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61.
Maureen E. Bowers George A. Buzzell Virginia Salo Sonya V. Troller-Renfree Colin A. Hodgkinson David Goldman Elena Gorodetsky Jennifer Martin McDermott Heather A. Henderson Nathan A. Fox 《Developmental psychobiology》2020,62(2):181-190
The Val158Met rs4680 single-nucleotide polymorphism (SNP) at the catechol-O-methyltransferase (COMT) gene, primarily involved in dopamine breakdown within prefrontal cortex, has shown relations with inhibitory control (IC) in both adults and children. However, little is known about how COMT genotype relates to developmental trajectories of IC throughout childhood. Here, our study explored the effects of the COMT genotype (Val/Val, Val/Met, and Met/Met) on IC trajectories between the ages of 5 and 10 years. Children (n = 222) completed a Go/Nogo task at ages 5, 7, and 10; IC was characterized using signal detection theory to examine IC performance (d′) and response strategy (RS) (criterion). COMT genotype was not related to initial levels of IC performance and RS at age 5 or change in RS from ages 5 to 10. In contrast, COMT genotype was related to change in IC performance between 5 and 10 years. While Val/Val children did not differ from Val/Met children in development of IC performance, children with the Met/Met genotype exhibited more rapid development of IC performance when compared with Val/Met peers. These results suggest that COMT genotype modulates the development of IC performance in middle childhood. 相似文献
62.
Domenico Nuzzo Pasquale Picone Luca Caruana Sonya Vasto Annalisa Barera Calogero Caruso Marta Di Carlo 《Inflammation》2014,37(3):639-648
Neurodegenerative diseases such as Alzheimer, Parkinson, amyotrophic lateral sclerosis, and Huntington are incurable and debilitating conditions that result in progressive death of the neurons. The definite diagnosis of a neurodegenerative disorder is disadvantaged by the difficulty in obtaining biopsies and thereby to validate the clinical diagnosis with pathological results. Biomarkers are valuable indicators for detecting different phases of a disease such as prevention, early onset, treatment, progression, and monitoring the effect of pharmacological responses to a therapeutic intervention. Inflammation occurs in neurodegenerative diseases, and identification and validation of molecules involved in this process could be a strategy for finding new biomarkers. The ideal inflammatory biomarker needs to be easily measurable, must be reproducible, not subject to wide variation in the population, and unaffected by external factors. Our review summarizes the most important inflammation biomarkers currently available, whose specificity could be utilized for identifying and monitoring distinctive phases of different neurodegenerative diseases. 相似文献
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Brenda Happell RN Cert Psych Nurs BA DipEd MEd PhD FACMHN Shifra Waks BA MIHP B Int Global Stud Aine Horgan PhD MSc BNS PGCert T&L RPN Sonya Greaney DipSPH PG Cert Peer Support Fionnuala Manning John Goodwin MA PGDip Bsc BA ALCM DipMgmt RPN Julia Bocking BPhil B Soc & Comm Stud Brett Scholz BHSci PhD Elisabeth Hals MA Arild Granerud PhD Rory Doody B.Soc.Sc. Chris Platania-Phung BA PhD Martha Griffin H. Dip in Community Youth Work Siobhan Russell BSc RPN PhD Liam MacGabhann BSc MSc DrNursSci Jarmo Pulli Annaliina Vatula BA Graeme Browne RN MHN PhD FACMHN Kornelis Jan van der Vaart BN MSci Jerry Allon Einar Bjornsson Heikki Ellilä RN MNSc PhD Mari Lahti MNSc PhD Pall Biering PhD 《Perspectives in psychiatric care》2020,56(4):811-819
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Variable sensitivity to noxious heat is mediated by differential expression of the CGRP gene 下载免费PDF全文
Mogil JS Miermeister F Seifert F Strasburg K Zimmermann K Reinold H Austin JS Bernardini N Chesler EJ Hofmann HA Hordo C Messlinger K Nemmani KV Rankin AL Ritchie J Siegling A Smith SB Sotocinal S Vater A Lehto SG Klussmann S Quirion R Michaelis M Devor M Reeh PW 《Proceedings of the National Academy of Sciences of the United States of America》2005,102(36):12938-12943
Heat sensitivity shows considerable functional variability in humans and laboratory animals, and is fundamental to inflammatory and possibly neuropathic pain. In the mouse, at least, much of this variability is genetic because inbred strains differ robustly in their behavioral sensitivity to noxious heat. These strain differences are shown here to reflect differential responsiveness of primary afferent thermal nociceptors to heat stimuli. We further present convergent behavioral and electrophysiological evidence that the variable responses to noxious heat are due to strain-dependence of CGRP expression and sensitivity. Strain differences in behavioral response to noxious heat could be abolished by peripheral injection of CGRP, blockade of cutaneous and spinal CGRP receptors, or long-term inactivation of CGRP with a CGRP-binding Spiegelmer. Linkage mapping supports the contention that the genetic variant determining variable heat pain sensitivity across mouse strains affects the expression of the Calca gene that codes for CGRPalpha. 相似文献
70.
Antiinflammatory effects of dexamethasone are partly dependent on induction of dual specificity phosphatase 1 总被引:3,自引:0,他引:3 下载免费PDF全文
Abraham SM Lawrence T Kleiman A Warden P Medghalchi M Tuckermann J Saklatvala J Clark AR 《The Journal of experimental medicine》2006,203(8):1883-1889
Glucocorticoids (GCs), which are used in the treatment of immune-mediated inflammatory diseases, inhibit the expression of many inflammatory mediators. They can also induce the expression of dual specificity phosphatase 1 (DUSP1; otherwise known as mitogen-activated protein kinase [MAPK] phosphatase 1), which dephosphorylates and inactivates MAPKs. We investigated the role of DUSP1 in the antiinflammatory action of the GC dexamethasone (Dex). Dex-mediated inhibition of c-Jun N-terminal kinase and p38 MAPK was abrogated in DUSP1-/- mouse macrophages. Dex-mediated suppression of several proinflammatory genes (including tumor necrosis factor, cyclooxygenase 2, and interleukin 1alpha and 1beta) was impaired in DUSP1-/- mouse macrophages, whereas other proinflammatory genes were inhibited by Dex in a DUSP1-independent manner. In vivo antiinflammatory effects of Dex on zymosan-induced inflammation were impaired in DUSP1-/- mice. Therefore, the expression of DUSP1 is required for the inhibition of proinflammatory signaling pathways by Dex in mouse macrophages. Furthermore, DUSP1 contributes to the antiinflammatory effects of Dex in vitro and in vivo. 相似文献