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171.
Hiramani Dhungana Tarja Malm Adam Denes Piia Valonen Sara Wojciechowski Johanna Magga Ekaterina Savchenko Neil Humphreys Richard Grencis Nancy Rothwell Jari Koistinaho 《Aging cell》2013,12(5):842-850
Ischemic stroke is confounded by conditions such as atherosclerosis, diabetes, and infection, all of which alter peripheral inflammatory processes with concomitant impact on stroke outcome. The majority of the stroke patients are elderly, but the impact of interactions between aging and inflammation on stroke remains unknown. We thus investigated the influence of age on the outcome of stroke in animals predisposed to systemic chronic infection. Th1‐polarized chronic systemic infection was induced in 18–22 month and 4‐month‐old C57BL/6j mice by administration of Trichuris muris (gut parasite). One month after infection, mice underwent permanent middle cerebral artery occlusion and infarct size, brain gliosis, and brain and plasma cytokine profiles were analyzed. Chronic infection increased the infarct size in aged but not in young mice at 24 h. Aged, ischemic mice showed altered plasma and brain cytokine responses, while the lesion size correlated with plasma prestroke levels of RANTES. Moreover, the old, infected mice exhibited significantly increased neutrophil recruitment and upregulation of both plasma interleukin‐17α and tumor necrosis factor‐α levels. Neither age nor infection status alone or in combination altered the ischemia‐induced brain microgliosis. Our results show that chronic peripheral infection in aged animals renders the brain more vulnerable to ischemic insults, possibly by increasing the invasion of neutrophils and altering the inflammation status in the blood and brain. Understanding the interactions between age and infections is crucial for developing a better therapeutic regimen for ischemic stroke and when modeling it as a disease of the elderly. 相似文献
172.
173.
D. Friedecký P. Bednář M. Procházka T. Adam 《Nucleosides, nucleotides & nucleic acids》2013,32(9-11):1233-1236
A pilot study using capillary electrophoresis with mass spectrometry for the analysis of nucleotides in human erythrocytes is presented. Erythrocytes were incubated with 5-amino-4-imidazolecarboxamide riboside in order to mimic situation in defect of purine metabolism—AICA-ribosiduria. Characteristic AICA-ribotides together with normal nucleotides were separated by capillary electrophoresis in acetate buffer (20 mmol/L, pH 4.4) and identified on line by mass spectrometry. 相似文献
174.
Annika Kers Inger Kers Adam Kraszewski Michal Sobkowski Tomas Szabó Mats Thelin ¶ 《Nucleosides, nucleotides & nucleic acids》2013,32(1-3):361-378
Abstract In this paper a short account of our recent research concerning development of new synthetic methods and new reagents for the preparation of DNA and RNA fragments and their analogues is given. 相似文献
175.
Michal Sobkowski Jadwiga Jankowska Adam Kraszewski Jacek Stawinski 《Nucleosides, nucleotides & nucleic acids》2013,32(10-12):1469-1484
Sixteen diribonucleoside (3′-5′)-H-phosphonates were synthesized via condensation of the protected ribonucleoside 3′-H-phosphonates with nucleosides, and the influence of a nucleoside sequence on the observed stereoselectivity was analyzed. 31P NMR spectroscopy was used to evaluate a relationship between chemical shift and absolute configuration at the phosphorous center of the H-phosphonate diesters as well as of the corresponding phosphorothioate diesters. Although for the most cases such correlation was found, there was however several exceptions to the rule where the relative positions of resonances arising from R P and S P diastereomers were reversed. 相似文献
176.
