全文获取类型
收费全文 | 31559篇 |
免费 | 89篇 |
国内免费 | 135篇 |
专业分类
系统科学 | 319篇 |
丛书文集 | 558篇 |
教育与普及 | 78篇 |
理论与方法论 | 90篇 |
现状及发展 | 14247篇 |
研究方法 | 1282篇 |
综合类 | 14880篇 |
自然研究 | 329篇 |
出版年
2013年 | 187篇 |
2012年 | 423篇 |
2011年 | 773篇 |
2010年 | 189篇 |
2008年 | 536篇 |
2007年 | 644篇 |
2006年 | 592篇 |
2005年 | 594篇 |
2004年 | 541篇 |
2003年 | 608篇 |
2002年 | 511篇 |
2001年 | 1079篇 |
2000年 | 1069篇 |
1999年 | 626篇 |
1994年 | 366篇 |
1992年 | 613篇 |
1991年 | 455篇 |
1990年 | 554篇 |
1989年 | 495篇 |
1988年 | 452篇 |
1987年 | 518篇 |
1986年 | 529篇 |
1985年 | 639篇 |
1984年 | 466篇 |
1983年 | 429篇 |
1982年 | 397篇 |
1981年 | 429篇 |
1980年 | 440篇 |
1979年 | 1064篇 |
1978年 | 819篇 |
1977年 | 788篇 |
1976年 | 642篇 |
1975年 | 666篇 |
1974年 | 934篇 |
1973年 | 795篇 |
1972年 | 719篇 |
1971年 | 862篇 |
1970年 | 1135篇 |
1969年 | 946篇 |
1968年 | 888篇 |
1967年 | 880篇 |
1966年 | 775篇 |
1965年 | 569篇 |
1959年 | 325篇 |
1958年 | 505篇 |
1957年 | 340篇 |
1956年 | 313篇 |
1955年 | 292篇 |
1954年 | 288篇 |
1948年 | 199篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
The involvement of the renin-angiotensin system in the regulation of cell proliferation in the rat endometrium 总被引:1,自引:0,他引:1
Oestrogens are known to enhance angiotensin biosynthesis by increasing the elaboration of its precursor, angiotensinogen.
On the other hand, we found that inhibition of angiotensin-converting enzyme (ACE) suppressed the proliferative response of
the rat anterior pituitary gland to oestrogens. To answer the question whether the angiotensin system is involved in the control
of the cell proliferation of the uterine epithelium, the effects of an ACE inhibitor, enalapril maleate, and of angiotensins
II and IV, alone or together with losartan, an antagonist of angiotensin receptor type 1 (AT1), on endometrial epithelial
cell proliferation have been studied. The experiments were performed on ovariectomized female Wistar rats. In the first experiment
the animals were injected with a single dose of oestradiol benzoate or received an injection of solvent only. Half of the
oestrogen-treated rats were injected additionally with enalapril maleate (EN, twice daily). The incorporation of bromodeoxyuridine
(BrDU) into endometrial cell nuclei was used as an index of cell proliferation. It was found that oestradiol alone dramatically
increased the BrDU labelling index (LI) of endometrial cell nuclei, and this effect was partially blocked by the simultaneous
treatment with EN. In the second experiment, the animals were injected intraperitoneally with angiotensin II (AII), angiotensin
IV (AIV) or saline, alone or together with losartan. It was found that AIV induced an increase in the LI in uterine epithelium,
and this effect was not blocked by the simultaneous treatment with losartan. The increase in LI in uterine epithelium was
also observed in the rats treated with AII and with losartan. These findings suggest an involvement of angiotensin IV in the
control of uterine epithelium cell proliferation.
Received 12 October 1998; received after revision 6 January 1999; accepted 2 February 1999 相似文献
992.
Cell surface heparan sulfate proteoglycans are involved in several aspects of the lipoprotein metabolism. Most of the biological activities of these proteoglycans are mediated via interactions of their heparan sulfate moieties with various protein ligands, including lipoproteins and lipases. The binding of lipoproteins to heparan sulfate is largely determined by their apoprotein composition, and apoproteins B and E display the highest affinity for heparan sulfate. Interactions of lipoproteins with heparan sulfate are important for the cellular uptake and turnover of lipoproteins, in part by enhancing the accessibility of lipoproteins to lipoprotein receptors and lipases. Apoprotein B may interact with receptors without involving heparan sulfate. Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease. Heparan sulfate thus binds and regulates the activity of growth factors, cytokines, superoxide dismutase and antithrombin, which contribute to aberrant cell proliferation, migration and matrix production, scavenging of reactive oxygen radicals and thrombosis. In this review we discuss the various roles of heparan sulfate proteoglycans in vascular biology, with emphasis on interactions of heparan sulfate with lipoproteins and lipases and the molecular basis of such interactions. 相似文献
993.
Glycine: a new anti-inflammatory immunonutrient 总被引:7,自引:0,他引:7
994.
