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81.
Postmortem brain loss of reelin is noted in schizophrenia patients. Accordingly, heterozygous reeler mutant mice have been proposed as a putative model of this disorder. Little is known, however, about the involvement of the two receptors for reelin, Very-Low-Density Lipoprotein Receptor (VLDLR) and Apolipoprotein E Receptor 2 (ApoER2), on pre-cognitive processes of relevance to deficits seen in schizophrenia. Thus, we evaluated sensorimotor gating in mutant mice heterozygous or homozygous for the two reelin receptors. Mutant mice lacking one of these reelin receptors were tested for prepulse inhibition (PPI) of the acoustic startle reflex prior to and following puberty, and on a crossmodal PPI task, involving the presentation of acoustic and tactile stimuli. Furthermore, because schizophrenia patients show increased sensitivity to N-methyl-d-aspartate (NMDA) receptor blockade, we assessed the sensitivity of these mice to the PPI-disruptive effects of the NMDA receptor antagonist phencyclidine. The results demonstrated that acoustic PPI did not differ between mutant and wildtype mice. However, VLDLR homozygous mice displayed significant deficits in crossmodal PPI, while ApoER2 heterozygous and homozygous mice displayed significantly increased crossmodal PPI. Both ApoER2 and VLDLR heterozygous and homozygous mice exhibited greater sensitivity to the PPI-disruptive effects of phencyclidine than wildtype mice. These results indicate that partial or complete loss of either one of the reelin receptors results in a complex pattern of alterations in PPI function that includes alterations in crossmodal, but not acoustic, PPI and increased sensitivity to NMDA receptor blockade. Thus, reelin receptor function appears to be critically involved in crossmodal PPI and the modulation of the PPI response by NMDA receptors. These findings have relevance to a range of neuropsychiatric disorders that involve sensorimotor gating deficits, including schizophrenia. 相似文献
82.
Matta SG Balfour DJ Benowitz NL Boyd RT Buccafusco JJ Caggiula AR Craig CR Collins AC Damaj MI Donny EC Gardiner PS Grady SR Heberlein U Leonard SS Levin ED Lukas RJ Markou A Marks MJ McCallum SE Parameswaran N Perkins KA Picciotto MR Quik M Rose JE Rothenfluh A Schafer WR Stolerman IP Tyndale RF Wehner JM Zirger JM 《Psychopharmacology》2007,190(3):269-319
Rationale This review provides insight for the judicious selection of nicotine dose ranges and routes of administration for in vivo
studies. The literature is replete with reports in which a dosaging regimen chosen for a specific nicotine-mediated response
was suboptimal for the species used. In many cases, such discrepancies could be attributed to the complex variables comprising
species-specific in vivo responses to acute or chronic nicotine exposure.
Objectives This review capitalizes on the authors’ collective decades of in vivo nicotine experimentation to clarify the issues and to
identify the variables to be considered in choosing a dosaging regimen. Nicotine dose ranges tolerated by humans and their
animal models provide guidelines for experiments intended to extrapolate to human tobacco exposure through cigarette smoking
or nicotine replacement therapies. Just as important are the nicotine dosaging regimens used to provide a mechanistic framework
for acquisition of drug-taking behavior, dependence, tolerance, or withdrawal in animal models.
Results Seven species are addressed: humans, nonhuman primates, rats, mice, Drosophila, Caenorhabditis elegans, and zebrafish. After an overview on nicotine metabolism, each section focuses on an individual species, addressing issues
related to genetic background, age, acute vs chronic exposure, route of administration, and behavioral responses.
Conclusions The selected examples of successful dosaging ranges are provided, while emphasizing the necessity of empirically determined
dose–response relationships based on the precise parameters and conditions inherent to a specific hypothesis. This review
provides a new, experimentally based compilation of species-specific dose selection for studies on the in vivo effects of
nicotine. 相似文献
83.
Nicotine appears to enhance attention, while nicotine withdrawal leads to attentional deficits in humans that are ameliorated with nicotine administration. However, there has been much debate as to whether nicotine improves performance under baseline conditions, or only ameliorates attentional deficits. Thus, we studied the effects of acute and chronic nicotine administration and nicotine withdrawal on attentional performance in the 5-choice serial reaction time task (5-CSRTT) in Wistar and Sprague Dawley (SD) rats under baseline conditions. Wistar rats performed with higher accuracy compared to SD rats. Acute nicotine administration induced small increases in accuracy and correct responses, impulsivity and speed of responding, and decreases in omission errors. These effects were more pronounced in less accurate rats or after task modifications were implemented to disrupt the rats' performance. Chronic nicotine administration via minipumps consistently increased accuracy during days 4-6 of nicotine infusion after the effect of nicotine on impulsivity during days 1-3 dissipated. By contrast, nicotine withdrawal induced decreases in correct responses, and increases in omissions and latencies to respond, but had no effect on accuracy. These results provide evidence that chronic, but not acute, nicotine administration induced accuracy improvement under baseline conditions, while nicotine withdrawal produced some limited performance deficits. 相似文献
84.
Shankaran S Pappas A McDonald SA Laptook AR Bara R Ehrenkranz RA Tyson JE Goldberg R Donovan EF Fanaroff AA Das A Poole WK Walsh M Higgins RD Welsh C Salhab W Carlo WA Poindexter B Stoll BJ Guillet R Finer NN Stevenson DK Bauer CR;Eunice Kennedy Shriver National Institute of Child Health Human Development Neonatal Research Network 《Pediatrics》2011,128(1):e112-e120
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