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