全文获取类型
收费全文 | 15528篇 |
免费 | 1009篇 |
国内免费 | 1314篇 |
出版年
2024年 | 24篇 |
2023年 | 267篇 |
2022年 | 257篇 |
2021年 | 502篇 |
2020年 | 435篇 |
2019年 | 524篇 |
2018年 | 403篇 |
2017年 | 436篇 |
2016年 | 519篇 |
2015年 | 569篇 |
2014年 | 737篇 |
2013年 | 905篇 |
2012年 | 546篇 |
2011年 | 644篇 |
2010年 | 560篇 |
2009年 | 700篇 |
2008年 | 753篇 |
2007年 | 846篇 |
2006年 | 715篇 |
2005年 | 676篇 |
2004年 | 652篇 |
2003年 | 571篇 |
2002年 | 508篇 |
2001年 | 421篇 |
2000年 | 422篇 |
1999年 | 371篇 |
1998年 | 410篇 |
1997年 | 319篇 |
1996年 | 339篇 |
1995年 | 300篇 |
1994年 | 247篇 |
1993年 | 229篇 |
1992年 | 246篇 |
1991年 | 219篇 |
1990年 | 176篇 |
1989年 | 173篇 |
1988年 | 142篇 |
1987年 | 119篇 |
1986年 | 107篇 |
1985年 | 146篇 |
1984年 | 113篇 |
1983年 | 74篇 |
1982年 | 107篇 |
1981年 | 93篇 |
1980年 | 66篇 |
1979年 | 72篇 |
1978年 | 55篇 |
1977年 | 41篇 |
1976年 | 26篇 |
1973年 | 22篇 |
排序方式: 共有10000条查询结果,搜索用时 22 毫秒
971.
Passport data for Mexico’s Guanajuato State were used to locate the sites where maize was collected in the 1940s and 1950s
in an effort to document and conserve diversity. A map presenting survey points illustrates that collections have occurred
repeatedly in the same locations. Observations of these locations reveal that urbanization and industrialization, not high
yielding varieties, are displacing traditional varieties. Non-linear principal components analysis was used to assess associations
between variables in areas where maize persists. Landraces appear to be associated with mountains and mesas, mixed cropping,
little or no access to irrigation and areas classified as having low agricultural capacity; conversely, landraces have more
commonly been replaced in areas of high agricultural capacity. The areas of high agriculture capacity, located in the riparian
areas and plains, also have been the easiest to develop for urban and industrial use. Increasingly high rates of urbanization
and development in areas of high agriculture capacity will impede the conservation of crop diversity in these areas. 相似文献
972.
In vivo genetic ablation of the periotic mesoderm affects cell proliferation survival and differentiation in the cochlea 总被引:1,自引:0,他引:1
Tbx1 is required for ear development in humans and mice. Gene manipulation in the mouse has discovered multiple consequences of loss of function on early development of the inner ear, some of which are attributable to a cell autonomous role in maintaining cell proliferation of epithelial progenitors of the cochlear and vestibular apparata. However, ablation of the mesodermal domain of the gene also results in severe but more restricted abnormalities. Here we show that Tbx1 has a dynamic expression during late development of the ear, in particular, is expressed in the sensory epithelium of the vestibular organs but not of the cochlea. Vice versa, it is expressed in the condensed mesenchyme that surrounds the cochlea but not in the one that surrounds the vestibule. Loss of Tbx1 in the mesoderm disrupts this peri-cochlear capsule by strongly reducing the proliferation of mesenchymal cells. The organogenesis of the cochlea, which normally occurs inside the capsule, was dramatically affected in terms of growth of the organ, as well as proliferation, differentiation and survival of its epithelial cells. This model provides a striking demonstration of the essential role played by the periotic mesenchyme in the organogenesis of the cochlea. 相似文献
973.
While recent work has implicated Tbx20 in myocardial maturation and proliferation, the role of Tbx20 in heart valve development remains relatively unknown. Tbx20 expression was manipulated in primary avian endocardial cells in order to elucidate its function in developing endocardial cushions. Tbx20 gain of function was achieved with a Tbx20-adenovirus, and endogenous Tbx20 expression was inhibited with Tbx20-specific siRNA in cultured endocardial cushion cells. With Tbx20 gain of function, the expression of chondroitin sulfate proteoglycans (CSPG), including aggrecan and versican, was decreased, while the expression of the matrix metalloproteinases (MMP) mmp9 and mmp13 was increased. Consistent results were observed with Tbx20 loss of function, where the expression of CSPG genes increased and MMP genes decreased. In addition, cushion mesenchyme proliferation increased with infection of a Tbx20-adenovirus and decreased with transfection of Tbx20-specfic siRNA. Furthermore, BMP2 treatment resulted in increased Tbx20 expression in endocardial cushion cells, and loss of Tbx20 led to increased Tbx2 and decreased N-myc gene expression. Taken together, these data support a role for Tbx20 in repressing extracellular matrix remodeling and promoting cell proliferation in mesenchymal valve precursor populations in endocardial cushions during embryonic development. 相似文献
974.
