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991.
992.
Zhao X. Chen L. Ren Q. Wu Z. Fang S. Jiang Y. Chen Y. Zhong Y. Wang D. Wu J. Zhang G. 《Applied Biochemistry and Microbiology》2021,57(3):344-350
Applied Biochemistry and Microbiology - A pyridine-transforming strain P2 was isolated from sewage collected from Guangzhou oil stain field(China).According to the system analysis, it was... 相似文献
993.
目的研究miR-106a-5p对鼻咽癌细胞SUNE2增殖和迁移的影响。
方法将体外培养的鼻咽癌细胞SUNE2分成对照组(细胞未做任何处理)、Anti-NC组(转染阴性对照抑制剂)、Anti-miR-106a-5p组(转染miR-106a-5p抑制剂)、后期实验另设Anti-miR-106a-5p-inhibitor+si-NC组(转染miR-106a-5p抑制剂、siRNA阴性对照)、Anti-miR-106a-5p-inhibitor+si-PTEN组(转染miR-106a-5p抑制剂、PTEN siRNA),采用Realtime PCR测定miR-106a-5p表达,MTT法检测增殖,Transwell小室检测细胞侵袭和迁移能力变化,用Western blot方法测定vimentin、E-cadherin蛋白表达。在线靶基因预测软件预测miR-106a-5p的靶基因可能为PTEN,双荧光素酶报告系统鉴定miR-106a-5p和PTEN的靶向关系。两组间比较用独立样本t检验,多组间比较采用单因素方差分析,组间两两比较采用LSD-t检验。
结果与正常鼻咽上皮细胞NP69比较,鼻咽癌细胞CNE-2、HK1、SUNE2中miR-106a-5p水平(1.00±0.11比1.84±0.13、2.19±0.14、2.87±0.25)升高,差异具有统计学意义(P < 0.05)。与对照组、Anti-NC组比较,Anti-miR-106a-5p组鼻咽癌细胞miR-106a-5p水平(1.00±0.10、0.99±0.12比0.76±0.08)降低,OD值(0.56±0.05、0.57±0.04比0.32±0.02),细胞侵袭数[(128.47±11.65)个、(129.84±10.93)个比(85.12±6.75)个],迁移数[(182.51±14.81)个、(180.68±17.64)个比(122.01±11.62)个],vimentin蛋白表达水平(0.84±0.09、0.82±0.07比0.30±0.05)降低,E-cadherin蛋白表达水平(0.29±0.04、0.28±0.05比0.76±0.08)升高,差异具有统计学意义(P均< 0.05)。与Anti-miR-106a-inhibitor+si-NC组比较,Anti-miR-106a-inhibitor+si-PTEN组细胞OD值(0.33±0.03比0.52±0.05)、侵袭数[(84.16±5.91)个比(105.79±8.63)个]、迁移数[(118.42±10.25)个比(164.28±12.05)个]、vimentin蛋白表达水平(0.34±0.06比0.68±0.05)均升高,E-cadherin蛋白表达水平(0.72±0.06比0.29±0.05)降低,差异具有统计学意义(P均< 0.05)。
结论miR-106a-5p可通过靶向调控PTEN抑制鼻咽癌细胞SUNE2增殖和迁移潜能。 相似文献
994.
Holcombe Sven A. Agnew Amanda M. Derstine Brian Wang Stewart C. 《Biomechanics and modeling in mechanobiology》2020,19(6):2227-2239
Biomechanics and Modeling in Mechanobiology - Finite element human body models (HBMs) are used to assess injury risk in a variety of impact scenarios. The ribs are a key structural component within... 相似文献
995.
Chloroplasts are bounded by a pair of outer membranes, the envelope, that is the only permanent membrane structure of the
different types of plastids. Chloroplasts have had a long and complex evolutionary past and integration of the envelope membranes
in cellular functions is the result of this evolution. Plastid envelope membranes contain a wide diversity of lipids and terpenoid
compounds serving numerous biochemical functions and the flexibility of their biosynthetic pathways allow plants to adapt
to fluctuating environmental conditions (for instance phosphate deprivation). A large body of knowledge has been generated
by proteomic studies targeted to envelope membranes, thus revealing an unexpected complexity of this membrane system. For
instance, new transport systems for metabolites and ions have been identified in envelope membranes and new routes for the
import of chloroplast-specific proteins have been identified. The picture emerging from our present understanding of plastid
envelope membranes is that of a key player in plastid biogenesis and the co-ordinated gene expression of plastid-specific
protein (owing to chlorophyll precursors), of a major hub for integration of metabolic and ionic networks in cell metabolism,
of a flexible system that can divide, produce dynamic extensions and interact with other cell constituents. Envelope membranes
are indeed one of the most complex and dynamic system within a plant cell. In this review, we present an overview of envelope
constituents together with recent insights into the major functions fulfilled by envelope membranes and their dynamics within
plant cells.