The Pendred syndrome gene encodes a chloride-iodide transport protein 总被引:24,自引:0,他引:24
Pendred syndrome is the most common form of syndromic deafness and characterized by congenital sensorineural hearing loss and goitre. This disorder was mapped to chromosome 7 and the gene causing Pendred syndrome (PDS) was subsequently identified by positional cloning. PDS encodes a putative transmembrane protein designated pendrin. Pendrin is closely related to a family of sulfate transport proteins that includes the rat sulfate-anion transporter (encoded by Sat-1; 29% amino acid sequence identity), the human diastrophic dysplasia sulfate transporter (encoded by DTD; 32%) and the human sulfate transporter 'downregulated in adenoma' (encoded by DRA; 45%). On the basis of this homology and the presence of a slightly modified sulfate-transporter signature sequence comprising its putative second transmembrane domain, pendrin has been proposed to function as a sulfate transporter. We were unable to detect evidence of sulfate transport following the expression of pendrin in Xenopus laevis oocytes by microinjection of PDS cRNA or in Sf9 cells following infection with PDS-recombinant baculovirus. The rates of transport for iodide and chloride were significantly increased following the expression of pendrin in both cell systems. Our results demonstrate that pendrin functions as a transporter of chloride and iodide, but not sulfate, and may provide insight into thyroid physiology and the pathophysiology of Pendred syndrome. 相似文献
995.
Jansen G Thijssen KL Werner P van der Horst M Hazendonk E Plasterk RH 《Nature genetics》1999,21(4):414-419
Caenorhabditis elegans is the first animal whose genomic sequence has been determined. One of the new possibilities in post-sequence genetics is the analysis of complete gene families at once. We studied the family of heterotrimeric G proteins. C. elegans has 20 Galpha, 2 Gbeta and 2 Ggamma genes. There is 1 homologue of each of the 4 mammalian classes of Galpha genes, G(i)/G(o)alpha, G(s)alpha , G(q)alpha and G12alpha, and there are 16 new alpha genes. Although the conserved Galpha subunits are expressed in many neurons and muscle cells, GFP fusions indicate that 14 new Galpha genes are expressed almost exclusively in a small subset of the chemosensory neurons of C. elegans. We generated loss-of-function alleles using target-selected gene inactivation. None of the amphid-expressed genes are essential for viability, and only four show any detectable phenotype (chemotaxis defects), suggesting extensive functional redundancy. On the basis of functional analysis, the 20 genes encoding Galpha proteins can be divided into two groups: those that encode subunits affecting muscle activity (homologues of G(i)/G(o)alpha, G(s)alpha and G(q)), and those (14 new genes) that encode proteins most likely involved in perception. 相似文献
996.
997.
Molecular cloning and sequence analysis of myosin genes from Arabidopsis thaliana and electron microscopic observation of a myosin from characean alga have revealed that overall structure of plant unconventional
myosins is similar to that of the class V myosins. These plant unconventional myosins have two heads, a coiled-coil tail of
varied length and a globular tail piece at the end. The tail piece is probably a site for membrane interaction. Characean
myosin is of special interest because it can translocate actin filaments at a velocity several times faster than muscle myosin,
which must have evolved to support the quick movement of animals in the struggle for their lives. 相似文献
998.
Genomic instability in Gadd45a-deficient mice. 总被引:19,自引:0,他引:19
M C Hollander M S Sheikh D V Bulavin K Lundgren L Augeri-Henmueller R Shehee T A Molinaro K E Kim E Tolosa J D Ashwell M P Rosenberg Q Zhan P M Fernández-Salguero W F Morgan C X Deng A J Fornace 《Nature genetics》1999,23(2):176-184
Gadd45a-null mice generated by gene targeting exhibited several of the phenotypes characteristic of p53-deficient mice, including genomic instability, increased radiation carcinogenesis and a low frequency of exencephaly. Genomic instability was exemplified by aneuploidy, chromosome aberrations, gene amplification and centrosome amplification, and was accompanied by abnormalities in mitosis, cytokinesis and growth control. Unequal segregation of chromosomes due to multiple spindle poles during mitosis occurred in several Gadd45a -/- cell lineages and may contribute to the aneuploidy. Our results indicate that Gadd45a is one component of the p53 pathway that contributes to the maintenance of genomic stability. 相似文献
999.
1000.
CACP, encoding a secreted proteoglycan, is mutated in camptodactyly-arthropathy-coxa vara-pericarditis syndrome. 总被引:3,自引:0,他引:3
J Marcelino J D Carpten W M Suwairi O M Gutierrez S Schwartz C Robbins R Sood I Makalowska A Baxevanis B Johnstone R M Laxer L Zemel C A Kim J K Herd J Ihle C Williams M Johnson V Raman L G Alonso D Brunoni A Gerstein N Papadopoulos S A Bahabri J M Trent M L Warman 《Nature genetics》1999,23(3):319-322
Altered growth and function of synoviocytes, the intimal cells which line joint cavities and tendon sheaths, occur in a number of skeletal diseases. Hyperplasia of synoviocytes is found in both rheumatoid arthritis and osteoarthritis, despite differences in the underlying aetiologies of the two disorders. We have studied the autosomal recessive disorder camptodactyly-arthropathy-coxa vara-pericarditis syndrome (CACP; MIM 208250) to identify biological pathways that lead to synoviocyte hyperplasia, the principal pathological feature of this syndrome. Using a positional-candidate approach, we identified mutations in a gene (CACP) encoding a secreted proteoglycan as the cause of CACP. The CACP protein, which has previously been identified as both 'megakaryocyte stimulating factor precursor' and 'superficial zone protein', contains domains that have homology to somatomedin B, heparin-binding proteins, mucins and haemopexins. In addition to expression in joint synovium and cartilage, CACP is expressed in non-skeletal tissues including liver and pericardium. The similarity of CACP sequence to that of other protein families and the expression of CACP in non-skeletal tissues suggest it may have diverse biological activities. 相似文献