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1  the result of impaired axonal transport and perikaryal accumulation in the large neuron sub-populati
2 rt into and along axons, resulting in severe perikaryal accumulation of neurofilaments and proximal a
3 aluminum neurotoxicity is accompanied by the perikaryal accumulation of tangles of phosphorylated neu
4 erosis (ALS), motor neurons contain abnormal perikaryal accumulations of phosphorylated neurofilament
5 d neurons that displayed increased p-NF-H in perikaryal accumulations that colocalized with Pin1 and
6 n proximity ligation assay labels very early perikaryal aggregates in morphologically intact neurons
7                                     Multiple perikaryal aggregates were present in almost all cortica
8 uminum impairs axonal transport and promotes perikaryal aggregation.
9 n induces deregulated Cdk5 hyperactivity and perikaryal aggregations of hyperphosphorylated Tau and n
10 logical conditions can involve both neuronal perikaryal and axonal damage, yet considerably less is k
11 es immunoreactive (IR) for PARV and NPY were perikaryal and dendritic and found within the infragranu
12                                              Perikaryal and dendritic labeling was mostly intracellul
13 s, specifically accumulation and bundling of perikaryal and dendritic neurofilaments.
14 sions in NADPH-diaphorase neurons, with less perikaryal and neuropil aggregation.
15                In the pons and medulla, both perikaryal and neuropil labeling were observed.
16 consistent with actions on GnRH-1 neurons at perikaryal and/or terminal levels.
17 tic abnormalities persisted and motor neuron perikaryal atrophy had appeared.
18 olabeling was found within the thin shell of perikaryal cytoplasm that contained the usual organelles
19 tributions: QKI-6 and QKI-7 are localized to perikaryal cytoplasm, whereas QKI-5 invariably is restri
20 se-dependent increase in myelin and neuronal perikaryal damage.
21                                          The perikaryal diameters and lengths of the immunoreactive d
22                                     The mean perikaryal diameters and median summed lengths of dendri
23                      In contrast, nuclear or perikaryal huntingtin aggregates were present in less th
24 ystin LR (mLR), or fostriecin (Fos) leads to perikaryal hyperphosphorylation of NF.
25 cause of the effects of NGF on memory is not perikaryal hypertrophy per se but rather an increased de
26 nsity of terminals, which always accompanies perikaryal hypertrophy.
27 y using affinity-purified antisera, we found perikaryal labeling was diffuse and/or punctate; immunor
28                                        Light perikaryal labeling was found in other areas of the brai
29 disease, BC200 RNA often assumed a clustered perikaryal localization, indicating that dendritic loss
30 nin-a2 interaction resulted in altered MAP1B perikaryal localization, leading to MT deacetylation and
31 ture of the glial and axonal coverage of the perikaryal membrane and the somatic spines in the MePD o
32 up) showed that the rat MePD has most of the perikaryal membrane covered by glial processes and a rel
33                       The percentage of GnRH perikaryal membrane occupied by synaptic density in the
34        Differences in the percentage of GnRH perikaryal membrane occupied by synaptic density were no
35 ty of somatic spines along the length of the perikaryal membrane was higher in the late proestrus tha
36  dephosphorylation by aluminum would promote perikaryal NF phosphorylation and foster precocious phos
37                          Thus, while neither perikaryal nor axonal neurofilaments are essential for S
38 size nor morphological traits of NPY-labeled perikaryal or dendritic profiles from lesioned compared
39                       Steady-state levels of perikaryal phospho-NF immunoreactivity are reduced and t
40 transport into axonal neurites and increased perikaryal phospho-NF immunoreactivity.
41          The H(2)O(2) and heat shock induced perikaryal phospho-NF-H accumulations, and neuronal apop
42 ibition of Pin1 inhibits OA-induced aberrant perikaryal phosphorylation of NF.
43 presynaptic component, and layer 6 displayed perikaryal postsynaptic staining, suggesting that cortic
44   These active kinases distributed mainly in perikaryal regions of neurons.
45 en these two corticostriatal neuron types in perikaryal size and laminar location in the cortex, and
46  their laminar location in the cortex, their perikaryal size, and the morphology of their intrastriat
47 eurons and a 28% increase in dopamine neuron perikaryal size.
48         Very few pyramidal neurons exhibited perikaryal staining.

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