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71.
The basal ganglia are a complex neuronal system that is impaired in several movement disorders, including Parkinson's disease, Huntington's disease, and dystonia. Empirical studies have provided valuable insights into the brain dysfunctions underlying these disorders. The systems‐level perspective, however, of how patients' motor, cognitive, and emotional impairments originate from known brain dysfunctions has been a challenge to empirical investigations. These causal relations have been analyzed via computational modeling, a method that describes the simulation of interacting brain processes in a computer system. In this article, we review computational insights into the brain dysfunctions underlying Parkinson's disease, Huntington's disease, and dystonia, with particular foci on dysfunctions of the dopamine system, basal ganglia pathways, and neuronal oscillations. © 2016 International Parkinson and Movement Disorder Society 相似文献
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Introduction: A conditioning volley to the ipsilateral tibial nerve (iTN) inhibits contralateral soleus (cSOL) electromyographic activity at latencies of 37–41 ms. This is evidence for spinal muscular communication in opposing limbs. The aim of our study was to determine whether the cSOL H‐reflex would be inhibited in a similar manner. Methods: Thirteen subjects participated in two experiments: (1) stimuli delivered to the iTN at 85% of the maximal peak‐to‐peak M‐wave (85% M‐max) with a pre‐contracted cSOL; (2) 510 stimuli delivered at 85% M‐max to the iTN with a test volley delivered to the contralateral tibial nerve at interstimulus intervals of ?6 to 100 ms. Results: Significant inhibition was observed in the cSOL H‐reflex when conditioning stimuli were delivered 3–33 ms before the test H‐reflex. Conclusions: The activity of this spinal pathway can be quantified using H‐reflex conditioning to provide a controlled model for further studies of this response. Muscle Nerve, 2011 相似文献
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Burnat K Van Der Gucht E Waleszczyk WJ Kossut M Arckens L 《The Journal of comparative neurology》2012,520(11):2414-2429
Binocular deprivation of pattern vision (BD) early in life permanently impairs global motion perception. With the SMI-32 antibody against neurofilament protein (NFP) as a marker of the motion-sensitive Y-cell pathway (Van der Gucht et al. [2001] Cereb. Cortex 17:2805-2819), we analyzed the impact of early BD on the retinal circuitry in adult, perceptually characterized cats (Burnat et al. [2005] Neuroreport 16:751-754). In controls, large retinal ganglion cells exhibited a strong NFP signal in the soma and in the proximal parts of the dendritic arbors. The NFP-immunoreactive dendrites typically branched into sublamina a of the inner plexiform layer (IPL), i.e., the OFF inner plexiform sublamina. In the retina of adult BD cats, however, most of the NFP-immunoreactive ganglion cell dendrites branched throughout the entire IPL. The NFP-immunoreactive cell bodies were less regularly distributed, often appeared in pairs, and had a significantly larger diameter compared with NFP-expressing cells in control retinas. These remarkable differences in the immunoreactivity pattern were typically observed in temporal retina. In conclusion, we show that the anatomical organization typical of premature Y-type retinal ganglion cells persists into adulthood even if normal visual experience follows for years upon an initial 6-month period of BD. Binocular pattern deprivation possibly induces a lifelong OFF functional domination, normally apparent only during development, putting early high-quality vision forward as a premise for proper ON-OFF pathway segregation. These new observations for pattern-deprived animals provide an anatomical basis for the well-described motion perception deficits in congenital cataract patients. 相似文献
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Fernando Pea Benito Ordaz Hugo Balleza‐Tapia Ramn Bernal‐Pedraza Abraham Mrquez‐Ramos Liliana Carmona‐Aparicio Magda Giordano 《Hippocampus》2010,20(1):78-96
