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111.
马鸿 《高技术通讯(英文版)》2009,15(4):416-422
A k-shortest path based algorithm considering layout density and signal integrity for good buffer candidate locations is proposed in this paper. Theoretical results for computing the maximal distance between buffers are derived under the timing, noise and slew rate constraints. By modifying the traditional uniform wire segmenting strategy and considering the impact of tile size on density penalty function, this work proposes k-shortest path algorithm to find the buffer insertion candidate locations. The experiments show that the buffers inserted can significantly optimize the design density, alleviate signal degradation, save the number of buffers inserted and the overall run time. 相似文献
112.
Lee JE Silhavy JL Zaki MS Schroth J Bielas SL Marsh SE Olvera J Brancati F Iannicelli M Ikegami K Schlossman AM Merriman B Attié-Bitach T Logan CV Glass IA Cluckey A Louie CM Lee JH Raynes HR Rapin I Castroviejo IP Setou M Barbot C Boltshauser E Nelson SF Hildebrandt F Johnson CA Doherty DA Valente EM Gleeson JG 《Nature genetics》2012,44(2):193-199
Tubulin glutamylation is a post-translational modification that occurs predominantly in the ciliary axoneme and has been suggested to be important for ciliary function. However, its relationship to disorders of the primary cilium, termed ciliopathies, has not been explored. Here we mapped a new locus for Joubert syndrome (JBTS), which we have designated as JBTS15, and identified causative mutations in CEP41, which encodes a 41-kDa centrosomal protein. We show that CEP41 is localized to the basal body and primary cilia, and regulates ciliary entry of TTLL6, an evolutionarily conserved polyglutamylase enzyme. Depletion of CEP41 causes ciliopathy-related phenotypes in zebrafish and mice and results in glutamylation defects in the ciliary axoneme. Our data identify CEP41 mutations as a cause of JBTS and implicate tubulin post-translational modification in the pathogenesis of human ciliary dysfunction. 相似文献
113.
Aragonés J Schneider M Van Geyte K Fraisl P Dresselaers T Mazzone M Dirkx R Zacchigna S Lemieux H Jeoung NH Lambrechts D Bishop T Lafuste P Diez-Juan A Harten SK Van Noten P De Bock K Willam C Tjwa M Grosfeld A Navet R Moons L Vandendriessche T Deroose C Wijeyekoon B Nuyts J Jordan B Silasi-Mansat R Lupu F Dewerchin M Pugh C Salmon P Mortelmans L Gallez B Gorus F Buyse J Sluse F Harris RA Gnaiger E Hespel P Van Hecke P Schuit F Van Veldhoven P Ratcliffe P Baes M Maxwell P Carmeliet P 《Nature genetics》2008,40(2):170-180
HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia. Hypoxia tolerance is not due to HIF-dependent angiogenesis, erythropoiesis or vasodilation, but rather to reduced generation of oxidative stress, which allows Phd1-deficient myofibers to preserve mitochondrial respiration. Hypoxia tolerance relies primarily on Hif-2alpha and was not observed in heterozygous Phd2-deficient or homozygous Phd3-deficient mice. Of medical importance, conditional knockdown of Phd1 also rapidly induces hypoxia tolerance. These findings delineate a new role of Phd1 in hypoxia tolerance and offer new treatment perspectives for disorders characterized by oxidative stress. 相似文献
114.
Existing home devices in home network provides only independent services limited on a homogeneous protocol and/or do not fully support an intelligent service provided by cooperating among heterogeneous protocol devices. This paper proposes an intelligent and integrated service binding architecture which allow the users to figure out the status of devices and to cooperate among home network devices regardless of supported protocols or operational characteristics. 相似文献
115.
提出了各种网络集成管理的TMN-DCN设计方法,并举出了应用示例.TMN-DCN设备可按各个网络配置.这些设备具有网络管理功能.规模非常大的网络分配多个TMN-DCN设备.下一阶段则利用作为TMN-DCN节点的TMN-DCN设备设计TMN-DCN的布局(物理结构). 相似文献
116.
