全文获取类型
收费全文 | 31351篇 |
免费 | 48篇 |
国内免费 | 68篇 |
专业分类
系统科学 | 154篇 |
丛书文集 | 717篇 |
教育与普及 | 79篇 |
理论与方法论 | 200篇 |
现状及发展 | 13501篇 |
研究方法 | 1347篇 |
综合类 | 15100篇 |
自然研究 | 369篇 |
出版年
2013年 | 174篇 |
2012年 | 419篇 |
2011年 | 832篇 |
2010年 | 180篇 |
2008年 | 552篇 |
2007年 | 539篇 |
2006年 | 596篇 |
2005年 | 591篇 |
2004年 | 517篇 |
2003年 | 567篇 |
2002年 | 566篇 |
2001年 | 978篇 |
2000年 | 896篇 |
1999年 | 598篇 |
1992年 | 569篇 |
1991年 | 462篇 |
1990年 | 486篇 |
1989年 | 489篇 |
1988年 | 490篇 |
1987年 | 498篇 |
1986年 | 490篇 |
1985年 | 599篇 |
1984年 | 494篇 |
1983年 | 404篇 |
1982年 | 346篇 |
1981年 | 340篇 |
1980年 | 448篇 |
1979年 | 967篇 |
1978年 | 855篇 |
1977年 | 846篇 |
1976年 | 580篇 |
1975年 | 630篇 |
1974年 | 931篇 |
1973年 | 785篇 |
1972年 | 804篇 |
1971年 | 1017篇 |
1970年 | 1339篇 |
1969年 | 1004篇 |
1968年 | 945篇 |
1967年 | 988篇 |
1966年 | 829篇 |
1965年 | 609篇 |
1964年 | 148篇 |
1959年 | 360篇 |
1958年 | 522篇 |
1957年 | 443篇 |
1956年 | 366篇 |
1955年 | 316篇 |
1954年 | 363篇 |
1948年 | 193篇 |
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
901.
Hazan J Fonknechten N Mavel D Paternotte C Samson D Artiguenave F Davoine CS Cruaud C Dürr A Wincker P Brottier P Cattolico L Barbe V Burgunder JM Prud'homme JF Brice A Fontaine B Heilig B Weissenbach J 《Nature genetics》1999,23(3):296-303
Autosomal dominant hereditary spastic paraplegia (AD-HSP) is a genetically heterogeneous neurodegenerative disorder characterized by progressive spasticity of the lower limbs. Among the four loci causing AD-HSP identified so far, the SPG4 locus at chromosome 2p2-1p22 has been shown to account for 40-50% of all AD-HSP families. Using a positional cloning strategy based on obtaining sequence of the entire SPG4 interval, we identified a candidate gene encoding a new member of the AAA protein family, which we named spastin. Sequence analysis of this gene in seven SPG4-linked pedigrees revealed several DNA modifications, including missense, nonsense and splice-site mutations. Both SPG4 and its mouse orthologue were shown to be expressed early and ubiquitously in fetal and adult tissues. The sequence homologies and putative subcellular localization of spastin suggest that this ATPase is involved in the assembly or function of nuclear protein complexes. 相似文献
902.
Many hormones and neurotransmitters evoke Ca2+ release from intracellular stores, often triggering agonist-specific signatures of intracellular Ca2+ concentration. Inositol trisphosphate (InsP3) and cyclic adenosine 5'-diphosphate-ribose (cADPR) are established Ca2+-mobilizing messengers that activate Ca2+ release through intracellular InsP3 and ryanodine receptors, respectively. However, in pancreatic acinar cells, neither messenger can explain the complex pattern of Ca2+ signals triggered by the secretory hormone cholecystokinin (CCK). We show here that the Ca2+-mobilizing molecule nicotinic acid adenine dinucleotide phosphate (NAADP), an endogenous metabolite of beta-NADP, triggers a Ca2+ response that varies from short-lasting Ca2+ spikes to a complex mixture of short-lasting (1-2s) and long-lasting (0.2-1 min) Ca2+ spikes. Cells were significantly more sensitive to NAADP than to either cADPR or InsP3, whereas higher concentrations of NAADP selectively inactivated CCK-evoked Ca2+ signals in pancreatic acinar cells, indicating that NAADP may function as an intracellular messenger in mammalian cells. 相似文献
903.
