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991.
992.
羰基铁镍纤维的磁场诱导制备及结构特性研究   总被引:2,自引:0,他引:2  
以羰基铁与羰基镍为原料,采用磁场诱导热分解法制备了羰基铁镍纤维.研究了羰基铁和羰基镍在不同的流量比下,所制备纤维的结构、形貌特征.结果发现:不同组份的羰基铁镍纤维,呈现不同的结构(bcc或fcc),且碳元素以不同形式存在,其形貌呈现直线型、“Y”型和“Z”形的特征.通过对羰基铁镍纤维生长机理的研究,发现纤维呈现不同形貌的原因,是由于受到晶体生长界面干扰的影响.通过对影响羰基铁镍纤维生长因素的调控(分解温度和磁场强度等),可改变羰基铁镍纤维的形貌和直径.  相似文献   
993.
J Dong  Z Hu  C Wu  H Guo  B Zhou  J Lv  D Lu  K Chen  Y Shi  M Chu  C Wang  R Zhang  J Dai  Y Jiang  S Cao  Z Qin  D Yu  H Ma  G Jin  J Gong  C Sun  X Zhao  Z Yin  L Yang  Z Li  Q Deng  J Wang  W Wu  H Zheng  G Zhou  H Chen  P Guan  Z Peng  Y Chen  Y Shu  L Xu  X Liu  L Liu  P Xu  B Han  C Bai  Y Zhao  H Zhang  Y Yan  CI Amos  F Chen  W Tan  L Jin  T Wu  D Lin  H Shen 《Nature genetics》2012,44(8):895-899
To find additional susceptibility loci for lung cancer, we tested promising associations from our previous genome-wide association study (GWAS) of lung cancer in the Chinese population in an extended validation sample size of 7,436 individuals with lung cancer (cases) and 7,483 controls. We found genome-wide significant (P < 5.0 × 10(-8)) evidence for three additional lung cancer susceptibility loci at 10p14 (rs1663689, close to GATA3, P = 2.84 × 10(-10)), 5q32 (rs2895680 in PPP2R2B-STK32A-DPYSL3, P = 6.60 × 10(-9)) and 20q13.2 (rs4809957 in CYP24A1, P = 1.20 × 10(-8)). We also found consistent associations for rs247008 at 5q31.1 (IL3-CSF2-P4HA2, P = 7.68 × 10(-8)) and rs9439519 at 1p36.32 (AJAP1-NPHP4, P = 3.65 × 10(-6)). Four of these loci showed evidence for interactions with smoking dose (P = 1.72 × 10(-10), P = 5.07 × 10(-3), P = 6.77 × 10(-3) and P = 4.49 × 10(-2) for rs2895680, rs4809957, rs247008 and rs9439519, respectively). These results advance our understanding of lung cancer susceptibility and highlight potential pathways that integrate genetic variants and smoking in the development of lung cancer.  相似文献   
994.
Increasing evidence demonstrates that Na+, K+-ATPase plays an important role in pulmonary inflammation, but the mechanism remains largely unknown. In this study, we used cardiotonic steroids as Na+, K+-ATPase inhibitors to explore the possible involvement of Na+, K+-ATPase in pulmonary epithelial inflammation. The results demonstrated that mice after ouabain inhalation developed cyclooxygenase-2-dependent acute lung inflammation. The in vitro experiments further confirmed that Na+, K+-ATPase inhibitors significantly stimulated cyclooxygenase-2 expression in lung epithelial cells of human or murine origin, the process of which was participated by multiple cis-elements and trans-acting factors. Most importantly, we first described here that Na+, K+-ATPase inhibitors could evoke a significant Hu antigen R nuclear export in lung epithelial cells, which stabilized cyclooxygenase-2 mRNA by binding with a proximal AU-rich element within its 3′-untranslated region. In conclusion, HuR-mediated mRNA stabilization opens new avenues in understanding the importance of Na+, K+-ATPase, as well as its inhibitors in inflammation.  相似文献   
995.
