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991.
Zhang F.Wu Q.Zeng G. 《复杂系统与复杂性科学》2017,(1):81-87
We consider an SIRS epidemic model with a general direct immunization rate on networks. By constructing suitable Lyapunov functions, we find that the dynamical behvaior of the model is completely determined by the epidemic threshold λc. When λ≤λc, the disease-free equilibrium is globally asymptotically stable; when λ>λc, the endemic equilibrium is globally asymptotically stable. In addition, we propose a uniform direct immunization and a targeted direct immunization. The results show that under the same average immunization rate s there exists a critical immunization-lost rate δc so that the epidemic threshold of the targeted direct immunization is smaller (larger) than that of the uniform direct immunization if δ<δc(δ>δc). © 2017, The Journal of Agency of Complex Systems and Complexity Science. All right reserved. 相似文献
992.
为研究有阻尼多跨连续梁在横向激励下的位移响应,采用整体分析的方法,在BernoulliEuler梁理论的基础上建立求解连续梁的横向振动方程,求得了有阻尼多跨连续梁的位移响应函数,同时求得了有阻尼条件下的固有频率方程和振型函数。 相似文献
993.
Xin Zhu Yinwen Liang Feng Gao Junmin Pan 《Cellular and molecular life sciences : CMLS》2017,74(18):3425-3437
Intraflagellar transport (IFT) is required for ciliogenesis by ferrying ciliary components using IFT complexes as cargo adaptors. IFT54 is a component of the IFT-B complex and is also associated with cytoplasmic microtubules (MTs). Loss of IFT54 impairs cilia assembly as well as cytoplasmic MT dynamics. The N-terminal calponin homology (CH) domain of IFT54 interacts with tubulins/MTs and has been proposed to transport tubulin during ciliogenesis, whereas the C-terminal coiled-coil (CC) domain binds IFT20. However, the precise function of these domains in vivo is not well understood. We showed that in Chlamydomonas, loss of IFT54 completely blocks ciliogenesis but does not affect spindle formation and proper cell cycle progression, even though IFT54 interacts with mitotic MTs. Interestingly, IFT54 lacking the CH domain allows proper flagellar assembly. The CH domain is required for the association of IFT54 with the axoneme but not with mitotic MTs, and also regulates the flagellar import of IFT54 but not IFT81 and IFT46. The C-terminal CC domain is essential for IFT54 to bind IFT20, and for its recruitment to the basal body and incorporation into IFT complexes. Complete loss of IFT54 or the CC domain destabilizes IFT20. ift54 mutant cells expressing the CC domain alone rescue the stability of IFT20 and form stunted flagella with accumulation of both IFT-A component IFT43 and IFT-B component IFT46, indicating that IFT54 also functions in IFT turn-around at the flagellar tip. 相似文献
994.
对甘肃省兰州市榆中县中试基地种植的11种甜高粱材料进行试验,以筛选出适合在兰州榆中地区种植的甜高粱材料。采用灰色关联度对材料的茎干鲜重、生物产量、茎杆平均含糖量进行分析,同时参考株高、穗长、穗颈长、物候期等指标,选定适合榆中地区不同用途的甜高粱材料。灰色关联度分析结果:茎秆鲜重、生物产量、茎秆平均含糖量三个指标中,茎秆平均含糖量灰色关联度最大,对结果影响最大;灰色综合评判排序显示08-2、2043、09-1、雅津43号分别排列前4位。08-2、2043、09-1、雅津43号综合表现最好,适合兰州榆中地区种植,可用于饲料生产和生物质能源储备种植。 相似文献
995.
Pan Li Guoying Zheng Yan Yang Chunguang Zhang Ping Xiong Yong Xu Min Fang Zheng Tan Fang Zheng Feili Gong 《Cellular and molecular life sciences : CMLS》2010,67(18):3197-3208
When they recognize a target cell, natural killer (NK) cells mount an attack to kill the target by exerting their cytotoxicity
via the exocytosis of cytotoxic granules. Although the details of this process (which includes the movement of cytotoxic granules
in the immune synapse and their fusion with the plasma membrane, releasing granzymes and perforin into the synaptic cleft)
are relatively better understood, the post-exocytosis regulation of the process is still largely unknown. Here we show that
a clathrin-dependent endocytosis stimulated by target cell occurs in NK92 cell line, which is closely correlated with granzyme
B recovery. Inhibition of the endocytosis significantly attenuates the cytotoxicity of NK92 cells. The NK cell recovery of
its released effector molecules, in turn, suggests that endocytosis may well play a key role in the post exocytosis regulation
of immune cells. 相似文献
996.
