全文获取类型
收费全文 | 31154篇 |
免费 | 135篇 |
国内免费 | 264篇 |
专业分类
系统科学 | 449篇 |
丛书文集 | 477篇 |
教育与普及 | 95篇 |
理论与方法论 | 113篇 |
现状及发展 | 11199篇 |
研究方法 | 1246篇 |
综合类 | 17185篇 |
自然研究 | 789篇 |
出版年
2014年 | 165篇 |
2013年 | 448篇 |
2012年 | 649篇 |
2011年 | 1444篇 |
2010年 | 444篇 |
2009年 | 380篇 |
2008年 | 723篇 |
2007年 | 862篇 |
2006年 | 867篇 |
2005年 | 783篇 |
2004年 | 623篇 |
2003年 | 528篇 |
2002年 | 539篇 |
2001年 | 1024篇 |
2000年 | 1055篇 |
1999年 | 658篇 |
1992年 | 539篇 |
1991年 | 455篇 |
1990年 | 474篇 |
1989年 | 470篇 |
1988年 | 447篇 |
1987年 | 429篇 |
1986年 | 432篇 |
1985年 | 497篇 |
1984年 | 442篇 |
1983年 | 363篇 |
1982年 | 337篇 |
1981年 | 319篇 |
1980年 | 368篇 |
1979年 | 872篇 |
1978年 | 680篇 |
1977年 | 687篇 |
1976年 | 523篇 |
1975年 | 604篇 |
1974年 | 850篇 |
1973年 | 698篇 |
1972年 | 693篇 |
1971年 | 856篇 |
1970年 | 1007篇 |
1969年 | 792篇 |
1968年 | 792篇 |
1967年 | 777篇 |
1966年 | 728篇 |
1965年 | 515篇 |
1959年 | 266篇 |
1958年 | 434篇 |
1957年 | 327篇 |
1956年 | 241篇 |
1955年 | 250篇 |
1954年 | 232篇 |
排序方式: 共有10000条查询结果,搜索用时 125 毫秒
511.
In this paper, we shall describe a new account of information in communicational contexts, namely, a causal-deflationary one. Our approach draws from Timpson's deflationary view and supplies the field of philosophy of information with new tools that will help to clarify the underlying structure of communication: information is an abstract entity that must be involved in a causal link in order to achieve communication. In light of our account, communication is not merely the existence of statistical correlations between source and receiver, as usually understood from a purely formal view. Instead, communication is an asymmetric phenomenon involving causal notions: the destination system must be able to be causally manipulated by intervening on the source for successful communication. In a nutshell, we shall support the following lemma: no communication without manipulation. 相似文献
512.
证明了若可积函数列{fn}在[a,b]上一致收敛,则nl→im∞∫abfn(x)dx中极限运算与积分运算可交换,从而揭示了"积分的极限"解法的内在本质,并且对于limn→∞∫01xnF(x)dx及nl→im∞∫ab[f(x)]ndx两种类型给出了更为具体有效的一般性解法. 相似文献
513.
[目的]针对协同训练算法在视图分割时未考虑噪声影响和两视图分类器对无标记样本标注不一致问题,提出了基于加权主成分分析和改进密度峰值聚类的协同训练算法.[方法]首先引入加权主成分分析对数据进行预处理,通过寻求初始有标记样本中特征和类标记之间的依赖关系求得各特征加权系数,再对加权变换后的数据进行降维并提取高贡献度特征进行视... 相似文献
514.
突发模式传送系统中前导字作为系统开销降低了数据传送效率,提出一种全数字无前导字突发模式8PSK接收机方案,接收机的时钟和载波恢复均采用前向同步技术,并对载波频偏恢复算法进行了详细推导,并通过仿真验证了算法的可行性和有效性。 相似文献
515.
I. Campia E. Gazzano G. Pescarmona D. Ghigo A. Bosia C. Riganti 《Cellular and molecular life sciences : CMLS》2009,66(9):1580-1594
Digoxin and ouabain are steroid drugs that inhibit the Na+/K+-ATPase, and are widely used in the treatment of heart diseases. They may also have additional effects, such as on metabolism
of steroid hormones, although until now no evidence has been provided about the effects of these cardioactive glycosides on
the synthesis of cholesterol. Here we report that digoxin and ouabain increased the synthesis of cholesterol in human liver
HepG2 cells, enhancing the activity and the expression of the
3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the rate-limiting enzyme of the cholesterol synthesis. This effect
was mediated by the binding of the sterol regulatory element binding protein-2 (SREBP-2) to the HMGCR promoter, and was lost
in cells silenced for SREBP-2 or loaded with increasing amounts of cholesterol. Digoxin and ouabain competed with cholesterol
for binding to the SREBP-cleavage-activating protein, and are critical regulators of cholesterol synthesis in human liver
cells.
Received 10 January 2009; received after revision 11 February 2009; accepted 6 March 2009 相似文献
516.