Simone Kreutmayer Adam Csordas Jan Kern Viola Maass Giovanni Almanzar Martin Offterdinger Robert Öllinger Matthias Maass Georg Wick 《Cell stress & chaperones》2013,18(3):259-268
We identified increased expression and redistribution of the intracellular protein 60-kDa human heat shock protein (hHSP60) (HSPD1) to the cell surface in human endothelial cells subjected to classical atherosclerosis risk factors and subsequent immunologic cross-reactivity against this highly conserved molecule, as key events occurring early in the process of atherosclerosis. The present study aimed at investigating the role of infectious pathogens as stress factors for vascular endothelial cells and, as such, contributors to early atherosclerotic lesion formation. Using primary donor-matched arterial and venous human endothelial cells, we show that infection with Chlamydia pneumoniae leads to marked upregulation and surface expression of hHSP60 and adhesion molecules. Moreover, we provide evidence for an increased susceptibility of arterial endothelial cells for redistribution of hHSP60 to the cellular membrane in response to C. pneumoniae infection as compared to autologous venous endothelial cells. We also show that oxidative stress has a central role to play in endothelial cell activation in response to chlamydial infection. These data provide evidence for a role of C. pneumoniae as a potent primary endothelial stressor for arterial endothelial cells leading to enrichment of hHSP60 on the cellular membrane and, as such, a potential initiator of atherosclerosis. 相似文献
177.
J. Adam Langley Thomas J. Mozdzer Katherine A. Shepard Shannon B. Hagerty J. Patrick Megonigal 《Global Change Biology》2013,19(5):1495-1503
Elevated CO2 and nitrogen (N) addition directly affect plant productivity and the mechanisms that allow tidal marshes to maintain a constant elevation relative to sea level, but it remains unknown how these global change drivers modify marsh plant response to sea level rise. Here we manipulated factorial combinations of CO2 concentration (two levels), N availability (two levels) and relative sea level (six levels) using in situ mesocosms containing a tidal marsh community composed of a sedge, Schoenoplectus americanus, and a grass, Spartina patens. Our objective is to determine, if elevated CO2 and N alter the growth and persistence of these plants in coastal ecosystems facing rising sea levels. After two growing seasons, we found that N addition enhanced plant growth particularly at sea levels where plants were most stressed by flooding (114% stimulation in the + 10 cm treatment), and N effects were generally larger in combination with elevated CO2 (288% stimulation). N fertilization shifted the optimal productivity of S. patens to a higher sea level, but did not confer S. patens an enhanced ability to tolerate sea level rise. S. americanus responded strongly to N only in the higher sea level treatments that excluded S. patens. Interestingly, addition of N, which has been suggested to accelerate marsh loss, may afford some marsh plants, such as the widespread sedge, S. americanus, the enhanced ability to tolerate inundation. However, if chronic N pollution reduces the availability of propagules of S. americanus or other flood‐tolerant species on the landscape scale, this shift in species dominance could render tidal marshes more susceptible to marsh collapse. 相似文献
178.
Rob S. A. Pickles Daniel Thornton Richard Feldman Adam Marques Dennis L. Murray 《Global Change Biology》2013,19(9):2645-2654
Climate change likely will lead to increasingly favourable environmental conditions for many parasites. However, predictions regarding parasitism's impacts often fail to account for the likely variability in host distribution and how this may alter parasite occurrence. Here, we investigate potential distributional shifts in the meningeal worm, Parelaphostrongylosis tenuis, a protostrongylid nematode commonly found in white‐tailed deer in North America, whose life cycle also involves a free‐living stage and a gastropod intermediate host. We modelled the distribution of the hosts and free‐living larva as a complete assemblage to assess whether a complex trophic system will lead to an overall increase in parasite distribution with climate change, or whether divergent environmental niches may promote an ecological mismatch. Using an ensemble approach to climate modelling under two different carbon emission scenarios, we show that whereas the overall trend is for an increase in niche breadth for each species, mismatches arise in habitat suitability of the free‐living larva vs. the definitive and intermediate hosts. By incorporating these projected mismatches into a combined model, we project a shift in parasite distribution accounting for all steps in the transmission cycle, and identify that overall habitat suitability of the parasite will decline in the Great Plains and southeastern USA, but will increase in the Boreal Forest ecoregion, particularly in Alberta. These results have important implications for wildlife conservation and management due to the known pathogenicity of parelaphostrongylosis to alternate hosts including moose, caribou and elk. Our results suggest that disease risk forecasts which fail to consider biotic interactions may be overly simplistic, and that accounting for each of the parasite's life stages is key to refining predicted responses to climate change. 相似文献
179.