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51.
Unraveling toxicological mechanisms and predicting toxicity classes with gene dysregulation networks
Tessa E. Pronk Eugene P. van Someren Rob H. Stierum Janine Ezendam Jeroen L.A. Pennings 《Journal of applied toxicology : JAT》2013,33(12):1407-1415
The use of genes for distinguishing classes of toxicity has become well established. In this paper we combine the reconstruction of a gene dysregulation network (GDN) with a classifier to assign unseen compounds to their appropriate class. Gene pairs in the GDN are dysregulated in the sense that they are linked by a common expression pattern in one class and differ in this pattern in another class. The classifier gives a quantitative measure on this difference by its prediction accuracy. As an in‐depth example, gene pairs were selected that were dysregulated between skin cells treated with either sensitizers or irritants. Pairs with known and novel markers were found such as HMOX1 and ZFAND2A, ATF3 and PPP1R15A, OXSR1 and HSPA1B, ZFP36 and MAFF. The resulting GDN proved biologically valid as it was well‐connected and enriched in known interactions, processes and common regulatory motifs for pairs. Classification accuracy was improved when compared with conventional classifiers. As the dysregulated patterns for heat shock responding genes proved to be distinct from those of other stress genes, we were able to formulate the hypothesis that heat shock genes play a specific role in sensitization, apart from other stress genes. In conclusion, our combined approach creates added value for classification‐based toxicogenomics by obtaining novel, well‐distinguishing and biologically interesting measures, suitable for the formulation of hypotheses on functional relationships between genes and their relevance for toxicity class differences. Copyright © 2012 John Wiley & Sons, Ltd. 相似文献
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Sabine Kuss David Polcari Matthias Geissler Daniel Brassard Janine Mauzeroll 《Proceedings of the National Academy of Sciences of the United States of America》2013,110(23):9249-9254
The emergence of resistance to multiple unrelated chemotherapeutic drugs impedes the treatment of several cancers. Although the involvement of ATP-binding cassette transporters has long been known, there is no in situ method capable of tracking this transporter-related resistance at the single-cell level without interfering with the cell’s environment or metabolism. Here, we demonstrate that scanning electrochemical microscopy (SECM) can quantitatively and noninvasively track multidrug resistance-related protein 1–dependent multidrug resistance in patterned adenocarcinoma cervical cancer cells. Nonresistant human cancer cells and their multidrug resistant variants are arranged in a side-by-side format using a stencil-based patterning scheme, allowing for precise positioning of target cells underneath the SECM sensor. SECM measurements of the patterned cells, performed with ferrocenemethanol and [Ru(NH3)6]3+ serving as electrochemical indicators, are used to establish a kinetic “map” of constant-height SECM scans, free of topography contributions. The concept underlying the work described herein may help evaluate the effectiveness of treatment administration strategies targeting reduced drug efflux. 相似文献
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Shahar Shmuel PhD Virginia Pate MS Marc J. Pepin PharmD BCPS BCGP Janine C. Bailey PharmD BCPS Yvonne M. Golightly PT MS PhD Laura C. Hanson MD MPH Til Stürmer MD MPH PhD Rebecca B. Naumann PhD Danijela Gnjidic PhD Jennifer L. Lund PhD 《Journal of the American Geriatrics Society》2021,69(11):3212-3224
56.
Practitioner Review: Pathways to care for ADHD – a systematic review of barriers and facilitators 下载免费PDF全文
57.
Asynchronism and right ventricular pacing 总被引:2,自引:0,他引:2
Thambo JB Bordachar P Lafitte S Crepin D Garrigue S Reuter S Roudaut R Haïssaguerre M Clementy J Jimenez M 《Archives des maladies du coeur et des vaisseaux》2005,98(5):519-523
In patients with congenital heart block (CHB), dual-chamber pacing restores physiological heart rate and atrio-ventricular synchronization. However, patients with narrow QRS junctional escape rhythm may be deleteriously affected by long-term, permanent, apical ventricular pacing. We assessed the impact of apical ventricular pacing on echocardiographic ventricular dyssynchrony and hemodynamic parameters. METHODS: Fourteen CHB adults (23 +/- years, 58% male), with a DDD transvenous pacemaker and a junctional escape rhythm (QRS<120 ms) before implantation, were studied. Echocardiography coupled with tissue Doppler imaging (TDI) and Strain rate was performed in spontaneous rhythm (VVI mode 30/mn) and during atrio-synchronized ventricular pacing. RESULTS: The heart rate (43 +/- 09 vs 68 +/- 07: p<0.01), cardiac output (2.9 +/- 0.7 vs 3.7 +/- 0.6 L/min) and left ventricular filling time (325 +/- 38 vs 412 +/- 51 ms; p<0.01) were significantly less in the escape spontaneous rhythm compared with atrio-ventricular synchronized apical pacing. However, interventricular dyssynchrony (28 +/- 12 vs 59 +/- 25 ms, p<0.05), intra-left ventricular dyssynchrony (36 +/- 11 vs 57 +/- 29 ms; p<0.05), extent of left ventricular myocardium displaying delayed longitudinal contraction (26 +/- 10 vs 39 +/- 17%: p<0.05) were significantly less in the escape rhythm compared with paced rhythm. CONCLUSION: Once implanted with a DDD pacemaker, CHB patients present with increased cardiac output secondary to the restoration of physiological heart rate and improved diastolic function. However, the apical site is not optimal, as it creates detrimental ventricular dyssynchrony in patients with previous nearly physiological ventricular activation. Alternative pacing sites should be investigated. 相似文献
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The insulin-like growth factor I receptor (IGF-IR) is expressed in many cell types and is critical for normal growth and development.
In the healthy mammary gland, the role of IGF-IR is not fully elucidated. However, IGF-IR, which is primarily expressed in
the mammary epithelial cells, is known to play an obligatory role in cellular transformation, facilitating the progression
to breast cancer. We have utilized the tetracycline regulatory (tet-on) system to generate an in vitro model system to allow
us to further investigate IGF-I/IGF-IR function in mammary epithelial cells. A plasmid construct containing a mutant IGF-I
receptor (IGF-IR-DN) fused to the tetracycline operator (tetOPhCMV-IGF-IR-DN) was stably transfected into MCF-7 human breast cancer cells. The conditional regulation of the IGF-IR-DN gene
expression was studied in four independent clonal lines. The translated IGF-IR-DN protein was detected only in the stably
transfected doxycycline-induced cells, and its expression was up-regulated (three- to sixfold) following induction. IGF-I
stimulated cell proliferation diminished (twofold) in doxycycline-induced cells compared to uninduced cells, demonstrating
that the transgene construct was functional and ruling out any pleiotropic effect that may be attributed to doxycycline. Interestingly,
autophosphorylation of the IGF-IR and phosphorylation of the downstream substrate, insulin receptor substrate-1 (IRS-1), was
not inhibited in doxycycline/IGF-I treated cells, suggesting the possibility that activation of downstream substrates other
than the IRS-1 may be critical for optimal cell proliferation. This novel in vitro model should allow us to more directly
examine the role of IGF-I/IGF-IR signaling and function in mammary epithelial cells. 相似文献
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