Wolfs JL Comfurius P Bekers O Zwaal RF Balasubramanian K Schroit AJ Lindhout T Bevers EM 《Cellular and molecular life sciences : CMLS》2009,66(2):314-323
The exposure of phosphatidylserine (PS) at the cell surface plays a critical role in blood coagulation and serves as a macrophage
recognition moiety for the engulfment of apoptotic cells. Previous observations have shown that a high extracellular [K+] and selective K+ channel blockers inhibit PS exposure in platelets and erythrocytes. Here we show that the rate of PS exposure in erythrocytes
decreases by ~50% when the intracellular [K+] increases from 0 to physiological concentrations. Using resealed erythrocyte membranes, we further show that lipid scrambling
is inducible by raising the intracellular [Ca2+] and that K+ ions have a direct inhibitory effect on this process. Lipid scrambling in resealed ghosts occurs in the absence of cell shrinkage
and microvesicle formation, processes that are generally attributed to Ca2+-induced lipid scrambling in intact erythrocytes. Thus, opening of Ca2+-sensitive K+ channels causes loss of intracellular K+ that results in reduced intrinsic inhibitory effect of these ions on scramblase activity.
Received 11 September 2008; received after revision 17 October 2008; accepted 27 October 2008 相似文献
517.
J. Kim D. C. Han J. M. Kim S. Y. Lee S. J. Kim J. R. Woo J. W. Lee S.-K. Jung K. S. Yoon H. G. Cheon S. S. Kim S. H. Hong B.-M. Kwon 《Cellular and molecular life sciences : CMLS》2009,66(10):1766-1781
Indenone KR-62776 acts as an agonist of PPARγ without inducing obesity in animal models and cells. X-ray crystallography reveals
that the indenone occupies the binding pocket in a different manner than rosiglitazone. 2-Dimensional gel-electrophoresis
showed that the expression of 42 proteins was altered more than 2.0-fold between KR-62776- or rosiglitazone-treated adipocyte
cells and control cells. Rosiglitazone down-regulated the expression of ERK1/2 and suppressed the phosphorylation of ERK1/2
in these cells. However, the expression of ERK1/2 was up-regulated in KR-62776-treated cells. Phosphorylated ERK1/2, activated
by indenone, affects the localization of PPARγ, suggesting a mechanism for indenone-inhibition of adipogenesis in 3T3-L1 preadipocyte
cells. The preadipocyte cells are treated with ERK1/2 inhibitor PD98059, a large amount of the cells are converted to adipocyte
cells. These results support the conclusion that the localization of PPARγ is one of the key factors explaining the biological
responses of the ligands.
Received 04 March 2009; received after revision 13 March 2009; accepted 17 March 2009 相似文献
518.
Functions and pathologies of BiP and its interaction partners 总被引:1,自引:1,他引:0
J. Dudek J. Benedix S. Cappel M. Greiner C. Jalal L. Müller R. Zimmermann 《Cellular and molecular life sciences : CMLS》2009,66(9):1556-1569
The endoplasmic reticulum (ER) is involved in a variety of essential and interconnected processes in human cells, including
protein biogenesis, signal transduction, and calcium homeostasis. The central player in all these processes is the ER-lumenal
polypeptide chain binding protein BiP that acts as a molecular chaperone. BiP belongs to the heat shock protein 70 (Hsp70)
family and crucially depends on a number of interaction partners, including co-chaperones, nucleotide exchange factors, and
signaling molecules. In the course of the last five years, several diseases have been linked to BiP and its interaction partners,
such as a group of infectious diseases that are caused by Shigella toxin producing E. coli. Furthermore, the inherited diseases Marinesco-Sj?gren syndrome, autosomal dominant polycystic liver disease, Wolcott-Rallison
syndrome, and several cancer types can be considered BiP-related diseases. This review summarizes the physiological and pathophysiological
characteristics of BiP and its interaction partners.
Received 20 November 2008; received after revision 09 December 2008; accepted 12 December 2008 相似文献
519.
Bitter peptides and bitter taste receptors 总被引:1,自引:0,他引:1
Bitter peptides are a structurally diverse group of oligopeptides often generated in fermented, aged, and hydrolyzed food
products that make them unfavorable for consumption. Humans perceive bitterness by a repertoire of 25 human bitter receptors,
termed T2Rs. Knowledge of the structural features of bitter receptors and of the factors that stimulate bitter receptors will
aid in understanding the mechanism responsible for bitter taste perception. This article reviews the current knowledge regarding
structural features of bitter peptides and bitter taste receptors.
Received 24 November 2008; received after revision 11 December 2008; accepted 16 December 2008 相似文献
520.
Apolipoprotein M (apoM) is a novel apolipoprotein found mainly in high-density lipoproteins (HDL). Its function is yet to
be defined. ApoM (25 kDa) has a typical lipocalin ?-barrel fold and a hydrophobic pocket. Retinoids bind apoM but with low
affinity and may not be the natural ligands. ApoM retains its signal peptide, which serves as a hydrophobic anchor to the
lipoproteins. This prevents apoM from being lost in the urine. Approximately 5% of HDL carries an apoM molecule. ApoM in plasma
(1 μM) correlates strongly with both low-density lipoprotein (LDL) and HDL cholesterol, suggesting a link to cholesterol metabolism.
However, in casecontrol studies, apoM levels in patients with coronary heart disease (CHD) and controls were similar, suggesting
apoM levels not to affect the risk for CHD in humans. Experiments in transgenic mice suggested apoM to have antiatherogenic
properties; possible mechanisms include increased formation of pre-? HDL, enhanced cholesterol mobilization from foam cells,
and increased antioxidant properties.
Received 28 November 2008; received after revision 15 December 2008; accepted 16 December 2008 相似文献