通过对入侵检测中模糊技术应用和移动模糊推理方法的研究,设计并实现了基于移动模糊推理的DoS攻击入侵检测系统.首先,描述了移动模糊推理方法与模糊推理步骤;其次,详细阐述了用时间差与IP地址分布变化的DoS攻击检测方法与基于移动模糊推理的攻击检测系统,创建了用于检测的模糊规则,确定网络攻击.最后,把DoS攻击工具与DARPA 98数据集作为入侵检测数据集,对基于移动模糊推理的方法与现行方法进行测试,验证了所提方法的有效性. 相似文献
117.
Liu GH Barkho BZ Ruiz S Diep D Qu J Yang SL Panopoulos AD Suzuki K Kurian L Walsh C Thompson J Boue S Fung HL Sancho-Martinez I Zhang K Yates J Izpisua Belmonte JC 《Nature》2011,472(7342):221-225
Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal human premature ageing disease, characterized by premature arteriosclerosis and degeneration of vascular smooth muscle cells (SMCs). HGPS is caused by a single point mutation in the lamin A (LMNA) gene, resulting in the generation of progerin, a truncated splicing mutant of lamin A. Accumulation of progerin leads to various ageing-associated nuclear defects including disorganization of nuclear lamina and loss of heterochromatin. Here we report the generation of induced pluripotent stem cells (iPSCs) from fibroblasts obtained from patients with HGPS. HGPS-iPSCs show absence of progerin, and more importantly, lack the nuclear envelope and epigenetic alterations normally associated with premature ageing. Upon differentiation of HGPS-iPSCs, progerin and its ageing-associated phenotypic consequences are restored. Specifically, directed differentiation of HGPS-iPSCs to SMCs leads to the appearance of premature senescence phenotypes associated with vascular ageing. Additionally, our studies identify DNA-dependent protein kinase catalytic subunit (DNAPKcs, also known as PRKDC) as a downstream target of progerin. The absence of nuclear DNAPK holoenzyme correlates with premature as well as physiological ageing. Because progerin also accumulates during physiological ageing, our results provide an in vitro iPSC-based model to study the pathogenesis of human premature and physiological vascular ageing. 相似文献
118.
《庚辛玉册》:中国炼丹术在历史上的最后一部巨著 总被引:1,自引:1,他引:0
《庚辛玉册》是朱权(1378-1448年)的一部有关炼丹术的著作。西方学者琼克尔(D.R.Jonker)认为这部书已经失佚。明代李时珍在《本划纲目》中多次引述此书。另外,有一些片段也散载在某些类书中。文章英译了多年来所辑得的引自此书的条文,并试从这点蛛丝马迹中探讨这部书。自从1958年和李约瑟博士合作研究中国炼丹术史以来,他们两人就一直注意这部书。作者数十年来访问海外学术机构多处,顺便查访此书,但还没有发现整本的《庚辛玉册》。1990年访问北京期间,薄树人陪作者和中山茂到北京图书馆查询此书,也无收获。今竟然读到1993年姚品文著《朱权研究》中有“北京图书馆有藏本”一句话。希望将来学者们能够对这部典籍做更全面的研究。 相似文献
119.
120.
Cissé M Halabisky B Harris J Devidze N Dubal DB Sun B Orr A Lotz G Kim DH Hamto P Ho K Yu GQ Mucke L 《Nature》2011,469(7328):47-52
Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. Here we show that amyloid-β oligomers bind to the fibronectin repeats domain of EphB2 and trigger EphB2 degradation in the proteasome. To determine the pathogenic importance of EphB2 depletions in Alzheimer's disease and related models, we used lentiviral constructs to reduce or increase neuronal expression of EphB2 in memory centres of the mouse brain. In nontransgenic mice, knockdown of EphB2 mediated by short hairpin RNA reduced NMDA receptor currents and impaired long-term potentiation in the dentate gyrus, which are important for memory formation. Increasing EphB2 expression in the dentate gyrus of human amyloid precursor protein transgenic mice reversed deficits in NMDA receptor-dependent long-term potentiation and memory impairments. Thus, depletion of EphB2 is critical in amyloid-β-induced neuronal dysfunction. Increasing EphB2 levels or function could be beneficial in Alzheimer's disease. 相似文献