纳米晶稀土永磁材料的理论,制备及应用研究   总被引:1,自引:0,他引:1  
本文系统综述了作者近年来在纳米晶稀土永磁材料领域所取犁 进展,包括理论,制备及应用等几方面,并对今后该领域的研究与发展提出了值得重视和努力的方向。  相似文献   
996.
The robust H∞ control problem for a class of uncertain Takagi-Sugeno fuzzy systems with timevarying state delays is studied. The uncertain parameters are supposed to reside in a polytope. Based on the delay-dependent Lyapunov functional method, a new delay-dependent robust H∞ fuzzy controller, which depends on the size of the delays and the derivative of the delays, is presented in term of linear matrix inequalities (LMIs). For all admissible uncertainties and delays, the controller guarantees not only the asymptotic stability of the system but also the prescribed H∞ attenuation level. In addition, the effectiveness of the proposed design method is demonstrated by a numerical example.  相似文献   
997.
Cyclin-dependent kinase 1 (CDK1) is a major component of the cell cycle progression engine. Recently, several investigations provided evidence demonstrating that unscheduled CDK1 activation may also be involved in apoptosis in cancerous cells. In this article, we demonstrate that X-ray irradiation induced G1 arrest in MOLT-4 lymphocytic leukemia cells, the arrest being accompanied by reduction in the activity of CDK2, but increased CDK1 activity and cell apoptosis in the G1 phase. Interestingly, this increase in CDK1 and apoptosis by ionizing radiation was prevented by pretreatment with the CDK1 inhibitor, roscovitine, suggesting that CDK1 kinase activity is required for radiation-induced apoptotic cell death in this model system. Furthermore, cyclin B1 and CDK1 were detected co-localizing and associating in G1 phase MOLT-4 cells, with the cellular lysates from these cells revealing a genotoxic stress-induced increase in CDK1 phosphorylation (Thr-161) and dephosphorylation (Tyr-15), as analyzed by postsorting immunoprecipitation and immunoblotting. Finally, X-irradiation was found to increase Bcl-2 phosphorylation in G1 phase cells. Taken together, these novel findings suggest that CDK1 is activated by unscheduled accumulation of cyclin B1 in G1 phase cells exposed to X-ray, and that CDK1 activation, at the wrong time and in the wrong phase, may directly or indirectly trigger a Bcl-2-dependent signaling pathway leading to apoptotic cell death in MOLT-4 cells. Received 30 March 2006; received after revision 23 June 2006; accepted 24 August 2006 J. Wu and Y. Feng contributed equally to this work.  相似文献   
998.
TREX1 acts in concert with the SET complex in granzyme A-mediated apoptosis, and mutations in TREX1 cause Aicardi-Goutières syndrome and familial chilblain lupus. Here, we report monoallelic frameshift or missense mutations and one 3' UTR variant of TREX1 present in 9/417 individuals with systemic lupus erythematosus but absent in 1,712 controls (P = 4.1 x 10(-7)). We demonstrate that two mutant TREX1 alleles alter subcellular targeting. Our findings implicate TREX1 in the pathogenesis of SLE.  相似文献   
999.
特征统计算法是为了解决复杂多极值优化问题而开发的一种新的全局优化算法。为了检验该算法的性能,应用它在一类具有代表性的NP组合优化问题-旅行商问题(TSP)上作了计算。结果发现,该算法虽不是专为TSP问题而开发,却在该问题上取得了很好的结果。所得到的结果表明,特征统计算法可以作为解决这类NP组合优化问题的一个新的途径。  相似文献   
1000.
基于车用柴油机微粒捕集器过滤体孔道内的加热再生模型,采用数值模拟的方法对加热再生过程中过滤体孔道内微粒燃烧与壁面温度沿轴向的分布规律以及不同再生条件下柴油机微粒捕集器再生过程的规律进行了研究.结果表明:过滤体的壁面温度从过滤体前端向后端逐渐升高,且整个过滤体的峰值温度出现在过滤体后端;提高过滤体初始温度,适当地增大再生气流质量流量、气流含氧量以及微粒沉积量都可加快再生过程,但过大的含氧量和微粒沉积量会造成壁面峰值温度过高,过大的气流质量流量会减慢再生过程.  相似文献   
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