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81.
Kathrin Edelmann Lena Glashauser Susanne Sprungala Birgit Hesl Maike Fritschle Jovica Ninkovic Leanne Godinho Prisca Chapouton 《The Journal of comparative neurology》2013,521(13):3099-3115
The zebrafish has recently become a source of new data on the mechanisms of neural stem cell (NSC) maintenance and ongoing neurogenesis in adult brains. In this vertebrate, neurogenesis occurs at high levels in all ventricular regions of the brain, and brain injuries recover successfully, owing to the recruitment of radial glia, which function as NSCs. This new vertebrate model of adult neurogenesis is thus advancing our knowledge of the molecular cues in use for the activation of NSCs and fate of their progeny. Because the regenerative potential of somatic stem cells generally weakens with increasing age, it is important to assess the extent to which zebrafish NSC potential decreases or remains unaltered with age. We found that neurogenesis in the ventricular zone, in the olfactory bulb, and in a newly identified parenchymal zone of the telencephalon indeed declines as the fish ages and that oligodendrogenesis also declines. In the ventricular zone, the radial glial cell population remains largely unaltered morphologically but enters less frequently into the cell cycle and hence produces fewer neuroblasts. The neuroblasts themselves do not change their behavior with age and produce the same number of postmitotic neurons. Thus, decreased neurogenesis in the physiologically aging zebrafish brain is correlated with an increasing quiescence of radial glia. After injuries, radial glia in aged brains are reactivated, and the percentage of cell cycle entry is increased in the radial glia population. However, this reaction is far less pronounced than in younger animals, pointing to irreversible changes in aging zebrafish radial glia. J. Comp. Neurol. 521: 3099–3115, 2013. © 2013 Wiley Periodicals, Inc. 相似文献
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Julia Lechinger Kathrin Bothe Gerald Pichler Gabriele Michitsch Johann Donis Wolfgang Klimesch Manuel Schabus 《Journal of neurology》2013,260(9):2348-2356
Patients suffering from disorders of consciousness still present a diagnostic challenge due to the fact that their assessment is mainly based on behavioral scales with their motor responses often being strongly impaired. We therefore focused on resting electroencephalography (EEG) in order to reveal potential alternative measures of the patient’s current state independent of rather complex abilities (e.g., language comprehension). Resting EEG was recorded in nine minimally conscious state (MCS) and eight vegetative state/unresponsive wakefulness syndrome (VS/UWS) patients. Behavioral assessments were conducted using the Coma-Recovery Scale—Revised (CRS-R). The signal was analyzed in the frequency domain and association between resting EEG and CRS-R score as well as clinical diagnosis were calculated using Pearson correlation and repeated-measures ANOVAs. The analyses revealed robust positive correlations between CRS-R score and ratios between frequencies above 8 Hz and frequencies below 8 Hz. Furthermore, the frequency of the spectral peak was also highly indicative of the patient’s CRS-R score. Concerning differences between clinical diagnosis and healthy controls, it could be revealed that while VS/UWS patients showed higher delta and theta activity than controls, MCS did not differ from controls in this frequency range. Alpha activity, on the other hand, was strongly decreased in both patient groups as compared to controls. The strong relationship between various resting EEG parameters and CRS-R score provides significant clinical relevance. Not only is resting activity easily acquired at bedside, but furthermore, it does not depend on explicit cooperation of the patient. Especially in cases where behavioral assessment is difficult or ambiguous, spectral analysis of resting EEG can therefore complement clinical diagnosis. 相似文献
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Stefanie Ostermann Marco Herbsleb Steffen Schulz Lars Donath Sandy Berger Daniela Eisentr?ger Tobias Siebert Hans-Josef Müller Christian Puta Andreas Voss Holger W. Gabriel Kathrin Koch Karl-Jürgen B?r 《Schizophrenia bulletin》2013,39(5):1139-1149
Maintaining and improving fitness are associated with a lower risk of premature death from cardiovascular disease. Patients with schizophrenia are known to exercise less and have poorer health behaviors than average. Physical fitness and physiological regulation during exercise tasks have not been investigated to date among patients with schizophrenia. We studied autonomic modulation in a stepwise exhaustion protocol in 23 patients with schizophrenia and in matched controls, using spirometry and lactate diagnostics. Parameters of physical capacity were determined at the aerobic, anaerobic, and vagal thresholds (VT), as well as for peak output. VT was correlated with psychopathology, as assessed by the Positive and Negative Syndrome Scale, with the inflammatory markers IL-1β, IL-6, and TNF-α and with peak output. The MANOVA for heart and breathing rates, as well as for vagal modulation and complexity behavior of heart rate, indicated a profound lack of vagal modulation at all intensity levels, even after the covariate carbon monoxide concentration was introduced as a measure of smoking behavior. Significantly decreased physical capacity was demonstrated at the aerobic, anaerobic, and VT in patients. After the exercise task, reduced vagal modulation in patients correlated negatively with positive symptoms and with levels of IL-6 and TNF-α. This study shows decreased physical capacity in patients with schizophrenia. Upcoming intervention studies need to take into account the autonomic imbalance, which might predispose patients to arrhythmias during exercise. Results of inflammatory parameters are suggestive of a reduced activity of the anti-inflammatory cholinergic pathway in patients, leading to a pro-inflammatory state.Key words: heart rate, physical exercise, respiration, schizophrenia, vagal threshold, cardiac death, inflammation, physical fitness 相似文献
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Julia Patzig Wiebke Möbius Benoit Barrette Tadzio L. Wagner Kathrin Kusch Julia M. Edgar Peter J. Brophy Hauke B. Werner 《Glia》2013,61(11):1832-1847
Deficiency of the major constituent of central nervous system (CNS) myelin, proteolipid protein (PLP), causes axonal pathology in spastic paraplegia type‐2 patients and in Plp1null‐mice but is compatible with almost normal myelination. These observations led us to speculate that PLP's role in myelination may be partly compensated for by other tetraspan proteins. Here, we demonstrate that the abundance of the structurally related tetraspanin‐2 (TSPAN2) is highly increased in CNS myelin of Plp1null‐mice. Unexpectedly, Tspan2null‐mutant mice generated by homologous recombination in embryonic stem cells displayed low‐grade activation of astrocytes and microglia in white matter tracts while they were fully myelinated and showed no signs of axonal degeneration. To determine overlapping functions of TSPAN2 and PLP, Tspan2null*Plp1null double‐mutant mice were generated. Strikingly, the activation of astrocytes and microglia was strongly enhanced in Tspan2null*Plp1null double‐mutants compared with either single‐mutant, but the levels of dysmyelination and axonal degeneration were not increased. In this model, glial activation is thus unlikely to be caused by axonal pathology, and vice versa does not potentiate axonal degeneration. Our results support the concept that multiple myelin proteins have distinct roles in the long‐term preservation of a healthy CNS, rather than in myelination per se. GLIA 2013;61:1832–1847 相似文献
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Qualls Lydia R. Hartmann Kathrin Paulson James F. Wells Nicole Kreiser 《Journal of autism and developmental disorders》2022,52(4):1678-1692
Journal of Autism and Developmental Disorders - Individuals with Autism Spectrum Disorder (ASD) and the Broad Autism Phenotype (BAP) are more likely than individuals with typical development (TD)... 相似文献