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281.
One type of ion-sensitive micro-electrode (K+ ligand Corning 477317) is sensitive to large quaternary ammonium ions such as choline or tetramethylammonium (TMA+). We have now used such electrodes for continuous electrophysiological measurements of changes in cell volume of motoneurons in the isolated frog spinal cord. The electrodes were double-barrelled with tip diameters of 1 m. The reference barrel was filled with 100 mM choline or 100 mM TMA+ in 1 M Mg2+-acetate, the sensitive barrel contained the Corning K+ ligand. After the impalement of a motoneuron, choline or TMA+ diffused into the cell and about 1 h later, a steady-state concentration of these ions in the range of 10–20 mM was reached. Following this period, the motoneurons were activated by repetitive electrical stimulation or by application of amino acids via the bathing solution. All these stimuli led to a transient rise of the intracellular concentrations of choline or TMA+ (indicating a cell shrinkage of 3–10% difference to control volume). 相似文献
282.
Derek M. Miller Cliff S. Klein Nina L. Suresh William Z. Rymer 《Clinical neurophysiology》2014,125(10):2070-2078
Objective
Indirect evidence suggests that lateralized changes in motoneuron behavior post-stroke are potentially due to a depolarizing supraspinal drive to the motoneuron pool, but the pathways responsible are unknown. In this study, we assessed vestibular evoked myogenic potentials (VEMPs) in the neck muscles of hemispheric stroke survivors with contralesional spasticity to quantify the relative levels of vestibular drive to the spastic-paretic and contralateral motoneuron pools.Methods
VEMPs were recorded from each sternocleidomastoid muscle in chronic stroke survivors. Side-to-side differences in cVEMP amplitude were calculated and expressed as an asymmetry ratio, a proxy for the relative amount of vestibular drive to each side.Results
Spastic-paretic VEMPs were larger than contralateral VEMPs in 13/16 subjects. There was a strong positive relationship between the degree of asymmetry and the severity of spasticity in this subset of subjects. Remaining subjects had larger contralateral responses.Conclusion
Vestibular drive to cervical motoneurons is asymmetric in spastic stroke survivors, supporting our hypothesis that there is an imbalance in descending vestibular drive to motoneuron pools post-stroke. We speculate this imbalance is a consequence of the unilateral disruption of inhibitory corticobulbar projections to the vestibular nuclei.Significance
This study sheds new light on the underlying mechanisms of post-stroke spasticity. 相似文献283.
Amyotrophic lateral sclerosis (ALS; Lou Gehrig's disease) is a progressive debilitating neurodegenerative disease with no cure. We propose a novel molecular model for the pathogenesis of ALS that involves an adenosine triphosphate (ATP)-dependent muscle neuronal lactate shuttle (MNLS) at the neuromuscular junction (NMJ) to regulate the flow of lactate from muscle to neurons and vice versa. Failure of the MNLS due to respiratory chain dysfunction is proposed to result in lactate toxicity and degeneration of nerve endings at the NMJ leading to nerve terminus dysjunction from the muscle cell. At a critical threshold where denervation outpaces reinnervation, a vicious cycle is established where the remaining innervated muscle fibers are required to work harder to compensate for normal function, and in so doing produce toxic lactate concentrations which induces further denervation and neuronal death. This mechanism explains the exponential progression of ALS leading to paralysis. The molecular events leading to the dysregulation of the MNLS and the dismantling of NMJ are explained in the context of known ALS familial mutations and age-related endocrine dyscrasia. Combination drug therapies that inhibit lactate accumulation at the NMJ, enhance respiratory chain function, and/or promote reinnervation are predicted to be effective therapeutic strategies for ALS. 相似文献
284.
285.
Jivan S Novikova LN Wiberg M Novikov LN 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》2006,170(2):245-254
It has been proposed clinically that delayed surgery after traumatic brachial plexus injury may adversely affect functional
outcome. In the present experimental study the neuroprotective and growth-promoting effects of early and delayed nerve grafting
following proximal seventh cervical spinal nerve (C7) axotomy were examined. The ventral branch of C7 spinal nerve was transected
and axons projecting out of the proximal nerve stump were labelled with Fast Blue (FB). At the same time, the biceps brachii
muscle was denervated by transecting the musculocutaneous nerve at its origin. Neuronal survival and muscle atrophy were then
assessed at 1, 4, 8 and 16 weeks after permanent axotomy. In the experimental groups, a peripheral nerve graft was interposed
between the transected C7 spinal nerve and the distal stump of the musculocutaneous nerve at 1 week [early nerve repair (ENR)]
or 8 weeks [delayed nerve repair (DNR)] after axotomy. Sixteen weeks after nerve repair had been performed, a second tracer
Fluoro-Ruby (FR) was applied distal to the graft to assess the efficacy of axonal regeneration. Counts of FB-labelled neurons
revealed that axotomy did not induce any significant cell loss at 4 weeks, but 15% of motoneurons and 32% of sensory neurons
died at 8 weeks after injury. At 16 weeks, the amount of cell loss in spinal cord and dorsal root ganglion (DRG) reached 29
and 50%, respectively. Both ENR and DNR prevented retrograde degeneration of spinal motoneurons and counteracted muscle atrophy,
but failed to rescue sensory neurons. Due to substantial cell loss at 8 weeks, the number of FR-labelled neurons after DNR
was significantly lower when compared to ENR. However, the proportion of regenerating neurons among surviving motoneurons
and DRG neurons remained relatively constant indicating that neurons retained their regenerative capacity after prolonged
axotomy. The results demonstrate that DNR could protect spinal motoneurons and reduce muscle atrophy, but had little effect
on sensory DRG neurons. However, the efficacy of neuroprotection and axonal regeneration will be significantly affected by
the amount of cell loss already presented at the time of nerve repair. 相似文献