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1 jury index, a quantitative representation of axoplasmic and myelinic pathologies, was significantly l
2 to estimate neurotubule density (rho(RNFL)), axoplasmic area (A(x)) mode, axon area (A(a)) mode, slop
3 ope (u) of the number of neurotubules versus axoplasmic area (neurotubule packing density), fractiona
5 wild-type axons induced a dramatic spike in axoplasmic Ca(2+) and termination of mitochondrial movem
7 The results reveal that dramatically higher axoplasmic Ca(2+) levels occur at the sites of axonal sp
9 tion of neuronal anterograde (or retrograde) axoplasmic flow, leading to axonal degeneration, especia
12 ld(S) for the first time in vivo, and higher axoplasmic levels in transgenic mice with Wld(S) redistr
13 d with mitochondria versus synaptic vesicles/axoplasmic matrix reveals significant differences in the
16 xons that lack Na+/K+ ATPase cannot exchange axoplasmic Na+ for K+ and are incapable of nerve transmi
17 ated axons causes sequential deregulation of axoplasmic Na, K and Ca; i.e., an initial influx of Na a
19 Equilibrium density fractionation of motile axoplasmic organelle preparations has revealed that p196
22 orates the cytoplasmic surface of 21% of the axoplasmic organelles, as demonstrated by immunogold ele
23 myosin antibody in Western blots of isolated axoplasmic organelles, has been previously proposed to b
28 rayfish medial giant axon (MGA), we analyzed axoplasmic proteins separately from proteins of the glia
29 PA receptors, release of toxic Ca2+ from the axoplasmic reticulum, overactivation of ionotropic and m
30 or availability of the NE transporter to the axoplasmic side of the membrane, causing massive carrier
33 e known to inhibit neuronal fast anterograde axoplasmic transport (FAAT) in a reversible and dose-dep
35 neurofilament compaction (NFC) and impaired axoplasmic transport (IAT) in distinct populations of ax
36 ong-term effects of infraorbital nerve (ION) axoplasmic transport attenuation with vinblastine on the
37 bre nociceptors following the application of axoplasmic transport blockers (colchicine and vinblastin
39 port, we hypothesized that the disruption of axoplasmic transport by nerve inflammation could cause t
40 e inflammation that causes the disruption of axoplasmic transport in patients with painful conditions
41 e body (MGB) was discovered in the cat using axoplasmic transport methods combined with immunocytoche
44 newly synthesized proteins destined for fast axoplasmic transport pass through the Golgi apparatus.
45 separate series of experiments, the block of axoplasmic transport proximal to a localized neuritis si
46 the latter is dependent exclusively on slow axoplasmic transport to maintain protein mass in a stead
47 icate that although transient attenuation of axoplasmic transport with vinblastine has limited effect
49 Because nerve inflammation also disrupts axoplasmic transport, we hypothesized that the disruptio
52 processing of polypeptides destined for fast axoplasmic transports, the fragmentation of the organell
56 axoplasm isolated from myelinated fibers as axoplasmic whole mounts and delipidated spinal nerve roo
57 of anaesthetized transgenic mice expressing axoplasmic yellow fluorescent protein were stimulated el
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