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1 uding causes such as axonal degeneration and retrograde degeneration.
2 ing axon protection in these acute models of retrograde degeneration.
3 d 90% of beta retinal ganglion cells die via retrograde degeneration.
4 reas undergoing secondary anterograde and/or retrograde degeneration.
5 nt with a shared mechanism for Wallerian and retrograde degeneration.
6 of eyes with optic neuritis, suggesting that retrograde degeneration after optic neuritis may not ext
7 s, a surviving intact branch suppresses both retrograde degeneration and regeneration of the injured
9 eing clarified in rodent models, focusing on retrograde degeneration following axonal damage, excitot
10 in this subtype than may be expected due to retrograde degeneration from either typical clinical or
11 nucleus; and (b) the lesions did not induce retrograde degeneration nor diminution of Fos label in t
13 lammatory process results in anterograde and retrograde degeneration of axons, leading to the tempora
14 Transection of the fimbria fornix leads to retrograde degeneration of axotomised septal cholinergic
18 e is experimental evidence of trans-synaptic retrograde degeneration of retinal ganglion cells follow
19 ization of visual pathways, including severe retrograde degeneration of retinal ganglion cells of the
21 tinal anatomy suggests that MME is caused by retrograde degeneration of the inner retinal layers, res
24 mary retinal neuronopathy, in the absence of retrograde degeneration of the retinal nerve fibre layer
25 r to assess the time course of Wallerian and retrograde degeneration of unmyelinated retinal ganglion
26 t require a separate intervention to prevent retrograde degeneration of upper motoneurons in the cort
28 in actively demyelinating cortical lesions, retrograde degeneration was mainly related to demyelinat
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