则会导致异常痛觉。该发现表明内源性钠一钾泵激动剂可以通过调控突触传递对神经系统功能产生重要的影响。 相似文献
46.
M. G. Monti G. Marverti S. Ghiaroni G. Piccinini L. Pernecco M. S. Moruzzi 《Cellular and molecular life sciences : CMLS》1994,50(10):953-957
Phosphatidylserine (PS), an activator of protein kinase C (PKC) in the assay of protein phosphorylation, inhibited this enzyme in a time-dependent manner following preincubation in the absence of Ca2+. The phospholipid-induced inactivation of kinase activity was dependent on the PS content and on the charge density of liposomes. This inactivation of PKC could be reduced, but not completely eliminated, by addition of Ca2+. In the present work the effect of a naturally occurring polyamine (spermine) on the PS-induced inactivation of PKC was investigated. The presence of spermine during preincubation without Ca2+ was effective in suppressing the PS-induced inactivation of PKC over the period (20 min) required for PS to inhibit the enzyme by 95%. PKC exists in two membrane-bound states: a reversible one which can be dissociated by Ca2+ chelators (membrane-associated form) and an irreversible one which is chelator-stable (membrane-inserted form). Gel filtration experiments on the PKC-PS complex formed in the presence of Ca2+ indicated that less insertion of enzyme into liposomes occurred in the presence of spermine and that the kinase activity of the reversibly membrane-associated PKC was protected from PS inactivation. 相似文献
47.
The colorimetric response of amine-terminated polydiacetylene (PDA) vesicles was initially demonstrated by varying the pH of the solution. Convenient colorimetric methods to detect glucose and acetylcholinesterase (AChE) activity were successfully established using amine-terminated PDA vesicles by taking advantage of the following features: (1) the amine-terminated PDA vesicles undergo a colorimetric transition as the pH of the solution changes; (2) glucose can be oxidized to gluconic acid in the presence of glucose oxidase; and (3) AChE catalyzes the hydrolysis of acetylcholine to acetic acid. The visual detection of glucose levels and AChE activity showed good selectivity and acceptable sensitivity. The detection limit of glucose was ~2.5 μmol/L and the level of AChE activity was assayed as low as 10.0 mU/mL. Moreover, the amine-terminated PDA vesicles can be used for screening the activity of inhibitors against AChE. 相似文献
48.
K. B. Clairmont W. Boll M. Ericsson T. Kirchhausen 《Cellular and molecular life sciences : CMLS》1997,53(7):611-619
The clathrin-associated adaptor protein (AP) complexes drive the polymerization of clathrin in coated pits to form coated
vesicles. It has previously been shown that the carboxyl-terminal hinge/ear domain of the β2 chain contains a binding site for clathrin and that removal of this domain from APs or from isolated β2 chains abrogates their ability to form clathrin coats in vitro. We show here that the hinge/ear domain is necessary for efficient
incorporation of AP complexes into coated pits and coated vesicles in cells, a result that is consistent with the view that
the β chains indeed provide an important interaction between the AP complexes and clathrin.
Received 7 April 1997; received after revision 22 May 1997; accepted 28 May 1997 相似文献
49.
SNAREs and SNARE regulators in membrane fusion and exocytosis 总被引:21,自引:0,他引:21
J. E. Gerst 《Cellular and molecular life sciences : CMLS》1999,55(5):707-734
Eukaryotes have a remarkably well-conserved apparatus for the trafficking of proteins between intracellular compartments
and delivery to their target organelles. This apparatus comprises the secretory (or ‘protein export’) pathway, which is responsible
for the proper processing and delivery of proteins and lipids, and is essential for the derivation and maintenance of those
organelles. Protein transport between intracellular compartments is mediated by carrier vesicles that bud from one organelle
and fuse selectively with another. Therefore, organelle-specific trafficking of vesicles requires specialized proteins that
regulate vesicle transport, docking and fusion. These proteins are generically termed SNAREs and comprise evolutionarily conserved
families of membrane-associated proteins (i.e. the synaptobrevin/VAMP, syntaxin and SNAP-25 families) which mediate membrane
fusion. SNAREs act at all levels of the secretory pathway, but individual family members tend to be compartment-specific and,
thus, are thought to contribute to the specificity of docking and fusion events. In this review, we describe the different
SNARE families which function in exocytosis, as well as discuss the role of possible negative regulators (e.g. ‘SNARE-masters’)
in mediating events leading to membrane fusion. A model to illustrate the dynamic cycling of SNAREs between fusion-incompetent
and fusion-competent states, called the SNARE cycle, is presented.
Received 8 October 1998; received after revision 26 November 1998; accepted 26 November 1998 相似文献
50.
Blockade of GABAB receptors was reported to improve cognitive performance in mammals. The physiological basis of this effect is poorly understood. We investigated the effect of the GABAB receptor antagonist CGP 35348 on long-term potentiation (LTP) in the CA1 area of the hippocampus in vitro and in vivo. In vitro the effect of CGP 35348 on LTP, induced either by two non-primed tetanic stimulations or by two primed bursts of stimuli, was investigated. In the presence of 1 mM CGP 35348 LTP was significantly facilitated following two non-primed tetanic trains, but was impaired following two primed burst stimulations. In vivo LTP was induced by applying non-primed trains of stimuli of increasing duration to the Schaffer collateral/commissural fibers. The potentiation of the population spike recorded in CA1 was significantly facilitated by CGP 35348 (100 mg/kg i.v.). In conclusion these findings demonstrate that the GABAB antagonist CGP 35348 facilitates LTP in vitro and in vivo if induced by non-primed tetanic stimulation. In vitro, the mode of stimulation determines the effect of the GABAB antagonist on LTP. 相似文献