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31.
Meenakshi Hegde Malini Mukherjee Zakaria Grada Antonella Pignata Daniel Landi Shoba A. Navai Amanda Wakefield Kristen Fousek Kevin Bielamowicz Kevin K.H. Chow Vita S. Brawley Tiara T. Byrd Simone Krebs Stephen Gottschalk Winfried S. Wels Matthew L. Baker Gianpietro Dotti Maksim Mamonkin Malcolm K. Brenner Jordan S. Orange Nabil Ahmed 《The Journal of clinical investigation》2021,131(13)
32.
Claudia Brogna Giorgia Coratti Rachele Rossi Marcella Neri Sonia Messina Adele D’ Amico Claudio Bruno Simona Lucibello Gianluca Vita Angela Berardinelli Francesca Magri Federica Ricci Marina Pedemonte Tiziana Mongini Roberta Battini Luca Bello Elena Pegoraro Giovanni Baranello Eugenio Mercuri 《Neuromuscular disorders : NMD》2021,31(6):479-488
The aim was to assess 3-year longitudinal data using 6MWT in 26 ambulant boys affected by DMD carrying nonsense mutations and to compare their results to other small mutations. We also wished to establish, within the nonsense mutations group, patterns of change according to several variables. Patients with nonsense mutations were categorized according to the stop codon type newly created by the mutation and also including the adjacent 5′ (upstream) and 3′ (downstream) nucleotides. No significant difference was found between nonsense mutations and other small mutations (p > 0.05) on the 6MWT. Within the nonsense mutations group, there was no difference in 6MWT when the patients were subdivided according to: Type of stop codon, frame status of exons involved, protein domain affected. In contrast, there was a difference when the stop codon together with the 3′ adjacent nucleotide (“stop+4 model”) was considered (p < 0.05) with patients with stop codon TGA and 3′ adjacent nucleotide G (TGAG) having a more rapid decline. Our finding suggest that the stop+4 model may help in predicting functional changes. This data will be useful at the time of interpreting the long term follow up of patients treated with Ataluren that are becoming increasingly available. 相似文献
33.
Martinotti Giovanni Bonanni Laura Barlati Stefano Miuli Andrea Sepede Gianna Prestia Davide Trabucco Alice Palumbo Claudia Massaro Alessandra Olcese Martina D’Ardes Damiano Cipollone Francesco Amore Mario Bondi Emi Russo Mirella Carrarini Claudia Onofrj Marco Sensi Stefano Luca Vita Antonio di Giannantonio Massimo 《Neurological sciences》2021,42(10):3981-3988
Neurological Sciences - Although recent data show that SARS-CoV-2 infection seems to affect the central nervous system (CNS), little is known about the neuropsychiatric effects resulting from this... 相似文献
34.
Donaldson Kandace Huntington Alyssa De Vita Raffaella 《Annals of biomedical engineering》2021,49(8):1788-1804
Annals of Biomedical Engineering - The uterosacral ligaments (USLs) are important anatomical structures that support the uterus and apical vagina within the pelvis. As these structures are... 相似文献
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E. Barca M. Aguennouz A. Mazzeo S. Messina A. Toscano G. L. Vita S. Portaro D. Parisi C. Rodolico 《Neurological sciences》2013,34(2):217-224
To investigate ANT1 and NF-κB expression in inclusion body myositis (IBM) muscle and to verify their possible roles in the pathogenesis of the disease, we collected muscle samples from five patients with IBM, polimyositis (PM) and controls. p65 form of NF-κB was analyzed using immunocytochemistry, Western blot and EMSA. Western blot of ANT1 was performed and confirmed by gene expression study. Mann–Whitney test was used for groups comparisons. NF-κB (p65) was found over-expressed both with western blot and EMSA, either in IBM or PM patients versus controls (p < 0.01). Expression of ANT1 were lower in IBM samples versus both PM and controls (p < 0.01). ANT1 reduction and NF-κB over-expression in IBM muscle could explain the lack of apoptosis in such disease. Normal ANT1 expression in PM could be related to the scarcity of mitochondrial abnormalities in the disease, but it could also suggest that these two conditions diverge in activating different anti-apoptotic pathways. 相似文献
39.
Francesca Novara Ambra Rizzo Gloria Bedini Vita Girgenti Silvia Esposito Chiara Pantaleoni Roberto Ciccone Francesca L. Sciacca Valentina Achille Erika Della Mina Simone Gana Orsetta Zuffardi Margherita Estienne 《European journal of medical genetics》2013,56(5):260-265
5q14.3 deletions including the MEF2C gene have been identified to date using genomic arrays in patients with severe developmental delay or intellectual disability, stereotypic behavior, epilepsy, cerebral malformations and a facial gestalt not really distinctive though characterized by broad and/or high, bulging forehead, upslanting palpebral fissures, flat nasal root and bridge, small, upturned nose, hypotonic small mouth resulting in cupid bow/tented upper lip. MEF2C mutations have been also identified in patients with overlapping phenotype so that it is considered the gene responsible for the 5q14.3 deletion syndrome. To date, one single duplication including MEF2C has been reported in a patient with intellectual disability but its clinical significance remains uncertain also because of the large size of the imbalance. Here we present two further patients with 5q14.3 duplications including MEF2C. Their phenotype indeed suggest the pathogenic effect of the MEF2C duplication although other duplicated genes also brain expressed might contribute to the clinical features. In none of them a clear-cut syndrome can be identified. A comparison between MEF2C deleted/mutated and duplicated patients is also presented. 相似文献
40.
Govoni M Bombardieri S Bortoluzzi A Caniatti L Casu C Conti F De Vita S Doria A Farina I Ferraccioli G Gremese E Mansutti E Mosca M Padovan M Piga M Tincani A Tola MR Tomietto P Taglietti M Trotta F Valesini G Zen M Mathieu A;Italian Society of Rheumatology 《Rheumatology (Oxford, England)》2012,51(1):157-168