Xue B Mizianty MJ Kurgan L Uversky VN 《Cellular and molecular life sciences : CMLS》2012,69(8):1211-1259
Many proteins and protein regions are disordered in their native, biologically active states. These proteins/regions are abundant
in different organisms and carry out important biological functions that complement the functional repertoire of ordered proteins.
Viruses, with their highly compact genomes, small proteomes, and high adaptability for fast change in their biological and
physical environment utilize many of the advantages of intrinsic disorder. In fact, viral proteins are generally rich in intrinsic
disorder, and intrinsically disordered regions are commonly used by viruses to invade the host organisms, to hijack various
host systems, and to help viruses in accommodation to their hostile habitats and to manage their economic usage of genetic
material. In this review, we focus on the structural peculiarities of HIV-1 proteins, on the abundance of intrinsic disorder
in viral proteins, and on the role of intrinsic disorder in their functions. 相似文献
997.
Ong CK Subimerb C Pairojkul C Wongkham S Cutcutache I Yu W McPherson JR Allen GE Ng CC Wong BH Myint SS Rajasegaran V Heng HL Gan A Zang ZJ Wu Y Wu J Lee MH Huang D Ong P Chan-on W Cao Y Qian CN Lim KH Ooi A Dykema K Furge K Kukongviriyapan V Sripa B Wongkham C Yongvanit P Futreal PA Bhudhisawasdi V Rozen S Tan P Teh BT 《Nature genetics》2012,44(6):690-693
Opisthorchis viverrini-related cholangiocarcinoma (CCA), a fatal bile duct cancer, is a major public health concern in areas endemic for this parasite. We report here whole-exome sequencing of eight O. viverrini-related tumors and matched normal tissue. We identified and validated 206 somatic mutations in 187 genes using Sanger sequencing and selected 15 genes for mutation prevalence screening in an additional 46 individuals with CCA (cases). In addition to the known cancer-related genes TP53 (mutated in 44.4% of cases), KRAS (16.7%) and SMAD4 (16.7%), we identified somatic mutations in 10 newly implicated genes in 14.8-3.7% of cases. These included inactivating mutations in MLL3 (in 14.8% of cases), ROBO2 (9.3%), RNF43 (9.3%) and PEG3 (5.6%), and activating mutations in the GNAS oncogene (9.3%). These genes have functions that can be broadly grouped into three biological classes: (i) deactivation of histone modifiers, (ii) activation of G protein signaling and (iii) loss of genome stability. This study provides insight into the mutational landscape contributing to O. viverrini-related CCA. 相似文献
998.
A long‐standing puzzle to financial economists is the difficulty of outperforming the benchmark random walk model in out‐of‐sample contests. Using data from the USA over the period of 1872–2007, this paper re‐examines the out‐of‐sample predictability of real stock prices based on price–dividend (PD) ratios. The current research focuses on the significance of the time‐varying mean and nonlinear dynamics of PD ratios in the empirical analysis. Empirical results support the proposed nonlinear model of the PD ratio and the stationarity of the trend‐adjusted PD ratio. Furthermore, this paper rejects the non‐predictability hypothesis of stock prices statistically based on in‐ and out‐of‐sample tests and economically based on the criteria of expected real return per unit of risk. Copyright © 2011 John Wiley & Sons, Ltd. 相似文献
999.
1000.
Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas 总被引:1,自引:0,他引:1
Wu G Broniscer A McEachron TA Lu C Paugh BS Becksfort J Qu C Ding L Huether R Parker M Zhang J Gajjar A Dyer MA Mullighan CG Gilbertson RJ Mardis ER Wilson RK Downing JR Ellison DW Zhang J Baker SJ;St. Jude Children's Research Hospital–Washington University Pediatric Cancer Genome Project 《Nature genetics》2012,44(3):251-253
To identify somatic mutations in pediatric diffuse intrinsic pontine glioma (DIPG), we performed whole-genome sequencing of DNA from seven DIPGs and matched germline tissue and targeted sequencing of an additional 43 DIPGs and 36 non-brainstem pediatric glioblastomas (non-BS-PGs). We found that 78% of DIPGs and 22% of non-BS-PGs contained a mutation in H3F3A, encoding histone H3.3, or in the related HIST1H3B, encoding histone H3.1, that caused a p.Lys27Met amino acid substitution in each protein. An additional 14% of non-BS-PGs had somatic mutations in H3F3A causing a p.Gly34Arg alteration. 相似文献