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排序方式: 共有3709条查询结果,搜索用时 15 毫秒
91.
Camille Nicolas Vincent Vuiblet Veronique Baudouin Marie-Alice Macher Isabele Vrillon Nathalie Biebuyck-Gouge Maud Dehennault Sophie Gié Denis Morin Hubert Nivet François Nobili Tim Ulinski Bruno Ranchin Maria Chiarra Marinozzi Stéphanie Ngo Véronique Frémeaux-Bacchi Christine Pietrement 《Pediatric nephrology (Berlin, Germany)》2014,29(1):85-94
Background
C3 glomerulopathy (C3G) is characterized by predominant C3 deposits in glomeruli and dysregulation of the alternative pathway of complement. Half of C3G patients have a C3 nephritic factor (C3NeF). C3G incorporated entities with a range of features on microscopy including dense deposit diseases (DDD) and C3 glomerulonephritis (C3GN). The aim of this work was to study children cases of C3G associated with C3NeF.Methods
We reviewed 18 cases of C3G with a childhood onset associated with C3NeF without identified mutations in CFH, CFI, and MCP genes.Results
Clinical histories started with recurrent hematuria for seven patients, nephrotic syndrome for four, acute post-infectious glomerulonephritis for three and acute renal failure for four. Twelve patients had a low C3 at first investigation. Kidney biopsy showed ten C3GN and eight DDD. Twenty-three percent of the patients tested presented elevated sC5b9. Seven patients relapsed 3 to 6 years after the onset. At the end of follow-up, two patients were under dialysis, 11 had a persistent proteinuria, five had none; four patients did not follow any treatment. Steroids were first used in 80 % of cases.Conclusions
C3NeF associated C3G has a heterogeneous presentation and outcome. Anti-proteinuric agents may control the disease during follow-up, even after nephrotic syndrome at the onset. The efficiency of immunosuppressive therapy remains questionable. 相似文献92.
Distribution of human papillomavirus genotypes,assessment of HPV 16 and 18 viral load and anal related lesions in HIV positive patients: A cross‐sectional analysis 下载免费PDF全文
93.
94.
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
95.
Fifteen fluorescent oligoamines with one or two fluorescent groups and two or three basic N-functions were prepared and tested for antiplatelet activity (Born-test). Five compounds involving three different fluorophores, i.e. 2-fluorenyl, 1-pyrenyl, and 9-phenanthryl, show an IC50 of 7–11 μmol/L. They are suitable to serve as probes in the field of oligoamine-biopolymere interactions. 相似文献
96.
97.
Hendrickx Gaelle De Roeck Veronique Russet Frdrick Dieleman Gwen Franic Tomislav Maras Athanasios McNicholas Fiona Paul Moli Santosh Paramala Schulze Ulrike Signorini Giulia Singh Swaran P. Street Cathy Tuomainen Helena Verhulst Frank Wolke Dieter Purper-Ouakil Diane Tremmery Sabine 《European child & adolescent psychiatry》2020,29(1):41-49
European Child & Adolescent Psychiatry - The majority of adolescents with mental health problems do not experience continuity of care when they reach the transition boundary of their child and... 相似文献
98.
Wiemann Greta Pertz Milena Kowalski Thomas Seidel Sabine Schlegel Uwe Thoma Patrizia 《Journal of neuro-oncology》2020,146(1):171-180
Journal of Neuro-Oncology - Evidence supporting routine postoperative antiepileptic drug (AED) prophylaxis following oncologic neurosurgery is limited, and actual practice patterns are largely... 相似文献
99.
Andreas Tzschach Ute Grasshoff Stefanie Beck-Woedl Claudia Dufke Claudia Bauer Martin Kehrer Christina Evers Ute Moog Barbara Oehl-Jaschkowitz Nataliya Di Donato Robert Maiwald Christine Jung Alma Kuechler Solveig Schulz Peter Meinecke Stephanie Spranger Jürgen Kohlhase J?rg Seidel Silke Reif Manuela Rieger Angelika Riess Marc Sturm Julia Bickmann Christopher Schroeder Andreas Dufke Olaf Riess Peter Bauer 《European journal of human genetics : EJHG》2015,23(11):1513-1518
X-linked intellectual disability (XLID) is a genetically heterogeneous disorder with more than 100 genes known to date. Most genes are responsible for a small proportion of patients only, which has hitherto hampered the systematic screening of large patient cohorts. We performed targeted enrichment and next-generation sequencing of 107 XLID genes in a cohort of 150 male patients. Hundred patients had sporadic intellectual disability, and 50 patients had a family history suggestive of XLID. We also analysed a sporadic female patient with severe ID and epilepsy because she had strongly skewed X-inactivation. Target enrichment and high parallel sequencing allowed a diagnostic coverage of >10 reads for ~96% of all coding bases of the XLID genes at a mean coverage of 124 reads. We found 18 pathogenic variants in 13 XLID genes (AP1S2, ATRX, CUL4B, DLG3, IQSEC2, KDM5C, MED12, OPHN1, SLC9A6, SMC1A, UBE2A, UPF3B and ZDHHC9) among the 150 male patients. Thirteen pathogenic variants were present in the group of 50 familial patients (26%), and 5 pathogenic variants among the 100 sporadic patients (5%). Systematic gene dosage analysis for low coverage exons detected one pathogenic hemizygous deletion. An IQSEC2 nonsense variant was detected in the female ID patient, providing further evidence for a role of this gene in encephalopathy in females. Skewed X-inactivation was more frequently observed in mothers with pathogenic variants compared with those without known X-linked defects. The mutation rate in the cohort of sporadic patients corroborates previous estimates of 5–10% for X-chromosomal defects in male ID patients. 相似文献