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排序方式: 共有5578条查询结果,搜索用时 15 毫秒
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Héctor Díaz-Zabala Xingyi Guo Jie Ping Wanqing Wen Xiao-Ou Shu Jirong Long Loren Lipworth Bingshan Li Mary Kay Fadden Tuya Pal William J. Blot Qiuyin Cai Christopher A. Haiman Julie R. Palmer Maureen Sanderson Wei Zheng 《Genetics in medicine》2022,24(7):1468-1475
PurposeStudies conducted primarily among European ancestry women reported 12 breast cancer predisposition genes. However, etiologic roles of these genes in breast cancer among African ancestry women have been less well-investigated.MethodsWe conducted a case-control study in African American women, which included 1117 breast cancer cases and 2169 cancer-free controls, and a pooled analysis, which included 7096 cases and 8040 controls of African descent. Odds ratios of associations with breast cancer risk were estimated.ResultsUsing sequence data, we identified 61 pathogenic variants in 12 breast cancer predisposition genes, including 11 pathogenic variants not yet reported in previous studies. Pooled analysis showed statistically significant associations of breast cancer risk with pathogenic variants in BRCA1, BRCA2, PALB2, ATM, CHEK2, TP53, NF1, RAD51C, and RAD51D (all P < .05). The associations with BRCA1, PALB2, and RAD51D were stronger for estrogen receptor (ER)-negative than for ER-positive breast cancer (P heterogeneity < .05), whereas the association with CHEK2 was stronger for ER-positive than for ER-negative breast cancer.ConclusionOur study confirmed previously identified associations of breast cancer risk with BRCA1, BRCA2, PALB2, ATM, TP53, NF1, and CHEK2 and provided new evidence to extend the associations of breast cancer risk with RAD51C and RAD51D, which was identified previously in European ancestry populations, to African ancestry women. 相似文献
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Guru Sonpavde MD Neeraj Agarwal MD Gregory Russell Pond PhD Rebecca J. Nagy MSc Roberto H. Nussenzveig PhD Andrew W. Hahn MD Oliver Sartor MD Theodore Stewart Gourdin MD Lakshminarayanan Nandagopal MD Elisa M. Ledet PhD Gurudatta Naik MPH Andrew J. Armstrong MD MSc Jue Wang MD Mehmet Asim Bilen MD Shilpa Gupta MD Petros Grivas MD PhD Sumanta K. Pal MD Richard B. Lanman MD AmirAli Talasaz PhD Michael B. Lilly MD 《Cancer》2019,125(9):1459-1469
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Lisa Kane Low PhD CNM FAAN Beverly Rosa Williams PhD Deepa R. Camenga MD MHS Jeni Hebert‐Beirne PhD MPH Sonya S. Brady PhD Diane K. Newman DNP ANP‐BC FAAN Aimee S. James PhD MPH Cecilia T. Hardacker MSN RN CNL Jesse Nodora DrPH Sarah E. Linke PhD MPH Kathryn L. Burgio PhD 《Journal of advanced nursing》2019,75(11):3111-3125
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Tina Hsu Nitya Nathwani Matthew Loscalzo Vincent Chung Joseph Chao Chatchada Karanes Marianna Koczywas Stephen Forman Dean Lim Tanya Siddiqi Anthony Stein Przemyslaw Twardowski Auayporn Nademanee Sumanta Pal Eduardo Siccion Marjorie Hein Chie Akiba Leanne Goldstein David Smith Huiyan Ma Tao Feng Arti Hurria 《Journal of the American Geriatrics Society》2019,67(5):978-986
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Hritika Sharma Anjali Bose Ruchi Sachdeva Monika Malik Uma Kumar Rahul Pal 《Immunology》2022,165(1):122-140
Haemoglobin (Hb) has well-documented inflammatory effects and is normally efficiently scavenged; clearance mechanisms can be overwhelmed during erythrocyte lysis. Whether Hb is preferentially inflammatory in lupus and triggers broad anti-self responses was assessed. Peripheral blood mononuclear cells (PBMCs) derived from SLE patients secreted higher levels of lupus-associated inflammatory cytokines when incubated with human Hb than did PBMCs derived from healthy donors, an effect negated by haptoglobin. Ferric murine Hb triggered the preferential release of lupus-associated cytokines from splenocytes, B cells, CD4 T cells, CD8 T cells and plasmacytoid dendritic cells isolated from ageing, lupus-prone NZM2410 mice, and also had mitogenic effects on B cells. Pull-downs, followed by mass spectrometry, revealed