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排序方式: 共有2992条查询结果,搜索用时 46 毫秒
71.
Severely elevated C‐reactive protein accompanied by prolonged high fever and leukocytosis in a healthy peripheral blood stem cell donor: an atypical granulocyte–colony‐stimulating factor reaction?
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Heiko Sic Helene Kraus Josef Madl Karl-Andreas Flittner Audrey Lilly von Münchow Kathrin Pieper Marta Rizzi Anne-Kathrin Kienzler Korcan Ayata Sebastian Rauer Burkhard Kleuser Ulrich Salzer Meike Burger Katja Zirlik Vassilios Lougaris Alessandro Plebani Winfried Römer Christoph Loeffler Samantha Scaramuzza Anna Villa Emiko Noguchi Bodo Grimbacher Hermann Eibel 《The Journal of allergy and clinical immunology》2014
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Kathrin Pieper Marta Rizzi Matthaios Speletas Cristian R. Smulski Heiko Sic Helene Kraus Ulrich Salzer Gina J. Fiala Wolfgang W. Schamel Vassilios Lougaris Alessandro Plebani Lennart Hammarstrom Mike Recher Anastasios E. Germenis Bodo Grimbacher Klaus Warnatz Antonius G. Rolink Pascal Schneider Luigi D. Notarangelo Hermann Eibel 《The Journal of allergy and clinical immunology》2014
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Vassilia Theodorou Afifa Ait Belgnaoui Simona Agostini Helene Eutamene 《Gut microbes》2014,5(3):430-436
The last ten years’ wide progress in the gut microbiota phylogenetic and functional characterization has been made evidencing dysbiosis in several gastrointestinal diseases including inflammatory bowel diseases and irritable bowel syndrome (IBS). IBS is a functional gut disease with high prevalence and negative impact on patient’s quality of life characterized mainly by visceral pain and/or discomfort, representing a good paradigm of chronic gut hypersensitivity. The IBS features are strongly regulated by bidirectional gut-brain interactions and there is increasing evidence for the involvement of gut bacteria and/or their metabolites in these features, including visceral pain. Further, gut microbiota modulation by antibiotics or probiotics has been promising in IBS. Mechanistic data provided mainly by animal studies highlight that commensals or probiotics may exert a direct action through bacterial metabolites on sensitive nerve endings in the gut mucosa, or indirect pathways targeting the intestinal epithelial barrier, the mucosal and/or systemic immune activation, and subsequent neuronal sensitization and/or activation. 相似文献
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LE Quenee TM Hermanas N Ciletti H Louvel NC Miller D Elli B Blaylock A Mitchell J Schroeder T Krausz J Kanabrocki O Schneewind 《The Journal of infectious diseases》2012,206(7):1050-1058
Nonpigmented Yersinia pestis (pgm) strains are defective in scavenging host iron and have been used in live-attenuated vaccines to combat plague epidemics. Recently, a Y. pestis pgm strain was isolated from a researcher with hereditary hemochromatosis who died from laboratory-acquired plague. We used hemojuvelin-knockout (Hjv(-/-)) mice to examine whether iron-storage disease restores the virulence defects of nonpigmented Y. pestis. Unlike wild-type mice, Hjv(-/-) mice developed lethal plague when challenged with Y. pestis pgm strains. Immunization of Hjv(-/-) mice with a subunit vaccine that blocks Y. pestis type III secretion generated protection against plague. Thus, individuals with hereditary hemochromatosis may be protected with subunit vaccines but should not be exposed to live-attenuated plague vaccines. 相似文献
78.
Swift F Franzini-Armstrong C Øyehaug L Enger UH Andersson KB Christensen G Sejersted OM Louch WE 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(10):3997-4001
Cardiomyocyte contraction and relaxation are controlled by Ca(2+) handling, which can be regulated to meet demand. Indeed, major reduction in sarcoplasmic reticulum (SR) function in mice with Serca2 knockout (KO) is compensated by enhanced plasmalemmal Ca(2+) fluxes. Here we investigate whether altered Ca(2+) fluxes are facilitated by reorganization of cardiomyocyte ultrastructure. Hearts were fixed for electron microscopy and enzymatically dissociated for confocal microscopy and electrophysiology. SR relative surface area and volume densities were reduced by 63% and 76%, indicating marked loss and collapse of the free SR in KO. Although overall cardiomyocyte dimensions were unaltered, total surface area was increased. This resulted from increased T-tubule density, as revealed by confocal images. Fourier analysis indicated a maintained organization of transverse T-tubules but an increased presence of longitudinal T-tubules. This demonstrates a remarkable plasticity of the tubular system in the adult myocardium. Immunocytochemical data showed that the newly grown longitudinal T-tubules contained Na(+)/Ca(2+)-exchanger proximal to ryanodine receptors in the SR but did not contain Ca(2+)-channels. Ca(2+) measurements demonstrated a switch from SR-driven to Ca(2+) influx-driven Ca(2+) transients in KO. Still, SR Ca(2+) release constituted 20% of the Ca(2+) transient in KO. Mathematical modeling suggested that Ca(2+) influx via Na(+)/Ca(2+)-exchange in longitudinal T-tubules triggers release from apposing ryanodine receptors in KO, partially compensating for reduced SERCA by allowing for local Ca(2+) release near the myofilaments. T-tubule proliferation occurs without loss of the original ordered transverse orientation and thus constitutes the basis for compensation of the declining SR function without structural disarrangement. 相似文献
79.
Delis F Benveniste H Xenos M Grandy D Wang GJ Volkow ND Thanos PK 《Alcoholism, clinical and experimental research》2012,36(5):815-825
Background: The need of an animal model of alcoholism becomes apparent when we consider the genetic diversity of the human populations, an example being dopamine D2 receptor (DRD2) expression levels. Research suggests that low DRD2 availability is associated with alcohol abuse, while higher DRD2 levels may be protective against alcoholism. This study aims to establish whether (i) the ethanol‐consuming mouse is a suitable model of alcohol‐induced brain atrophy and (ii) DRD2 protect the brain against alcohol toxicity. Methods: Adult Drd2+/+ and Drd2?/? mice drank either water or 20% ethanol solution for 6 months. At the end of the treatment period, the mice underwent magnetic resonance (MR) imaging under anesthesia. MR images were registered to a common space, and regions of interest were manually segmented. Results: We found that chronic ethanol intake induced a decrease in the volume of the temporal and parietal cortices as well as the caudal thalamus in Drd2?/? mice. Conclusions: The result suggests that (i) normal DRD2 expression has a protective role against alcohol‐induced brain atrophy and (ii) in the absence of Drd2 expression, prolonged ethanol intake reproduces a distinct feature of human brain pathology in alcoholism, the atrophy of the temporal and parietal cortices. 相似文献
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