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SHOT, a SHOX-related homeobox gene, is implicated in craniofacial, brain, heart, and limb development 总被引:2,自引:0,他引:2 下载免费PDF全文
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Gabbi C Kim HJ Hultenby K Bouton D Toresson G Warner M Gustafsson JA 《Proceedings of the National Academy of Sciences of the United States of America》2008,105(39):15052-15057
Liver X receptors (LXRs) α and β are nuclear oxysterol receptors with a key role in cholesterol, triglyceride, and glucose metabolism. In LXRβ−/− mice on a normal diet, there is a reduction in size of perigonadal fat pad and, on high-fat diet there is resistance to obesity. In the present study, we investigated the reason for the resistance of LXRβ−/− mice to weight gain. In LXRβ−/− mice we found pancreatic exocrine insufficiency with reduced serum levels of amylase and lipase, reduced proteolytic activity in feces, chronic inflammatory infiltration, and, in the ductal epithelium, an increased apoptosis without compensatory proliferation. Electron microscopy revealed ductal dilatation with intraductal laminar structures characteristic of cystic fibrosis. To investigate the relationship between LXRβ and pancreatic secretion, we studied the expression of LXRβ and the water channel, aquaporin-1 (AQP1), in the ductal epithelium of the pancreas. In WT mice, ductal epithelial cells expressed LXRβ in the nuclei and AQP1 on the plasma membrane. In LXRβ−/− mice neither LXRβ nor AQP1 was detectable. Moreover, in WT mice the LXR agonist (T2320) increased AQP1 gene expression. These data demonstrate that in LXRβ−/− mice dietary resistance to weight gain is caused by pancreatic insufficiency and that LXRβ regulates pancreatic exocrine secretion through the control of AQP1 expression. Pancreatic exocrine insufficiency is the main cause of malabsorption syndrome responsible for weight loss in adults and growth failure in children. Several genes are known to be involved in the pathogenesis and susceptibility to pancreatic insufficiency. LXRβ should be included in that list. 相似文献
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Rabia Shahswar Gernot Beutel Piroska Klement Alina Rehberg Razif Gabdoulline Christian Koenecke Dominik Markel Hendrik Eggers Matthias Eder Michael Stadler Lothar Hambach Steve Ehrlich Gudrun Göhring Brigitte Schlegelberger Elke Dammann Marlene Reuter Martin Wichmann Blerina Neziri Arnold Ganser Felicitas Thol Michael Heuser 《British journal of haematology》2020,188(3):e11-e15
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Jos María MayaManzano Gudrun Pusch Cordula Ebner von Eschenbach Elke Bartusel Thomas Belzner Erwin Karg Ulrich Bardolatzy Michael Scheja Carsten SchmidtWeber Jeroen Buters 《Clinical and translational allergy》2022,12(4)
BackgroundIndoor allergens (i.e. from mite, cat and dog) are carried by airborne particulate matter. Thus, removal of particles would reduce allergen exposure. This work aims to assess the performance of air filtration on particulate matter and thus allergen removal in 22 bedrooms.MethodsIndoor air was sampled (with and without air filtration) with a cascade impactor and allergens were measured using enzyme‐linked immunosorbent assay (ELISA). Particulate matter (including ultrafine particles) was also monitored.ResultsThe median of allergen reduction was 75.2% for Der f 1 (p < 0.001, n = 20), 65.5% for Der p 1 (p = 0.066, n = 4), 76.6% for Fel d 1 (p < 0.01, n = 21) and 89.3% for Can f 1 (p < 0.01, n = 10). For size fractions, reductions were statistically significant for Der f 1 (all p < 0.001), Can f 1 (PM>10 and PM2.5–10, p < 0.01) and Fel d 1 (PM2.5–10, p < 0.01), but not for Der p 1 (all p > 0.05). PM was reduced in all fractions (p < 0.001). The allergens were found in all particle size fractions, higher mite allergens in the PM>10 and for pet allergens in the PM2.5–10.ConclusionsAir filtration was effective in removing mites, cat and dog allergens and also particulate matter from ambient indoor air, offering a fast and simple solution to mitigate allergen exposome. 相似文献
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Thomas Unger Peter J. Horst Martin Bauer Gudrun Demmert Rainer Rettig Peter Rohmeiss 《Brain research》1989,486(1):33-38
The effects of intracerebroventricular (i.c.v.) injections of angiotensin II (ANG II, 10 pg, 100 pg and 10 ng) on renal sodium excretion were investigated in conscious rats instrumented with a chronic urethral catheter. ANG II increased renal sodium excretion dose-dependently with a threshold i.c.v. dose of 10 pg. Only after the highest dose was a concomitant increase in arterial blood pressure and urinary flow observed. The ANG II-induced natriuresis began within 5 min of the i.c.v. injection and lasted for more than 1 h. The angiotensin receptor antagonist saralasin (1 ng, i.c.v.) largely prevented the natriuretic effect of i.c.v. injected ANG II (100 pg). Our results lend further support to the hypothesis that brain ANG II by its potent natriuretic actions may be instrumental in central osmotic control. 相似文献
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Inga Ebermann Jennifer B. Phillips Max C. Liebau Robert K. Koenekoop Bernhard Schermer Irma Lopez Ellen Sch?fer Anne-Francoise Roux Claudia Dafinger Antje Bernd Eberhart Zrenner Mireille Claustres Bernardo Blanco Gudrun Nürnberg Peter Nürnberg Rebecca Ruland Monte Westerfield Thomas Benzing Hanno J. Bolz 《The Journal of clinical investigation》2010,120(6):1812-1823
Usher syndrome is a genetically heterogeneous recessive disease characterized by hearing loss and retinitis pigmentosa (RP). It frequently presents with unexplained, often intrafamilial, variability of the visual phenotype. Although 9 genes have been linked with Usher syndrome, many patients do not have mutations in any of these genes, suggesting that there are still unidentified genes involved in the syndrome. Here, we have determined that mutations in PDZ domain–containing 7 (PDZD7), which encodes a homolog of proteins mutated in Usher syndrome subtype 1C (USH1C) and USH2D, contribute to Usher syndrome. Mutations in PDZD7 were identified only in patients with mutations in other known Usher genes. In a set of sisters, each with a homozygous mutation in USH2A, a frame-shift mutation in PDZD7 was present in the sister with more severe RP and earlier disease onset. Further, heterozygous PDZD7 mutations were present in patients with truncating mutations in USH2A, G protein–coupled receptor 98 (GPR98; also known as USH2C), and an unidentified locus. We validated the human genotypes using zebrafish, and our findings were consistent with digenic inheritance of PDZD7 and GPR98, and with PDZD7 as a retinal disease modifier in patients with USH2A. Pdzd7 knockdown produced an Usher-like phenotype in zebrafish, exacerbated retinal cell death in combination with ush2a or gpr98, and reduced Gpr98 localization in the region of the photoreceptor connecting cilium. Our data challenge the view of Usher syndrome as a traditional Mendelian disorder and support the reclassification of Usher syndrome as an oligogenic disease. 相似文献