interactions of Hb with several lupus-associated autoantigens; co-incubation of ferric Hb with apoptotic blebs (structures that contain packaged autoantigens) revealed synergies—in terms of cytokine release and autoantibody production in vitro—that were also restricted to the lupus genotype. Murine ferric Hb activated multiple signalling pathways and, in combination with apoptotic blebs, preferentially triggered MAP kinase signalling specifically in splenocytes isolated from lupus-prone mice. Infusion of murine ferric Hb into lupus-prone mice led to enhanced release of lupus-associated cytokines, the generation of a spectrum of autoantibodies and enhanced-onset glomerulosclerosis. Given that the biased recognition of ferric Hb in a lupus milieu, possibly in concert with lupus-associated autoantigens, triggers inflammatory responses and the generation of lupus-associated cytokines, and also stimulates the generation of potentially pathogenic lupus-associated autoantibodies, neutralization of Hb could have beneficial effects. 相似文献
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Thomas Powles Michael B. Atkins Bernard Escudier Robert J. Motzer Brian I. Rini Lawrence Fong Richard W. Joseph Sumanta K. Pal Mario Sznol John Hainsworth Walter M. Stadler Thomas E. Hutson Alain Ravaud Sergio Bracarda Cristina Suarez Toni K. Choueiri James Reeves Allen Cohn David F. McDermott 《European urology》2021,79(5):665-673
BackgroundThe use of immune checkpoint inhibitors combined with vascular endothelial growth factor (VEGF)-targeted therapy as second-line treatment for metastatic clear cell renal cancer (mRCC) has not been evaluated prospectively.ObjectiveTo evaluate the efficacy and safety of atezolizumab + bevacizumab following disease progression on atezolizumab or sunitinib monotherapy in patients with mRCC.Design, setting, and participantsIMmotion150 was a multicenter, randomized, open-label, phase 2 study of patients with untreated mRCC. Patients randomized to the atezolizumab or sunitinib arm who had investigator-assessed progression as per RECIST 1.1 could be treated with second-line atezolizumab + bevacizumab.InterventionPatients received atezolizumab 1200 mg intravenously (IV) plus bevacizumab 15 mg/kg IV every 3 wk following disease progression on either atezolizumab or sunitinib monotherapy.Outcome measurements and statistical analysisThe secondary endpoints analyzed during the second-line part of IMmotion150 included objective response rate (ORR), progression-free survival (PFS), and safety. PFS was examined using Kaplan-Meier methods.Results and limitationsFifty-nine patients in the atezolizumab arm and 78 in the sunitinib arm were eligible, and 103 initiated second-line atezolizumab + bevacizumab (atezolizumab arm, n = 44; sunitinib arm, n = 59). ORR (95% confidence interval [CI]) was 27% (19–37%). The median PFS (95% CI) from the start of second line was 8.7 (5.6–13.7) mo. The median event follow-up duration was 19.4 (12.9–21.9) mo among the 25 patients without a PFS event. Eighty-six (83%) patients had treatment-related adverse events; 31 of 103 (30%) had grade 3/4 events. Limitations were the small sample size and selection for progressors.ConclusionsThe atezolizumab + bevacizumab combination had activity and was tolerable in patients with progression on atezolizumab or sunitinib. Further studies are needed to investigate sequencing strategies in mRCC.Patient summaryPatients with advanced kidney cancer whose disease had worsened during treatment with atezolizumab or sunitinib began second-line treatment with atezolizumab + bevacizumab. Tumors shrank in more than one-quarter of patients treated with this combination, and side effects were manageable. 相似文献
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Nina Streefkerk Marianne J. Heins Jop C. Teepen Elizabeth A. M. Feijen Dorine Bresters Eline van Dulmen‐den Broeder Margriet van der Heiden‐van der Loo Marry M. van den Heuvel‐Eibrink Flora E. van Leeuwen Jacqueline J. Loonen Helena J. H. van der Pal Ccile M. Ronckers A. Birgitta Versluys Wim J. E. Tissing Joke C. Korevaar Leontien C. M. Kremer 《Pediatric blood & cancer》2019,66(8)