Cytotoxic T-cell immunity to virus-infected non-haematopoietic cells requires presentation of exogenous antigen 总被引:16,自引:0,他引:16
Cytotoxic T lymphocytes (CTLs) are thought to detect viral infections by monitoring the surface of all cells for the presence of viral peptides bound to major histocompatibility complex (MHC) class I molecules. In most cells, peptides presented by MHC class I molecules are derived exclusively from proteins synthesized by the antigen-bearing cells. Macrophages and dendritic cells also have an alternative MHC class I pathway that can present peptides derived from extracellular antigens; however, the physiological role of this process is unclear. Here we show that virally infected non-haematopoietic cells are unable to stimulate primary CTL-mediated immunity directly. Instead, bone-marrow-derived cells are required as antigen-presenting cells (APCs) to initiate anti-viral CTL responses. In these APCs, the alternative (exogenous) MHC class I pathway is the obligatory mechanism for the initiation of CTL responses to viruses that infect only non-haematopoietic cells. 相似文献
904.
A spelling device for the paralysed 总被引:29,自引:0,他引:29
Birbaumer N Ghanayim N Hinterberger T Iversen I Kotchoubey B Kübler A Perelmouter J Taub E Flor H 《Nature》1999,398(6725):297-298
905.
Molecular basis of triclosan activity 总被引:19,自引:0,他引:19
Levy CW Roujeinikova A Sedelnikova S Baker PJ Stuitje AR Slabas AR Rice DW Rafferty JB 《Nature》1999,398(6726):383-384
906.
A capsaicin-receptor homologue with a high threshold for noxious heat 总被引:60,自引:0,他引:60
907.
Trans-gender induction of hair follicles 总被引:24,自引:0,他引:24
908.
909.
Glucose/galactose malabsorption (GGM) is an autosomal recessive disease manifesting within the first weeks of life and characterized by a selective failure to absorb dietary glucose and galactose from the intestine. The consequent severe diarrhoea and dehydration are usually fatal unless these sugars are eliminated from the diet. Intestinal biopsies of GGM patients have revealed a specific defect in Na(+)-dependent absorption of glucose in the brush border. Normal glucose absorption is mediated by the Na+/glucose cotransporter in the brush border membrane of the intestinal epithelium. Cellular influx is driven by the transmembrane Na+ electrochemical potential gradient; thereafter the sugar moves to the blood across the basolateral membrane via the facilitated glucose carrier. We have previously cloned and sequenced a Na+/glucose cotransporter from normal human ileum and shown that this gene, SGLT1, resides on the distal q arm of chromosome 22. We have now amplified SGLT1 complementary DNA and genomic DNA from members of a family affected with GGM by the polymerase chain reaction. Sequence analysis of the amplified products has revealed a single missense mutation in SGLT1 which cosegregates with the GGM phenotype and results in a complete loss of Na(+)-dependent glucose transport in Xenopus oocytes injected with this complementary RNA. 相似文献
910.
Viable metacyclic forms of T. cruzi, Y strain, treated with an adequate dose of actinomycin D (50 micrograms Act-D/ml/10(7) parasites/ml for 72 h at 28 degrees C) showed the following properties: 1) they lost their ability to replicate in culture medium, in blood and in tissues of normal mice and were no longer able to incorporate tritiated thymidine; 2) they could not penetrate into Vero cells and could not replicate inside normal macrophages; 3) they retained their immunogenicity and the ability to protect mice against a virulent infection; 4) they did not induce histological lesions as described in chronic experimental Chagas' disease. 相似文献