Special Issue of Photosynthesis Research in honor of Andrew A. Benson. 相似文献
996.
During 30-months of storage at 4°C, potato (Solanum tuberosum L.) tubers progressively lose the ability to produce superoxide in response to wounding, resist microbial infection, and
develop a suberized wound periderm. Using differentially aged tubers, we demonstrate that Strboh A is responsible for the wound-induced oxidative burst in potato and aging attenuates its expression. In vivo superoxide production
and NADPH oxidase (NOX) activity from 1-month-old tubers increased to a maximum 18–24 h after wounding and then decreased
to barely detectable levels by 72 h. Wounding also induced a 68% increase in microsomal protein within 18 h. These wound-induced
responses were lost over a 25- to 30-month storage period. Superoxide production and NOX activity were inhibited by diphenylene
iodonium chloride, a specific inhibitor of NOX, which in turn effectively inhibited wound-healing and increased susceptibility
to microbial infection and decay in 1-month-old tubers. Wound-induced superoxide production was also inhibited by EGTA-mediated
destabilization of membranes. The ability to restore superoxide production to EGTA-treated tissue with Ca+2 declined with advancing tuber age, likely a consequence of age-related changes in membrane architecture. Of the five homologues
of NOX (Strboh A-D and F), wounding induced the expression of Strboh A in 6-month-old tubers but this response was absent in tubers stored for 25–30 months. Strboh
A thus mediates the initial burst of superoxide in response to wounding of potato tubers; loss of its expression increases
the susceptibility to microbial infection and contributes to the age-induced loss of wound-healing ability. 相似文献
997.
Simulation and experiment have been used to establish that significant artifacts can be generated in X-pulse CPMG relaxation dispersion experiments recorded on heteronuclear ABX spin-systems, such as 13C
i
–13C
j
–1H, where 13C
i
and 13C
j
are strongly coupled. A qualitative explanation of the origin of these artifacts is presented along with a simple method
to significantly reduce them. An application to the measurement of 1H CPMG relaxation dispersion profiles in an HIV-2 TAR RNA molecule where all ribose sugars are protonated at the 2′ position,
deuterated at all other sugar positions and 13C labeled at all sugar carbons is presented to illustrate the problems that strong 13C–13C coupling introduces and a simple solution is proposed. 相似文献
998.
Herr I Gassler N Friess H Büchler MW 《Apoptosis : an international journal on programmed cell death》2007,12(2):271-291
More than a quarter of a century ago, the phenomenon of glucocorticoid-induced apoptosis in the majority of hematological
cells was first recognized. More recently, glucocorticoid-induced antiapoptotic signaling associated with apoptosis resistance
has been identified in cells of epithelial origin, most of malignant solid tumors and some other tissues. Despite these huge
amount of data demonstrating differential pro- and anti-apoptotic effects of glucocortioids, the underlying mechanisms of
cell type specific glucocorticoid signaling are just beginning to be described. This review summarizes our present understanding
of cell type-specific pro- and anti-apoptotic signaling induced by glucocorticoids. In the first section we give a summary
and update of known glucocorticoid-induced pathways mediating apoptosis in hematological cells. We shortly introduce mechanisms
of glucocorticoid resistance of hematological cells. We highlight and discuss the emerging molecular evidence of a general
induction of survival signaling in epithelial cells and carcinoma cells by glucocorticoids. We provide a model for glucocorticoid-induced
resistance in cells growing in a tissue formation. Thus, attachment to the extracellular matrix and cell-cell contacts typical
for e.g. epithelial and tumor cells may be crucially involved in switching the balance of several interacting pathways to
survival upon treatment with glucocorticoids. 相似文献
999.
Pectinase was immobilized on a sodium alginate support using glutaraldehyde and retained 66% activity. The optimal pH for
activity shifted from 3.0 to 3.5 after immobilization; however, the optimum temperature remained unchanged at 40°C. The immobilized
enzyme also had a higher thermal stability and reusability than the free enzyme, and retained 80% of initial activity after
11 batch reactions. 相似文献
1000.