Basak S Raju K Babiarz J Kane-Goldsmith N Koticha D Grumet M 《Developmental biology》2007,311(2):408-422
The cell adhesion molecule neurofascin (NF) has a major neuronal isoform (NF186) containing a mucin-like domain followed by a fifth fibronectin type III repeat while these domains are absent from glial NF155. Neuronal NF isoforms lacking one or both of these domains are expressed transiently in embryonic dorsal root ganglia (DRG). These two domains are co-expressed in mature NF186, which peaks in expression prior to birth and then persists almost exclusively at nodes of Ranvier on myelinated axons. In contrast, glial NF155 is only detected postnatally with the onset of myelination. All these forms of NF bound homophilically and to Schwann cells but only the mature NF186 isoform inhibits cell adhesion, and this activity may be important in formation of the node of Ranvier. Schwann cells deficient in NF155 myelinated DRG axons in a delayed manner and they showed significantly decreased clustering of both NF and Caspr in regions where paranodes normally form. The combined results suggest that NF186 is expressed prenatally on DRG neurons and it may modulate their adhesive interactions with Schwann cells, which express NF155 postnatally and require it for development of axon-glial paranodal junctions. 相似文献
975.
976.
977.
During craniofacial development, Meckel's cartilage and the mandible bone derive from the first branchial arch, and their development depends upon the contribution of cranial neural crest (CNC) cells. We previously demonstrated that conditional inactivation of Tgfbr2 in the neural crest of mice (Tgfbr2fl/fl;Wnt1-Cre) results in severe defects in mandibular development, although the specific cellular and molecular mechanisms by which TGF-β signaling regulates the fate of CNC cells during mandibular development remain unknown. We show here that loss of Tgfbr2 does not affect the migration of CNC cells during mandibular development. TGF-β signaling is specifically required for cell proliferation in Meckel's cartilage and the mandibular anlagen and for the formation of the coronoid, condyle and angular processes. TGF-β-mediated connective tissue growth factor (CTGF) signaling is critical for CNC cell proliferation. Exogenous CTGF rescues the cell proliferation defect in Meckel's cartilage of Tgfbr2fl/fl;Wnt1-Cre mutants, demonstrating the biological significance of this signaling cascade in chondrogenesis during mandibular development. Furthermore, TGF-β signaling controls Msx1 expression to regulate mandibular osteogenesis as Msx1 expression is significantly reduced in Tgfbr2fl/fl;Wnt1-Cre mutants. Collectively, our data suggest that there are differential signal cascades in response to TGF-β to control chondrogenesis and osteogenesis during mandibular development. 相似文献
978.
FGF9 regulates early hypertrophic chondrocyte differentiation and skeletal vascularization in the developing stylopod 总被引:1,自引:0,他引:1
Gain-of-function mutations in fibroblast growth factor (FGF) receptors result in chondrodysplasia and craniosynostosis syndromes, highlighting the critical role for FGF signaling in skeletal development. Although the FGFRs involved in skeletal development have been well characterized, only a single FGF ligand, FGF18, has been identified that regulates skeletal development during embryogenesis. Here we identify Fgf9 as a second FGF ligand that is critical for skeletal development. We show that Fgf9 is expressed in the proximity of developing skeletal elements and that Fgf9-deficient mice exhibit rhizomelia (a disproportionate shortening of proximal skeletal elements), which is a prominent feature of patients with FGFR3-induced chondrodysplasia syndromes. Although Fgf9 is expressed in the apical ectodermal ridge in the limb bud, we demonstrate that the Fgf9-/- limb phenotype results from loss of FGF9 functions after formation of the mesenchymal condensation. In developing stylopod elements, FGF9 promotes chondrocyte hypertrophy at early stages and regulates vascularization of the growth plate and osteogenesis at later stages of skeletal development. 相似文献
979.
980.
Laminin alpha5 is necessary for submandibular gland epithelial morphogenesis and influences FGFR expression through beta1 integrin signaling 总被引:3,自引:0,他引:3
Rebustini IT Patel VN Stewart JS Layvey A Georges-Labouesse E Miner JH Hoffman MP 《Developmental biology》2007,308(1):15-29
Laminin alpha chains have unique spatiotemporal expression patterns during development and defining their function is necessary to understand the regulation of epithelial morphogenesis. We investigated the function of laminin alpha5 in mouse submandibular glands (SMGs). Lama5(-/-) SMGs have a striking phenotype: epithelial clefting is delayed, although proliferation occurs; there is decreased FGFR1b and FGFR2b, but no difference in Lama1 expression; later in development, epithelial cell organization and lumen formation are disrupted. In wild-type SMGs alpha5 and alpha1 are present in epithelial clefts but as branching begins alpha5 expression increases while alpha1 decreases. Lama5 siRNA decreased branching, p42 MAPK phosphorylation, and FGFR expression, and branching was rescued by FGF10. FGFR siRNA decreased Lama5 suggesting that FGFR signaling provides positive feedback for Lama5 expression. Anti-beta1 integrin antibodies decreased FGFR and Lama5 expression, suggesting that beta1 integrin signaling provides positive feedback for Lama5 and FGFR expression. Interestingly, the Itga3(-/-):Itga6(-/-) SMGs have a similar phenotype to Lama5(-/-). Our findings suggest that laminin alpha5 controls SMG epithelial morphogenesis through beta1 integrin signaling by regulating FGFR expression, which also reciprocally regulates the expression of Lama5. These data link changes in basement membrane composition during branching morphogenesis with FGFR expression and signaling. 相似文献