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排序方式: 共有2041条查询结果,搜索用时 15 毫秒
41.
Jacqueline M. Smits Jens Gottlieb Erik Verschuuren Patrick Evrard Rogier Hoek Christiane Knoop György Lang Johanna M. Kwakkel-van Erp Robin Vos Geert Verleden Benoit Rondelet Daniel Hoefer Frank Langer Rene Schramm Konrad Hoetzenecker Diana van Kessel Bart Luijk Leonard Seghers Tobias Deuse Roland Buhl Christian Witt Agita Strelniece Dave Green Erwin de Vries Guenter Laufer Dirk Van Raemdonck 《Transplant international》2020,33(5):544-554
The aim of this study was to investigate whether there is an impact of donation rates on the quality of lungs used for transplantation and whether donor lung quality affects post-transplant outcome in the current Lung Allocation Score era. All consecutive adult LTx performed in Eurotransplant (ET) between January 2012 and December 2016 were included (N = 3053). Donors used for LTx in countries with high donation rate were younger (42% vs. 33% ≤45 years, P < 0.0001), were less often smokers (35% vs. 46%, P < 0.0001), had more often clear chest X-rays (82% vs. 72%, P < 0.0001), had better donor oxygenation ratios (20% vs. 26% with PaO2/FiO2 ≤ 300 mmHg, P < 0.0001), and had better lung donor score values (LDS; 28% vs. 17% with LDS = 6, P < 0.0001) compared with donors used for LTx in countries with low donation rate. Survival rates for the groups LDS = 6 and ≥7 at 5 years were 69.7% and 60.9% (P = 0.007). Lung donor quality significantly impacts on long-term patient survival. Countries with a low donation rate are more oriented to using donor lungs with a lesser quality compared to countries with a high donation rate. Instead of further stretching donor eligibility criteria, the full potential of the donor pool should be realized. 相似文献
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Detlef Van der Velde-Zimmermann Veronique A. J. Smits Marina A. M. Verdaasdonk Louk H. P. M. Rademakers Naomi Werner Diana C. J. Spierings Roel A. De Weger Jan G. Van den Tweel Piet Joling 《International journal of cancer. Journal international du cancer》1996,66(2):225-233
Migration patterns of leukemic cells in bone marrow are largely regulated by cell contacts between leukemic cells and stromal cells or extra-cellular matrix. The mechanism of this interaction with bone-marrow stromal cells was studied in a human in vitro model. Migration behavior of erythroleukemia cell line K562, derived from a patient with chronic myeloid leukemia, was compared with that of the erythroleukemia cell line HEL92.1.7 and the promyelocytic leukemia cell line HL60 from acute leukemias. Interaction varied between low binding affinity (K562) to intensive cell interaction (HEL92.1.7) followed by invasion into the stromal cell monolayer. Some of the HL60 cells adhered to stromal cells, while the remainder migrated into the stromal cell monolayer. The role of adhesion molecules in these cell interactions was determined. Distinct expression of β1-integrins ICAM-I, CD44 and VCAM-I was detected on the different cell lines. Inhibition studies pointed to a dominant role of VLA-4- and VLA-5-mediated interactions. K562 lacked VLA-4 and a low affinity of the VLA-5 on these cells resulted in an absence of binding to the bone-marrow stroma. These results indicate the VLA-5/fibronectin, VLA-4/fibronectin and the VLA-4/VCAM-I interaction pathways between leukemic cells and bone-marrow stroma. © 1996 Wiley-Liss, Inc. 相似文献
47.
Hua Huang Maria Georganaki Lei Liu Conze Brbara Lavia Luuk van Hooren Kalyani Vemuri Tiarne van de Walle Mohanraj Ramachandran Lei Zhang Fredrik Pontn Michael Bergqvist Anja Smits Christer Betsholtz Elisabetta Dejana Peetra U Magnusson Liqun He Roberta Lugano Anna Dimberg 《Neuro-oncology》2022,24(3):398
48.
The role of oncogenes, tumour suppressor genes and growth factors in oral squamous cell carcinoma: a case of apoptosis versus proliferation 总被引:1,自引:0,他引:1
Mutation, deactivation and disregulated expression of oncogenes and tumour-suppressor genes may be involved in the pathogenesis of oral squamous cell carcinoma (SCC). Deactivation of the p53 tumour-suppressor gene allows cell proliferation and blocks apoptosis of malignant oral keratinocytes. Mutation in the ras oncog-ene results in persistent mitogenic signalling. Upregul-ated c-Myc expression, in the presence of growth factors, provides an additional proliferative signal. Loss of retino-blastoma tumour-suppressor gene (Rb) function may contribute to oral keratinocyte hyperproliferation and recent evidence suggests that simultaneous deactivation of both p53 and Rb is required for tumourigenesis. Enhanced Bcl-2 and reduced Fas expression inhibit tumour cell apoptosis and may convey resistance to cyto-toxic drugs and T cell-mediated cytotoxicity, respectively. Exogenous mutagens such as tobacco, alcohol and viral oncogenes may cause altered expression of oncogenes and tumour-suppressor genes in some cases of oral SCC. The impact of these mechanisms on future therapies for oral SCC is highlighted. 相似文献
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Normal phenotype in two brothers with a full FMR1 mutation 总被引:6,自引:2,他引:6
Smeets H.J.M.; Smits A.P.T.; Verheij C.E.; Theelen J.P.G.; Willemsen R.; Burgt I.van de; Hoogeveen A.T.; Oosterwijk J.C.; Oostra B.A. 《Human molecular genetics》1995,4(11):2103-2108
The fragile X syndrome is associated with an expanding CGG repeatin the 5' untranslated region of the first exon of the FMR1gene. Subsequent methylation of the promoter region inhibitsexpression of the FMR1 gene. In two clinically normal brotherslarge, expanded CGG repeats and cytogenetically visible fragilesites were found. The FMR1 promoter was unmethylated and bothRNA and protein could be detected. This indicates that inactivationof the FMR1 gene and not repeat expansion itself results inthe fragile X phenotype. We conclude that repeat expansion doesnot necessarily induce methylation and that methylation is noabsolute requirement for the induction of fragile sites. 相似文献