Early cognitive deficit characteristic of early Alzheimer's disease seems to be produced by the soluble forms of β‐amyloid protein. Such cognitive deficit correlates with neuronal network dysfunction that is reflected as alterations in the electroencephalogram of both Alzheimer patients and transgenic murine models of such disease. Correspondingly, recent studies have demonstrated that chronic exposure to βAP affects hippocampal oscillatory properties. However, it is still unclear if such neuronal network dysfunction results from a direct action of βAP on the hippocampal circuit or it is secondary to the chronic presence of the protein in the brain. Therefore, we aimed to explore the effect of acute exposure to βAP25–35 on hippocampal network activity both in vitro and in vivo, as well as on intrinsic and synaptic properties of hippocampal neurons. We found that βAP25–35, reversibly, affects spontaneous hippocampal population activity in vitro. Such effect is not produced by the inverse sequence βAP35–25 and is reproduced by the full‐length peptide βAP1–42. Correspondingly βAP25–35, but not the inverse sequence βAP35–25, reduces theta‐like activity recorded from the hippocampus in vivo. The βAP25–35‐induced disruption in hippocampal network activity correlates with a reduction in spontaneous neuronal activity and synaptic transmission, as well as with an inhibition in the subthreshold oscillations produced by pyramidal neurons in vitro. Finally, we studied the involvement of Fyn‐kinase on the βAP25–35‐induced disruption in hippocampal network activity in vitro. Interestingly, we found that such phenomenon is not observed in slices obtained from Fyn‐knockout mice. In conclusion, our data suggest that βAP acutely affects proper hippocampal function through a Fyn‐dependent mechanism. We propose that such alteration might be related to the cognitive impairment observed, at least, during the early phases of Alzheimer's disease. © 2009 Wiley‐Liss, Inc. 相似文献
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Khaleel A. Razak Terese Zumsteg Zoltan M. Fuzessery 《The Journal of comparative neurology》2009,515(2):231-242
Auditory thalamocortical connections are organized as parallel pathways originating in various nuclei of the medial geniculate body (MGB). The development of these pathways has not been studied. Therefore it remains unclear whether thalamocortical connections segregate before the onset of hearing or whether refinement of exuberant thalamocortical connections occurs following hearing onset. We studied this issue in the pallid bat. In adult pallid bats, parallel thalamocortical pathways represent two different sounds used in two different behaviors. The suprageniculate (SG) nucleus of the dorsal division of the MGB (MGBd) projects to a high‐frequency cortical region selective for the echolocation calls, but not to a low‐frequency cortical region sensitive to noise transients used in the localization of prey. Conversely, the ventral division (MGBv) projects to the low‐frequency, but not the high‐frequency, cortical region. Here we studied the development of these parallel pathways. Based on retrograde tracer injections in electrophysiologically characterized cortical loci, we show that there is an asymmetrical overlap in projection patterns from postnatal (P) day 15–60. The low‐frequency region receives extensive input from both the SG and the MGBv. In contrast, the high‐frequency region receives the great majority of its input from the SG, as in adults, whereas projections from the MGBv appear to make only a minor contribution, if any. By P150, these pathways are segregated and adult‐like. These data suggest that these anatomically segregated pathways arise through postnatal refinement of initially overlapping connections. J. Comp. Neurol. 515:231–242, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
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The efferent association fibers from the caudal part of the prefrontal cortex to posterior cortical areas course via several pathways: the three components of the superior longitudinal fasciculus (SLF I, SLF II, and SLF III), the arcuate fasciculus (AF), the fronto-occipital fasciculus (FOF), the cingulate fasciculus (CING F), and the extreme capsule (Extm C). Fibers from area 8Av course via FOF and SLF II, merging in the white matter of the inferior parietal lobule (IPL) and terminating in the caudal intraparietal sulcus (IPS). A group of these fibers turns ventrally to terminate in the caudal superior temporal sulcus (STS). Fibers from the rostral part of area 8Ad course via FOF and SLF II to the IPS and IPL and via the AF to the caudal superior temporal gyrus and STS. Some fibers from the rostral part of area 8Ad are conveyed to the medial parieto-occipital region via FOF, to the STS via Extm C, and to the caudal cingulate gyrus via CING F. Fibers from area 8B travel via SLF I to the supplementary motor area and area 31 in the caudal dorsal cingulate region and via the CING F to cingulate areas 24 and 23 and the cingulate motor areas. Fibers from area 9/46d course via SLF I to the superior parietal lobule and medial parieto-occipital region, via SLF II to the IPL. Fibers from area 9/46v travel via SLF III to the rostral IPL and the frontoparietal opercular region and via the CING F to the cingulate gyrus. 相似文献